Q2 2024 Cue Biopharma Inc Earnings Call and Business Update

Operator: Good day and welcome to the Cue Biopharma second quarter 2024 earnings call. All participants will be in a listen only mode.

Operator: Good day and welcome to the Cue Biopharma second quarter 2024 earnings call.

Operator: Good day, and welcome to the Cue Biopharma second quarter 2024 earnings call. All participants will be in a listen-only mode. Should you need assistance, please signal conference specialists by pressing the star key followed by zero.

Good day and welcome to the cue Biopharma second quarter 2024 earnings call. All participants will be in a listen only mode should you need assistance. Please signal conference specialist by pressing the star key followed by zero after.

Operator: All participants will be in a listen only mode.

Operator: Should you need assistance, please signal conference specialists by pressing the star key followed by zero. After today's presentation, there will be an opportunity to ask questions. To ask a question, you may press star then 1 on your touchtone phone.

Operator: Should you need assistance, please signal conference specialists, by pressing the star key followed by zero.

Operator: After today's presentation, there will be an opportunity to ask questions.

Operator: After today's presentation, there will be an opportunity to ask questions. To ask a question, you may press star, then one on your touch-tone phone. And to withdraw your question, please press star, then two. Please note this event is being recorded.

After todays presentation, there will be an opportunity to ask questions to ask a question you May Press Star then one on your Touchtone phone and to withdraw your question. Please press Star then two please.

Operator: To ask a question, you may press star than one on your touchtone phone, and to withdraw your question, please press star than two.

Operator: Please note this event is being recorded.

Speaker Change: Please note. This event is being recorded I would now like to turn the conference over to our Chief Executive Officer. Mr. Danforth Gary. Please go ahead Sir.

Daniel Passeri: I would now like to turn the conference over to our Chief Executive Officer, Mr. Dan Passeri. Please go ahead, sir. Okay, thank you, and good afternoon, everyone. As a reminder, this presentation and discussion is being recorded and will be available on our website for the next 30 days. Also, please be aware that the slides accompanying today's update may be advanced directly by those listening in, and we will notify you on what slide we're on throughout the presentation. Joining me on today's call is Dr. Anish Suri, our President and Chief Scientific Officer, and Dr. Mateo Levisetti, our Chief Medical Officer.

Operator: I would now like to turn the conference over to our chief executive officer,

Operator: And to withdraw your question, please press star then 2. Please note this event is being recorded. I would now like to turn the conference over to our Chief Executive Officer, Mr. Dan Passeri. Please go ahead, sir.

Daniel Passeri: Mr. Dan Passeri, please go ahead, sir.

Daniel Passeri: Okay, thank you and good afternoon, everyone.

Daniel Passeri: Okay, thank you. And good afternoon, everyone. As a reminder, this presentation and discussion is being recorded and will be available on our website for the next 30 days. Also, please be aware that the slides accompanying today's update may be advanced directly by those listening in, and we will notify you on what slide we're on throughout the presentation. Joining me on today's call is Dr. Anish Suri, our President and Chief Scientific Officer, and Dr. Matteo Levisetti, our Chief Medical Officer, are shown here on slide two.

Danforth Gary: Okay. Thank you and good afternoon, everyone.

Daniel Passeri: As a reminder, this presentation and discussion is being recorded, and will be available on our website for the next 30 days.

Speaker Change: As a reminder, this presentation and discussion is being recorded and will be available on our website for the next 30 days.

Daniel Passeri: Also, please be aware that the slides accompanying today's update may be advanced directly, by those listening in and we will notify you on what slide we're on throughout the presentation.

Also please be aware that the slides accompanying today's update may be advanced directly by those listening in.

Speaker Change: And we will notify you on what slide we're on throughout the presentation. Joining me on today's call is Dr. Any Siri, our president and Chief Scientific Officer and Dr material ever said, Hey, our Chief Medical Officer.

Daniel Passeri: Joining me on today's call is Dr. Anish Suri, our president and chief scientific officer,

Daniel Passeri: and Dr. Matteo Levasetti, our chief medical officer.

Daniel Passeri: Shown here on slide two, this presentation and overview may contain some forward-looking, statements and any forward-looking statements made during this call represents the company's views only as of today, August 19th, 2024.

Daniel Passeri: Shown here on slide two.

Speaker Change: Shown here on slide two.

Daniel Passeri: This presentation and overview may contain some forward-looking statements, and any forward-looking statements made during this call represents the company's views only as of today, August 19, 2024. I'd like to begin the call by providing you with some context pertaining to our recent announcement focused upon near-term developments with our autoimmune programs and associated corporate restructuring. I'll begin with a brief synopsis of the objectives underlying these measures, and just to underscore, we carefully assessed our strategic positioning and evaluated various options for optimizing probabilities of success within the challenges and constraints of the current capital market condition.

Daniel Passeri: This presentation and overview may contain some forward-looking statements, and any forward-looking statements made during this call represent the company's views only as of today, August 19, 2024.

Speaker Change: This presentation and overview may contain some forward looking statements in any forward looking statements made during this call represents the company's views only as of today August 19th 2024.

Daniel Passeri: I'd like to begin the call by providing you with some context pertaining to our recent announcement focused upon near-term developments with our autoimmune programs and associated corporate restructuring. I'll begin with a brief synopsis of the objectives underlying these measures, and just to underscore, we carefully assessed our strategic positioning and evaluated various options for optimizing probabilities of success within the challenges and constraints of the current capital market conditions. The measures recently implemented aim to reduce our capital requirements while also achieving enhanced productivity through what we consider to be basically a balanced business model focusing upon accessing capital and additional resources through a series of anticipated strategic partnerships.

Daniel Passeri: I'd like to begin the call by providing you with some context pertaining, to our recent announcement focused upon near-term developments with our autoimmune programs and associated corporate restructuring.

Daniel Passeri: The measures recently implemented aim to reduce our capital requirements while also achieving enhanced productivity through what we consider to be basically a balanced business model focusing upon accessing capital and additional resources through a series of anticipated strategic partnerships. Furthermore, we've taken measures for our clinical data to further mature to enhance competitive positioning, particularly relating to patient survival data, enabling near-term cost savings and delaying the launch of a capital-intensive trial towards registration.

Speaker Change: I'd like to begin the call by providing you with some context pertaining to our recent announcement focused upon near term developments with our autoimmune programs and associated corporate restructuring.

Daniel Passeri: I'll begin with a brief synopsis of the objectives underlying these measures, and just to underscore, we carefully assessed our strategic positioning and evaluated various options for optimizing probabilities of success within the challenges and constraints of the current capital market conditions. The measures recently implemented aim to reduce our capital requirements, while also achieving enhanced productivity through what we consider to be basically a balanced business model focusing upon accessing capital and additional resources through a series of anticipated strategic partnerships.

Speaker Change: I'll begin with a brief synopsis of the objectives unwind. These message these measures.

Speaker Change: And just to underscore we carefully assessed our strategic positioning and evaluated various options for optimizing probabilities of success within the challenges and constraints of the current capital market conditions.

Speaker Change: The measures our recently implemented aimed to reduce our capital requirements, while also achieving enhanced productivity through what we consider to be a.

Speaker Change: Basically our balanced business model, focusing upon accessing capital and additional resources through a series of anticipated strategic partnerships.

Daniel Passeri: Furthermore, we've taken measures for our clinical data to further mature, to enhance competitive positioning, particularly relating to patient survival data, enabling near-term cost savings and delaying the launch of a capital-intensive trial towards registration. This path provides a higher probability of success as more matured businesses, and more mature data should bolster the veracity of our mechanistic advantages for establishing the potential of a new standard of care for cancer patients.

Daniel Passeri: Furthermore, we've taken measures for our clinical data to further mature to enhance competitive positioning, particularly relating to patient survival data, enabling near-term cost savings and delaying the launch of a capital intensive trial towards registration. This path provides a higher probability of success, as more mature data should bolster the veracity of our mechanistic advantages for establishing the potential of a new standard of care for cancer patients.

Speaker Change: Furthermore, we've taken measures for our clinical data to further mature to enhanced competitive positioning, particularly relating to patient survival data, enabling near term cost savings and delaying the launch of a capital intensive trial towards registration.

Daniel Passeri: This path provides a higher probability of success as more mature data should bolster the veracity of our mechanistic advantages for establishing the potential of a new standard of care for cancer patients, as shown in slide number three. We believe we've developed a breakthrough proprietary therapeutic approach, to establish a new standard of care for treating both cancer and autoimmune diseases by restoring immune balance to the patient's immune system. As Matteo will elaborate upon shortly, our data from the ongoing Q101 Phase 1B trial clearly demonstrates evidence of substantial prolongation of survival in patients treated with Q101 monotherapy in the second line plus setting, and emerging data from the combination trial and frontline with Keytruda, as Pembrolizumab, that also appears to be following a similar pattern as what we saw with the monotherapy trial. We believe this data to be quite remarkable, underscoring what we believe to be the true competitive positioning of our approach.

Speaker Change: This past provides a higher probability of success is more mature data should bolster the veracity of our mechanistic advantages for establishing the potential of a new standard of care for cancer patients.

Daniel Passeri: As shown on slide number three, we believe we've developed a breakthrough proprietary therapeutic approach to establish a new standard of care for treating both cancer and autoimmune diseases by restoring immune balance to the patient's immune system. As Mateo will elaborate upon shortly, our data from the ongoing Q101 Phase 1 B trial clearly demonstrates evidence of substantial prolongation of survival in patients treated with Q101 monotherapy in the second line plus setting. and emerging data from the combination trial in frontline with Catrutas, Pembrolyzumab, that also appears to be following a similar pattern, as what we saw with the monotherapy trial.

Daniel Passeri: As shown in slide number three, we believe we've developed a breakthrough proprietary, therapeutic approach to establish a new standard of care for treating both cancer and autoimmune diseases by restoring immune balance to the patient's immune system.

Speaker Change: As shown in slide number three.

Speaker Change: We believe we've developed a breakthrough proprietary therapeutic approach.

Speaker Change: To establish a new standard of care for treating both cancer and autoimmune diseases by restoring immune balance to the patient's immune system.

Daniel Passeri: As Matteo will elaborate upon shortly, our data from the ongoing Q101 phase 1B trial clearly demonstrates evidence of substantial prolongation of survival in patients treated with Q101 monotherapy in the second line plus setting, and emerging data from the combination trial and frontline with Keytruda, that's Pembrolizumab, that also appears to be following a similar pattern as what we saw with the monotherapy trial.

Speaker Change: As Matteo will elaborate upon shortly.

Matteo: Our data from the ongoing Q1 O one phase one b trial.

Speaker Change: Daily demonstrates evidence of substantial prolongation of survival in patients treated with Q1 O. One monotherapy in second line.

Matteo: Plus setting.

Speaker Change: Emerging data from the combination trial in frontline <unk> with.

Speaker Change: With Keytruda September lithium app.

Speaker Change: That also appears to be following a similar pattern as what we saw with the monotherapy trial.

Daniel Passeri: We believe this data to be quite remarkable, underscoring what we believe to be the true competitive positioning of our approach. As such, it's our intention with the measures taken to enable clinical data to further develop and mature in support of our foundational platform, that we believe can induce effective and long-lasting anti-tumor activity, or can be harnessed to rebalance the aberrant immune responses to address autoimmune disease.

Daniel Passeri: We believe this data to be quite remarkable, underscoring what we believe to be the true competitive positioning of our approach.

Speaker Change: We believe this data to be quite remarkable underscoring what we believe to be the true competitive positioning of our approach.

Daniel Passeri: As such, it's our intention, with the measures taken, to enable clinical data to further develop and mature in support of our foundational platform that we believe can induce effective and long-lasting anti-tumor activity or can be harnessed to rebalance the aberrant immune responses to address autoimmune disease. We've also made significant progress with our lead autoimmune disease program, Q401, being developed in collaboration with our partner Ono Pharmaceutical to address multiple autoimmune and inflammatory diseases such as rheumatoid arthritis, graft-versus-host disease, lupus, inflammatory bowel disease, psoriasis, multiple sclerosis, amongst others, representing large, multi-billion dollar market potential addressing significant unmet medical needs. Through this partnership, we've made impressive progress to date in moving towards selection of a lead candidate, which we anticipate in the first quarter of the coming year.

Daniel Passeri: As such, it's our intention, with the measures taken, to enable clinical data to further develop and mature in support of our foundational platform that we believe can induce effective and long-lasting anti-tumor activity, or can be harnessed to rebalance the aberrant immune responses to address autoimmune disease.

Speaker Change: As such it's our intention with the measures taken to enable clinical data to further develop and mature in support of our foundational platform that we believe can induce effective and long lasting anti tumor activity or it can be harnessed to rebalance the aberrant immune responses to address autoimmune disease.

Speaker Change: Yeah.

Daniel Passeri: We've also made significant progress with our lead autoimmune disease program Q401, being developed in collaboration with our partner, Ono Pharmaceutical, to address multiple autoimmune and inflammatory diseases, such as rheumatoid arthritis, graft-versus-host disease, lupus, inflammatory bowel disease, psoriasis, and multiple sclerosis, amongst others, representing large multi-billion dollar market potential, addressing significant unmet medical need. Through this partnership, we've made impressive progress to date and are moving towards selection of a lead candidate, which we anticipate in the first quarter of the coming year. Our collaboration with Ono has been highly productive and supportive, resulting in a growing body of promising data, demonstrating the ability of Q401 to generate and expand regulatory T-cells, or T-regs, fostering disease control, and several disease models tested to date.

Daniel Passeri: We've also made significant progress, with our lead autoimmune disease program, Q401, being developed in collaboration with our partner, Ono Pharmaceutical, to address multiple, autoimmune and inflammatory diseases, such as rheumatoid arthritis, graft-versus-host disease, lupus, inflammatory bowel disease, psoriasis, multiple sclerosis, amongst others, representing large, multibillion-dollar market potential, addressing significant unmet medical need. Through this partnership, we've made, impressive progress to date, and moving towards selection of a lead candidate, which we anticipate in the first quarter of the coming year.

Speaker Change: We've also made significant progress with our lead autoimmune disease program Q4 O one.

Speaker Change: Being developed in collaboration with our partner Ono pharmaceutical to address multiple autoimmune and inflammatory diseases, such as rheumatoid arthritis.

Speaker Change: Graft versus host disease.

Speaker Change: Lucas inflammatory bowel disease, psoriasis psoriasis multiple sclerosis, amongst others, representing large multibillion dollar market potential addressing significant unmet medical need.

Speaker Change: Through this partnership we've made impressive progress to date and moving towards selection of a lead candidate, which we anticipate in the first quarter of the coming year.

Daniel Passeri: Our collaboration with Ono has been highly productive and supportive, resulting in a growing body of promising data demonstrating the ability of Q401. To generate and expand regulatory T-cells are Tregs fostering disease control in several disease models tested to date. As a reminder, Cue Biopharma has retained an option to a 50% U.S. co-development, co-marketing right to Q401. Turning to 501, this program continues to advance and progress forward with the potential of, eliminating autoreactive B-cells with a highly selective and well-tolerated biologic, program has the promise of addressing multiple B-cell mediated autoimmune diseases, such as lupus, myasthenia gravis.

Daniel Passeri: Our collaboration with Ono has been, highly productive and supportive, resulting in a growing body of promising data demonstrating the ability of Q401 to generate and expand regulatory T-cells, or Tregs, fostering disease control in several disease models tested to date. As a reminder, Q Biopharma has retained an option, to a 50% U.S. co-development, co-marketing right to Q401.

Speaker Change: Our collaboration with Ono has been highly productive and supportive.

Speaker Change: Resulting in a growing body of promising data demonstrating the ability of cure for Q.

Speaker Change: 401.

Speaker Change: To generate and expand regulatory T cells or T regs fostering disease control in several disease models tested to date.

Daniel Passeri: As a reminder, QBIO Pharma has retained an option to a 50% U.S. Co-development co-marketing right to Q401.

Speaker Change: As a reminder, cue biopharma has retained an option to a 50% U S. Co development co marketing right to Q4 O one.

Daniel Passeri: Turning to 501, this program continues to advance and progress forward with a potential of eliminating auto-reactive B-cells with a highly selective and well-tolerated biologic. This program has the promise of addressing multiple B-cell mediated autoimmune diseases, such as lupus, myasthenia gravis, Sjögren's disease, and myositis, amongst others, representing significant unmet medical needs with large multi-billion dollar market potential. Furthermore, the same mechanism of action that we would be seeing in B-cell oblation for autoimmune disease may be deployed to address B-cell malignancies, such as B-cell lymphoma, with presently assessing strategic partnering alternatives for furthering the development of this promising program, and look forward to providing updates as they become available.

Daniel Passeri: Turning to 501, this program continues to advance and progress forward with the potential of eliminating autoreactive B-cells with a highly selective and well-tolerated biologic. This program has the promise of addressing, multiple B-cell-mediated autoimmune diseases, such as lupus, myasthenia gravis, Sjogren's disease, and myositis, amongst others representing significant unmet medical needs with large, multibillion-dollar market potential. Furthermore, the same mechanism of action, that we would be seeing in B-cell ablation for autoimmune disease may be deployed to address B-cell malignancies, such as B-cell lymphoma.

Speaker Change: Turning to 501. This program continues to advance and progress forward with the potential of <unk>.

Speaker Change: Eliminating auto reactive T cells with a highly selective and well tolerated biologic. This program has the promise of addressing multiple b cell mediated autoimmune diseases, such as lupus myasthenia gravis, shoguns disease, and myositis amongst others.

Daniel Passeri: Sjogren's disease, and myositis, amongst others representing significant unmet medical needs with large multi-billion dollar market potential. Furthermore, the same mechanism of action that we would be seeing in B-cell ablation for autoimmune disease may be deployed to address B-cell malignancies, such as B-cell lymphoma. We're presently assessing strategic partnering alternatives for furthering the development of this promising program and look forward to providing updates as they become available.

Speaker Change: Any significant unmet medical needs with large multibillion dollar market potential.

Speaker Change: Furthermore, the same mechanism of action that we would be seen in our b.

Speaker Change: B cell ablation for auto immune disease may be deploy to address b cell malignancies, such as B cell lymphoma.

Daniel Passeri: We're presently assessing strategic partnering alternatives, for furthering the development of this promising program and look forward to providing updates as they become available.

Speaker Change: We're presently assessing strategic partnering alternatives for furthering the development of this promising program and look forward to providing updates as they become available.

Daniel Passeri: We have positioned ourselves with a growing portfolio of highly promising drug candidates in both oncology and autoimmune disease, all of which represent significant market opportunities addressing major unmet medical needs. We believe we've de-risked and validated our therapeutics platform with the existing data sets from our Q101 and Q102 programs, and have established foundational pre-clinical data pertaining to our autoimmune programs with potential to rebalance the patient's immune system to restore health. We've implemented a cash-efficient business model enabling a reduction of capital requirements with an emphasis on validating net-term partner infrastructures.

Daniel Passeri: We have positioned ourselves with a growing portfolio of highly promising drug candidates in both oncology and autoimmune disease, all of which represent significant market opportunities addressing major unmet medical needs. We believe we've de-risked and validated our therapeutics platform with the existing data sets from our Q101 and Q102 programs and have established foundational preclinical data pertaining to our autoimmune programs with potential to rebalance the patient's immune system to restore health. We've implemented a cash-efficient business model enabling a reduction of capital requirements with an emphasis on validating near-term partnering structures.

Daniel Passeri: We have positioned ourselves with a growing portfolio, of highly promising drug candidates in both oncology and autoimmune disease, all of which represent significant market opportunities addressing major unmet medical needs.

Speaker Change: We have positioned ourselves with a growing portfolio of highly promising drug candidates in both oncology and autoimmune disease.

Speaker Change: All of which represent significant market opportunities addressing major unmet medical needs, we believe with deep we've derisked and validated our therapeutics platform with the existing data SaaS from our Q1 O. One in Q1 O two programs and have established foundational preclinical data pertaining to our autoimmune.

Daniel Passeri: We believe we've de-risked and validated, our therapeutics platform with the existing datasets from our Q101 and Q102 programs and have established foundational preclinical data pertaining to our autoimmune programs with potential to rebalance the patient's immune system to restore health.

Speaker Change: Programs with potential to rebalance the patient's immune system to restore health.

Daniel Passeri: We've implemented a cash-efficient business model enabling a reduction of, capital requirements with an emphasis on validating near-term partnering

Speaker Change: We've implemented a cash efficient business model, enabling a reduction of capital requirements with an emphasis on validating near term partnering structures.

Daniel Passeri: structures.

Daniel Passeri: I'm going to now turn the call over to Anish, who will describe the core attributes and advantages of our approach to treating autoimmune disease, as well as provide some additional context on our underlying platform developments for both oncology and autoimmune disease.

Daniel Passeri: I'm going to now turn the call over to Anish, who will describe the core attributes and advantages of our approach for treating autoimmune disease, as well as provide some additional context on our underlying platform developments for both oncology and autoimmune disease. After Anish, Matteo will provide further updates on the Q101 and Q102 clinical trials and highlight the importance of the maturing datasets, particular attention to the survival metrics that are emerging. I'll then return for a brief summary before opening the call up to questions.

Anish: I'm going to now turn the call over to a niche or describe the core attributes and advantages of our approach to treating autoimmune disease as well as provide some additional context on our underlying platform developments for both oncology and autoimmune disease and after a niche Matteo will.

Anish Suri: After Anish, Matteo will provide further updates on the Q101 and one on two clinical trials and highlight the importance of the maturing data sets with particular attention to the survival metrics that are emerging.

Matteo: To provide further updates on the Q1 O one and one or two clinical trials and highlight the importance of the maturing datasets with particular attention to the survival metrics that are emerging I'll then return for a brief summary, before opening the call up to questions a niche.

Anish Suri: I'll then return for a brief summary before opening the call up to question, Anish.

Daniel Passeri: I'm going to now turn the call over to Anish who will describe the core attributes and advantages of our approach for treating autoimmune disease as well as provide some additional context on our underlying platform developments for both oncology and autoimmune disease.

Anish Suri: Thanks, Dan, and good afternoon to all listening in on today's call. I'll start by briefly summarizing our platform and the significant potential of our approach for restoring immune balance, for treating cancers and autoimmune diseases. As described previously, the Immunostat platform enables selective modulation of disease-relevant immune cells while avoiding broad perturbations of the immune system. This approach allows us to maximize efficacy while preserving patient safety. As Dan indicated previously, and as summarized on slide three.

Anish Suri: Thanks, Dan, and good afternoon to all listening in on today's call. I'll start by briefly summarizing our platform and the significant potential of our approach for restoring immune balance for treating cancers and autoimmune diseases. As described previously, the immunostat platform enables selective modulation of disease-relevant immune cells while avoiding broad perturbations of the immune system. This approach allows us to maximize efficacy while preserving patient safety. As Dan indicated previously and as summarized on slide three, we have now clinically validated immunostats via the Q100 series that selectively and safely delivers the potent cytokine IL-2, along with the TCR activating signal, to preferentially activate tumor-specific T cells while sparing all other irrelevant T cells.

Anish: Thanks, Dan and good afternoon to all listening in on today's call I'll start by briefly summarizing our platform and the significant potential of our approach for restoring immune balance for treating cancers and autoimmune diseases.

Daniel Passeri: After Anish,

Speaker Change: As described previously the immuno stat platform enables selective modulation of disease relevant immune cells, while avoiding broad perturbations of the immune system. This approach allows us to maximize efficacy while preserving patient safety as Dan indicated previously and are summarized on slide three.

Anish Suri: We have now clinically validated immunostats via the Q100 series that selectively and safely delivers the potent cytokine IL-2 along with a TCR activating signal to preferentially activate tumor-specific T cells while sparing all other irrelevant T cells. This selective stimulation allows for the generation of a therapeutic index for IL-2, which has eluded many others trying to develop IL-2-based cancer therapies. In over 120 patients dosed, we have demonstrated a remarkable increase in efficacy with favorable tolerability.

Speaker Change: We have now clinically validated immuno stats via the cue 100 series.

Dan: Selectively and safely delivers the potent cytokine IL two along with the TCR activating signal to preferentially activate tumor specific T cells, while sparing all other irrelevant T cells there.

Anish Suri: This selective stimulation allows for the generation of a therapeutic index for IL-2, which has eluded many others trying to develop IL-2-based cancer therapies. In over 120 patients dozed, we have demonstrated a remarkable increase in efficacy with favorable tolerability. Mateo will provide further details on the latest clinical data that continue to demonstrate impressive benefit for patients being treated with Q101 and Q102.

Speaker Change: Selective stimulation allows for the generation of a therapeutic index for IL, two which is alluded many others trying to develop IL two based cancer therapies in over 120 patients dosed, we have demonstrated a remarkable increase in efficacy with favorable tolerability.

Daniel Passeri: Matteo will provide further updates on the Q101 and Q102 clinical trials and highlight the importance of the maturing data sets with particular attention to the survival metrics that are emerging.

Daniel Passeri: I'll then return for a brief summary

Anish Suri: Matteo will provide further details on the latest clinical data that continue to demonstrate impressive benefit for patients being treated with Q101 and Q102. On the autoimmune front, we have focused on two distinct and highly promising approaches to reset immune balance. Q401 is a novel bispecific that stimulates the generation and expansion of regulatory T-cells. Regulatory T-cells, or Tregs, possess the ability to dampen and control autoreactive lymphocytes, hence are an important cell type to maintain immune homeostasis and health.

Daniel Passeri: before opening the call up to questions.

Speaker Change: <unk> will provide further details on the latest clinical data that continue to demonstrate impressive benefit for patients being treated with cue 101 in Q1 or two on.

Anish Suri: Anish?

Anish Suri: Thanks Dan and good afternoon to all listening in on today's call.

Anish Suri: On the autoimmune front, we have focused on two distinct and highly promising approaches to reset immune balance. Q101 is a novel by Specific that stimulates the generation and expansion of regulatory T cells. Regulatory T cells or T-regs possess the ability to dampen and control or reactive lymphocytes; hence, are an important cell type to maintain immune homeostasis and health. Q101 has been partnered with ONO Pharmaceuticals, and this collaboration continues to move forward strongly. In addition to Q101, we've also made significant progress developing Q501 from the Q500 series to enable T cell-mediated depletion of B cells. This approach has the potential to deliver CAR-T-like efficacy in a biologic while preserving patient safety, which offers significant differentiation from other competing approaches.

Speaker Change: On the autoimmune front, we are focused on two distinct and highly promising approaches to reset the immune balance.

Anish Suri: I'll start by briefly summarizing our platform and the significant potential of our approach for restoring immune balance for treating cancers and autoimmune diseases. As described previously, the Immunostat platform enables selective modulation of disease relevant immune cells while avoiding broad perturbations of the immune system. This approach allows us to maximize efficacy while preserving patient safety.

Speaker Change: Q4 O. One is a novel bi specific that stimulates the generation in expansion of regulatory T cells regulatory T cells or T. Regs possess the ability to dampen and control Autoreactive lymphocytes, hence are unimportant cell type to maintain immune homeostasis and help Q4 hundred one has been partnered with owner.

Anish Suri: As Dan indicated previously and as summarized on slide 3, we have now, clinically validated Immunostats via the Q100 series that selectively and safely delivers the potent cytokine IL-2 along with a TCR activating signal to preferentially activate tumor-specific T cells while sparing all other irrelevant T cells.

Anish Suri: This selective stimulation allows for the generation of a therapeutic index for IL-2, which has eluded many others trying to develop IL-2 based cancer therapies.

Anish Suri: In over 120 patients dosed, we have demonstrated a remarkable increase in efficacy with favorable tolerability.

Anish Suri: Q401 has been partnered with Ono Pharmaceuticals, and this collaboration continues to move forward strongly. In addition to Q401, we've also made significant progress developing Q501 from the Q500 series to enable T cell-mediated depletion of B cells. This approach has the potential to deliver CAR T-like efficacy in a biologic while preserving patient safety, which offers significant differentiation from other competing approaches. Both Q401 and Q500 series are designed to address large patient populations across numerous autoimmune and inflammatory diseases with a multi-billion dollar market potential. We will expand on both programs in the next few slides. The next slide, slide 4, exemplifies the unique attributes of Q401 in induction and expansion of Tregs.

Anish Suri: Mateo will provide further details on the latest clinical data that continue to demonstrate impressive benefit for patients being treated with Q101 and Q102.

Speaker Change: Pharmaceuticals, and this collaboration continues to move forward strongly in addition to Q4 O. One. We've also made significant progress developing Q 501 from the Q 500 series to enable T cell mediated depletion of B cells. This approach has the potential to deliver car T like efficacy by law.

Speaker Change: Logic, while preserving patient safety, which offers significant differentiation from other competing approaches.

Anish Suri: On the autoimmune front, we have focused on two distinct and highly, promising approaches to reset immune balance. Q401 is a novel bispecific that stimulates the generation and expansion of regulatory T cells. Regulatory T cells or Tregs possess the ability to dampen and control autoreactive lymphocytes, hence are an important cell type to maintain immune homeostasis and health.

Anish Suri: Both Q101 and Q500 series are designed to address large patient populations across numerous autoimmune and inflammatory diseases, with a multi-billion dollar market potential. We will expand on both programs in the next few slides. The next slide, slide 4, exemplifies the unique attributes of Q101 in the induction and expansion of T-regs. Q101 is a bi-specific composed of the two key cytokines IL-2 and TG of beta that are known to convert peripheral CD4 T cells into T-regs, as well as expand pre-existing natural T-regs. This ability to induce new populations of T-regs provides Q101 with the prospects of significant superiority over other approaches deploying IL-2 variants to focus on only the pre-existing natural.

Both Q4 hundred one in Q 500 series designed to address large patient populations across numerous autoimmune and inflammatory diseases with a multibillion dollar market potential we will expand on both programs in the next few slides.

Anish Suri: Q401 has been partnered with Ono Pharmaceuticals and this collaboration, continues to move forward strongly.

Speaker Change: The next slide slide four exemplifies the unique attributes of Q4 to one in induction and expansion of T. Regs Q4 to one is a bi specific composed of the two key cytokines IL two and TGF beta that are known to convert peripheral CD four T cells into T. Rex.

Anish Suri: Q401 is a bispecific composed of the two key cytokines IL-2 and TGF-beta that are known to convert peripheral CD4 T cells into Tregs, as well as expand preexisting natural Tregs. This ability to induce new populations of Tregs provides Q401 with the prospects of significant superiority over other approaches deploying IL-2 variants to focus on only the preexisting natural Tregs. As shown in slide 4, we believe the mechanism of action of Q401 to enhance Tregs is qualitatively and quantitatively superior to IL-2 mutines targeting CD25, which is the high affinity subunit of the IL-2 receptor expressed on regulatory Tregs.

Speaker Change: As well as expand preexisting natural T. Rex this ability to induce new populations of T. Regs provides Q4 O one with the prospects of significant superiority over other approaches deploying IL two variance to focus on only the preexisting natural T. Rex as shown on slide four we believe the mechanism of action of Q4, one to enhance directs.

Anish Suri: T-Rex. As shown on slide 4, we believe the mechanism of action of Q401 to enhance T-Rex is qualitatively and quantitatively superior to IL-2 Mutine's targeting CD25, which is the high affinity subunit of the IL-2 receptor expressed on regulatory T cells. Slide 5 highlights data sets that show superiority of Q401 over an IL-2 Mutine analog currently in clinical development for T-Rex generation. As shown on the left side of this slide, in an in vitro human emilar assay, which is an in vitro model for graft-versus-horse disease, Q401 induces differentiation and expansion of T-Rex. In contrast, a T-Rex-directed IL-2 mutine is unable to achieve these effects.

Speaker Change: Qualitatively and quantitatively superior to add two mid teens targeting CD 25, which is the high affinity subunit of the IL two receptor expressed on regulatory T cells.

Anish Suri: Slide 5 highlights datasets that show superiority of Q401 over an IL-2 mutine analog currently in clinical development for Treg generation. As shown on the left side of the slide, in an in vitro human MLR assay, which is an in vitro model for graft-versus-host disease, Q401 induces differentiation and expansion of Tregs. In contrast, a Treg-directed IL-2 mutine is unable to achieve these effects. The bottom left panel confirms that both IL-2 and TGF-beta signals are needed for Treg generation. Either alone is unable to achieve this effect.

Speaker Change: <unk> five highlights datasets that show superiority of Q4 O. One over an IL two mutant analogue currently in clinical development for T Reg generation.

Speaker Change: As shown on the left side of this slide and in in vitro human MLR assay, which is an in vitro model for graft versus host disease Q4, O. One induces differentiation and expansion of T. Regs. In contrast, 18 red directed aisle to mute team is unable to achieve these effects the bottom left panel confirms at both IL.

Anish Suri: The bottom left panel confirms that both IL-2 and TGF beta signals are needed for T-Rex generation; either alone is unable to achieve this effect. As shown on the right side, and as previously discussed, short-term administration of Q401 results in long-term protection from auto-munity, in this case auto-mium gas tritis. In our ongoing collaboration with ONO Pharmaceuticals, we have further extended the in vivo efficacy with Q401 in several other disease models where we have noted a significant increase in T-Rex accompanied by a notable decrease in pro-inflammatory cytokines.

Speaker Change: <unk> and TGF beta signals are needed for T. Rowe generation either alone is unable to achieve this effect.

Anish Suri: As shown on the right side and as previously discussed, short-term administration of Q401 results in long-term protection from autoimmunity, in this case autoimmune gastritis. In our ongoing collaboration with Ono Pharmaceuticals, we have further extended the in vivo efficacy with Q401 in several other disease models where we have noted a significant increase in Tregs accompanied by a notable decrease in pro-inflammatory side effects. Let's now move to slide 6 to provide an overview and update on the Q500 series for B-cell depletion.

Speaker Change: One on the right side and as previously discussed short term administration of Q4 O. One results in long term protection for motor immunity in this case autoimmune gastritis.

Speaker Change: Our ongoing collaboration with Ono Pharmaceuticals, we have further extended the in vivo efficacy with Q4 O one and several other disease models, where we have noted a significant increase in T. Rex accompanied by a notable decrease in pro inflammatory cytokines.

Anish Suri: Let's now move to slide 6 to provide an overview and update on the Q500 series for B-cell depletion. The primary goal behind the design of the Q500 T-cell engages was to achieve T-cell mediated depletion of B-cells while avoiding the adverse effects of systemic immune activation and broad engagement of all T-cells. Our approach enables the potential to achieve cartilic efficacy while avoiding the safety pitfalls of pan-T-cell engages. By design, the Q500 series immunostats bind to CD-19 on B-cells and effectively paint the B-cells with a viral epitope, such as CMV. These B-cells are then readily recognized and killed by the memory antiviral T-cells, as shown in the slide.

Anish Suri: In addition to Q401, we've also made significant progress developing Q501 from the Q500 series to enable T cell mediated depletion of B cells. This approach has the potential to deliver CAR T-like efficacy in a biologic while preserving patient safety, which offers, significant differentiation from other competing approaches.

Speaker Change: Let's now move to slide six to provide an overview and update on the Q 500 series for B cell depletion. The primary goal behind the design of the Q 500 diesel engages was to achieve T cell mediated depletion of b cells, while avoiding the adverse effects of systemic immune activation and broad engagement of all T cells.

Anish Suri: The primary goal behind the design of the Q500 T-cell engages was to achieve T-cell mediated depletion of B-cells while avoiding the adverse effects of systemic immune activation and broad engagement of all, Our approach enables the potential to achieve CAR T-like efficacy while avoiding the safety pitfalls of pan T-cell engages. By design, the Q500 series immunostats bind to CD19 and B-cells and effectively paint the B-cells with a viral epitope, such as CMV. These B-cells are then readily recognized and killed by the memory antiviral T-cells as shown in this slide.

Anish Suri: Both Q401 and Q500 series are designed to address large patient populations across, numerous autoimmune and inflammatory diseases with a multi-billion dollar market potential. We will expand on both programs in the next few slides.

Anish Suri: The next slide, slide 4, exemplifies the unique attributes of Q401 in induction, and expansion of Tregs. Q401 is a bispecific composed of the two key cytokines IL-2 and TGF-beta that are known to convert peripheral CD4 T cells into Tregs as well as expand pre-existing natural Tregs.

Anish Suri: This ability to induce new populations of Tregs provides Q401 with the prospects of significant superiority over other approaches deploying IL-2 variants to focus on only the pre-existing natural Tregs.

Anish Suri: As shown in slide 4, we believe the mechanism of action of Q401 to enhance Tregs is qualitatively, and quantitatively superior to IL-2 mutines targeting CD25, which is the high affinity subunit of the IL-2 receptor expressed on regulatory T cells.

Speaker Change: Our approach enables the potential to achieve car T lack efficacy, while avoiding the safety pitfalls of patent T cell engages by design. The Q 500 series immuno stats bind to <unk> 19 on b cells and effectively paint the b cells, but the viral epitope such as CMV. These b cells are then readily <unk>.

Anish Suri: Slide 5 highlights datasets that show superiority of Q401 over an IL-2 mutine analog currently, in clinical development for Treg generation. As shown on the left side of the slide, in an in vitro human MLR assay, which is an, in vitro model for graft-versus-host disease, Q401 induces differentiation and expansion of Tregs.

Anish Suri: In contrast, a Treg-directed IL-2 mutine is unable to achieve these effects.

Speaker Change: Nice and killed by the memory anti viral T cells as shown in this slide engaging virus specific T cells or Vst's offers several advantages. These are trained killer T cells present in high frequency across the human population. They are localized in diseased tissue and perform rapid killing of cog.

Anish Suri: Engaging virus-specific T-cells, or VSTs, offers several advantages. These are trained killer T-cells present in high frequency across the human population. They are localized in diseased tissue and perform rapid killing of targets.

Anish Suri: Engaging virus-specific T-cells or VSTs offers several advantages. These are trained K-cells present in high frequency across the human population. They are localized in disease tissue and perform rapid killing of targets. And due to their specificity of virus antigens, the VSTs avoid the risk of potential reactivity against self-tissue or systemic immune activation, as would be with pan-T-cell engages. Importantly, and as shown in slide 7, VSTs in this case, CMV-specific memory T-cells can achieve the same degree of killing of B-cells as pan-T-cell engages, in this case an anti-CD-19, anti-CD-3 by specific molecule. Note here that the killing is specific to the engagement of CMV T-cells, since a Q500 molecule expressing an HIV epitope is unable to mediate B-cell killing, since HIV-specific T-cells are largely absent in most individuals.

Anish Suri: And due to their specificity of virus antigens, the VSTs avoid the risk of potential reactivity against cell tissue or systemic immune activation, as would be with pan-T-cell engagement. Importantly, and as shown in slide 7, VSTs, in this case CMV-specific memory T-cells, can achieve the same degree of killing of B-cells as pan-T-cell engages, in this case an anti-CD19, anti-CD3 bispecific molar. Note here that the killing is specific to the engagement of CMVT cells since a Q500 molecule expressing an HIV epitope, is unable to mediate B-cell killing since HIV-specific T-cells are largely absent in most individuals.

Speaker Change: And due to the specificity of a virus antigens <unk> avoid the risk of potential reactivity against south tissue or systemic immune activation as it would be with patent diesel engages.

Speaker Change: Importantly, and as shown on slide seven <unk> in this case CMV specific memory T cells can achieve the same degree of killing of B cells as band T cell engages in this case, an anti CD 19 anti CD three bi specific molecule note here that the killing of specific to the engagement of CMV T cells since our Q4.

Speaker Change: 500 molecule expressing an HIV epitope is unable to meet the eight b cell, killing since HIV specific T cells are largely absent in most individuals' slide eight further exemplifies the difference in safety inside of pen production between Q five or one in pad N T cell engages due to the high selective.

Anish Suri: Slide 8 further exemplifies the difference in safety and cytokine production between Q501 and pan-T cell engagers. Due to their high selective engagement, the Q501 molecule does not result in copious production of inflammatory cytokines such as interferon gamma and TNF, as shown here. In contrast, a pan-T cell engager molecule, due to its anti-CD3 binding to all T cells, results in significantly high levels of cytokine release, which ultimately compromises patient safety and drug tolerability.

Anish Suri: Slide 8 further exemplifies the difference in safety and side-up and production between Q501 and pan-T-cell engages. Due to the high selective engagement, the Q501 molecule does not result in copious production of inflammatory cytokines such as interferon gamma and TNF, as shown here. In contrast, a pan-T-cell engage a molecule due to its anti-CD-3 binding to all T-cells results in significantly high levels of cytokine released, which ultimately compromises patient safety and drug tolerability.

Speaker Change: Engagement the Q five of one molecule does not result in copious production of inflammatory cytokines, such as interferon gamma and TNF shown here in contrast, a patent diesel engage a molecule due to its anti CD three binding to all T cells results in significantly high levels of cytokine release, which.

Speaker Change: Ultimately compromises patient safety and drug Tolerability.

Anish Suri: The following slide, slide 9, highlights some of the notable points of differentiation between Q500, CARTI approaches, and pan-T cell-engaging molecules. Note that all three approaches involve T cell-mediated killing of target B cells, but it's only the Q500 series that can selectively engage trained memory killer T cells and redirect them to kill B cells. The selective engagement while avoiding systemic activation results in a significant reduction in cytokine release and related toxicities, which it favors patient safety while preserving efficacy. We believe the Q500 series of biologics are likely positioned as the best in class T cell engages for B cell depletion and could address a very large segment of autoimmune patients across many indications.

Anish Suri: The following slide, slide nine, highlights some of the notable points of differentiation between Q500 CAR-T approaches and PAN-T cell engager molecules. Note that all three approaches involve T-cell mediated killing of target B-cells, but it's only the Q500 series that can selectively engage trained memory killer T-cells and redirect them to kill B-cells. The selective engagement while avoiding systemic activation results in a significant reduction in cytokine release and related toxicities, which should favor patient safety while preserving efficacy.

Speaker Change: The following slide slide nine highlights some of the notable points of differentiation between Q 500 car T approaches and N T cell engaging molecules note that all three approaches involve T cell mediated killing of target b cells, but it's only the Q 500 series that can selectively engage trained memory.

Speaker Change: T cells and redirect them to kill B cells, the selective engagement, while avoiding systemic activation results in a significant reduction in cytokine release and related toxicities, which should favor patient safety, while preserving efficacy.

Anish Suri: We believe the Q500 series of biologics are likely positioned as the best-in-class T cell engagers for B cell depletion and could address a very large segment of autoimmune patients across many indicators. In summary, there are three key takeaway messages.

We believe that Q 500 series of biologics are likely positioned as the best in class diesel engages with B cell depletion and could address a very large segment of autoimmune patients across many indications in summary, there are three key takeaway messages for.

Anish Suri: The bottom left panel confirms that both IL-2 and TGF-beta signals are needed for Treg generation. Either alone is unable to achieve this effect.

Anish Suri: In summary, there are three key takeaway messages. First, due to the shared core structural framework, the clinical de-risking and validation of amino-stats in oncology via Q101 and Q102, including lack of clinically relevant immunogenicity, bolsters and supports the clinical application of Q500 series for B cell depletion in autoimmunity. Second, selective harnessing of anti-viral memory T cells to kill B cells circumvents the safety risk associated with systemic T cell activation, as noted with anti-cell engages. And third, data demonstrating comparable killing while avoiding high levels of pro-inflammatory cytokine production positions the Q500 series to achieve desirable efficacy while not compromising patient safety, which is of highest clinical relevance when considering therapeutic applications in autoimmune diseases.

Matteo Levisetti: First, due to the shared core structural framework, the clinical de-risking and validation of immunostats in oncology via Q101 and Q102, including lack of clinically relevant immunogenicity, bolsters and supports the clinical application of Q500 series for B-cell depletion in autoimmune disease. Second, selective harnessing of antiviral memory T-cells to kill B-cells circumvents the safety risk associated with systemic T-cell activation, as noted with pan-T-cell engages. And third, data demonstrating comparable killing while avoiding high levels of pro-inflammatory cytokine production positions the Q500 series to achieve desirable efficacy while not compromising patient safety, which is of highest clinical relevance when considering therapeutic applications in autoimmune diseases. With that background and update, I'll turn the call over to Matteo to describe the maturing clinical data from the ongoing oncology trials. Matteo?

Speaker Change: Due to the shared cost structural framework that clinical derisking and validation of immuno stats in oncology, we had Q1 O. One in Q1 or two including lack of clinically relevant immunogenicity bolsters and supports the clinical application of Q 500 series for B cell depletion and auto immunity second selective harnessing of anti viral.

Speaker Change: Memory T cells to kill B cells circumvents, the safety risks associated with systemic T cell activation as noted with patent diesel engages and third data demonstrating comparable killing while avoiding high levels of protein Framatome cytokine production positions. The Q 500 series to achieve desired efficacy while not corporate.

Speaker Change: Rising patient safety, which is of highest clinical relevance when considering therapeutic applications in autoimmune diseases with that background and update I'll turn the call over to Matteo to describe the mature and clinical data from the ongoing oncology trials.

Anish Suri: As shown on the right side, and as previously discussed, short-term administration of Q401, results in long-term protection from autoimmunity, in this case, autoimmune gastritis.

Matteo Levisetti: With that background and update, I'll turn the call over to Mateo to describe the mature and clinical data from the ongoing oncology trials. Mateo? Thanks, Anish. Good afternoon to everyone listening in on today's call. The maturing clinical data from the ongoing Q101 trial continues to demonstrate highly encouraging and robust metrics of clinical benefit for patients newly diagnosed with recurrent metastatic HPV-positive head neck cancer treated in combination with Pemberlizumet. And for heavily pre-treated recurrent metastatic HPV-positive head neck cancer patients treated with monotherapy. The latest data continues to bolster prior observations. Further enhancing our confidence in Q101 as a potential new standard of care therapeutic to improve outcomes for patients battling HPV-positive head and neck cancer.

Speaker Change: Yep.

Matteo Levisetti: Thanks, Anish. Good afternoon to everyone listening in on today's call. The maturing clinical data from the ongoing Q101 trial continues to demonstrate highly encouraging and robust metrics of clinical benefit for patients newly diagnosed with recurrent metastatic HPV positive head and neck cancer treated in combination with pembrolizumab and for heavily pretreated recurrent metastatic HPV positive head and neck cancer patients treated with monotherapy. The latest data continues to bolster prior observations, further enhancing our confidence in Q101 as a potential new standard of care therapeutic to improve outcomes for patients battling HPV-positive head and neck.

Speaker Change: Thanks <unk> good.

Anish Suri: In our ongoing collaboration with Ono Pharmaceuticals, we have further extended the in vivo efficacy, with Q401 in several other disease models where we have noted a significant increase in Tregs accompanied by a notable decrease in pro-inflammatory cytokines.

Anish Suri: Let's now move to slide 6 to provide an overview and update on the Q500 series for B-cell depletion.

Speaker Change: Good afternoon to everyone listening in on today's call the maturing clinical data from the ongoing cue 101 trial continues to demonstrate highly encouraging and robust metrics clinical benefit for patients newly diagnosed with recurrent metastatic HPV positive head and neck cancer treated in combination with pepper livsey met.

Anish Suri: The primary goal behind the design of the Q500 T-cell engages was to achieve T-cell, mediated depletion of B-cells while avoiding the adverse effects of systemic immune activation and broad engagement of all T-cells.

Speaker Change: And for heavily pretreated recurrent metastatic HPV positive head and neck cancer patients treated with monotherapy.

Speaker Change: Latest data continues to bolster prior observations further enhancing our confidence in Q1 O. One as a potential new standard of care therapeutics to improve outcomes for patients battling HPV positive head and neck cancer.

Matteo Levisetti: As previously and consistently stated, we believe Q101's unique mechanism of action, as evidenced by the data generated to date, enables effective and tolerated dosing and selective expansion of the targeted tumor-specific T-cells. Pemberlizumet is approved as this current standard of care treatment of first-line patients with recurrent metastatic head neck cancer that have tumors with the combined positive score or CPS score of greater than or equal to 1%, which is a measure of PDL expression. The approval of Pemberlizumet in this setting was based on a median overall survival of 12.3 months and with an objective response rate of 19% as observed in the Keynote 48 studies.

Anish Suri: Our approach enables the potential to achieve CAR T-like efficacy while avoiding the safety, pitfalls of pan-T-cell engages.

Matteo Levisetti: As previously and consistently stated, we believe Q101's unique mechanism of action, as evidenced by the data generated to date, enables effective and tolerated dose, and Selective Expansion of the Targeted Tumor-Specific T-Cell. Pembrolizumab is approved as the current standard of care treatment of first-line patients with recurrent metastatic head and neck cancer that have tumors with a combined positive score or CPS score of greater than or equal to 1%, which is a measure of PDL expression.

Anish Suri: By design, the Q500 series immunostats bind to CD19 and B-cells and effectively paint, the B-cells with a viral epitope, such as CMV. These B-cells are then readily recognized and killed by the memory antiviral T-cells, as shown in the slide.

Speaker Change: As previously and consistently stated we believe Q1 O ones unique mechanism of action as evidenced by the data generated to date enables effective and tolerated dosing and selective expansion of the targeted tumor specific.

Anish Suri: Engaging virus-specific T-cells, or VSTs, offers several advantages.

Anish Suri: These are trained killer T-cells present in high frequency across the human population. They are localized in diseased tissue and perform rapid killing of targets.

Anish Suri: And due to their specificity of virus antigens, the VSTs avoid the risk of potential reactivity, against cell tissue or systemic immune activation, as would be with pan-T-cell engages.

Anish Suri: Importantly, and as shown in slide 7, VSTs, in this case CMV-specific memory T-cells, can achieve the same degree of killing of B-cells as pan-T-cell engages, in this case an anti-CD19, anti-CD3 bispecific molecule.

Anish Suri: Note here that the killing is specific to the engagement of CMV T-cells, since a Q500, molecule expressing an HIV epitope is unable to mediate B-cell killing, since HIV-specific, T-cells are largely absent in most individuals.

Anish Suri: Slide 8 further exemplifies the difference in safety and cytopan production between Q501, and pan-T-cell engages.

Anish Suri: Due to their high selective engagement, the Q501 molecule does not result in copious production, of inflammatory cytokines, such as interferon gamma and TNF, as shown here.

Anish Suri: In contrast, a pan-T-cell engages molecule due to its anti-CD3 binding to all T-cells, results in significantly high levels of cytokine release, which ultimately compromises patient safety and drug tolerability.

Speaker Change: T cells.

Speaker Change: Member Luiza Mab is approved as the current standard of care treatment of first line patients with recurrent metastatic head and neck cancer that have tumors with a combined positive score or cps score of greater than or equal to 1%, which is a measure of PDL expression.

Matteo Levisetti: The approval of pembrolizumab in this setting was based on a median overall survival of 12.3 months and with an objective response rate of 19 percent, as observed in the Keynote 48 study. As presented at ASCO in June, following combination treatment with Q101, The objective response rate of 46%, as shown on slide 10, observed in patients with CPS greater than or equal to one represents a greater than doubling compared to the historical ORR of 19% observed with pembrolizumab monotherapy.

Speaker Change: Approval of <unk> in this setting was based on a median overall survival of 12, three months and with an objective response rate of 19% as observed in the keynote 48 study.

Anish Suri: The following slide, slide 9, highlights some of the notable points of differentiation between Q500 CAR-T approaches and PAN T-cell engager molecules.

Matteo Levisetti: As presented at ASCO in June, following combination treatment with Q101, the objective response rate of 46%, as shown on slide 10, observed in patients with CPS greater than or equal to 1, represents a greater than doubling compared to the historical ORR of 19% observed with Pembronizumab monotherapy. As shown on the waterfall plot, out of 24 valuable patients, we have observed significant tumor reductions across many of these patients, including confirmed partial responses in 10 patients and a confirmed complete response in one patient. Importantly, four patients remain on treatment, including one with stable disease that exhibits a reduction in their target lesions of minus 28%.

Speaker Change: As presented at Astro in June following combination treatment with Q1 at one.

Speaker Change: The objective response rate of 46% as shown on slide 10 observed in patients with Cps greater than or equal to one represents a greater than doubling compared to the historical O R or a 19% observed with Penguin did you Mad monotherapy.

Matteo Levisetti: As shown on the waterfall plot, out of 24 valuable patients, we have observed significant tumor reductions across many of these patients, including confirmed partial responses in 10 patients and a confirmed complete response in 1 patient. Importantly, four patients remain on treatment, including one with stable disease that exhibits a reduction in their target lesions of minus 28%. Notably, for patients with low CPS scores, or scores of 1 to 19, an ORR of 50% was observed with Q101 and pembrolizumab, which represents a greater than tripling of the historical ORR of approximately 15% observed with pembrolizumab alone.

As shown on the waterfall plot out of 24 Evaluable patients we have observed significant tumor reductions across many of these patients including confirmed partial responses and 10 patients and a confirmed complete response in one patient importantly, four patients remain on treatment, including one with stable disease.

Speaker Change: That exhibits a reduction in their target lesions of minus 28%.

Matteo Levisetti: Notably, for patients with low CPS scores, or scores of 1 to 19, an ORR of 50% was observed with Q101 and Pembronizumab, which represents a greater than tripling of the historical ORR of approximately 15% observed with Pembronizumab alone. In totality, our data suggests that not only does Q101 appear to demonstriply enhance the response rate of PD1 inhibitions, but also does so by substantially enhancing responses in patients that are traditionally less likely to respond. This is particularly important since patients with low CPS scores represent approximately 50% of all patients that are CPS positive and eligible for treatment with Pembronizumab in the front line setting.

Speaker Change: Notably for patients with low CPA scores are scores of 1% to 19 and O R or a 50% was observed with Q1 and one in pember, Lizzie met which represents a greater than tripling of the historical or are of approximately 15% observed with Tampa division that alone.

Anish Suri: Note that all three approaches involve T-cell mediated killing of target B-cells, but it's only the Q500 series that can selectively engage trained memory killer T-cells and redirect them to kill B-cells.

Matteo Levisetti: In totality, our data suggests that not only does Q101 appear to demonstrably enhance the response rate of PD-1 inhibition, but also does so by substantially enhancing responses in patients that are traditionally less likely to respond. This is particularly important since patients with low CPS scores represent approximately 50% of all patients that are CPS positive and eligible for treatment with pembrolizumab in the frontline setting. The responses observed in these patients have been durable, as reflected in the 12-month OS and median OS, which is shown on the next slide. Slide 11.

Speaker Change: <unk> our data suggests that not only just Q1 O one appear to demonstrably enhance the response rate of PD one inhibition.

Speaker Change: But also does so by substantially enhancing responses in patients that are traditionally less likely to respond.

Speaker Change: This is particularly important since patients with low Cps score is represented approximately 50% of all patients that are cps positive and eligible for treatment with <unk> in the frontline setting the.

Matteo Levisetti: The responses observed in these patients have been durable, as reflected in the 12-month OS and median OS, which is shown on the next slide, Slide 11. For patients treated with Q101 and Pembronizumab as first line treatment, the median PFS of 5.8 months compares favorably to the median PFS of 3.2 months that was observed in the Pembronizumab arm of the 8 months observed in patients with CPS greater than or equal to 1, treated with combination treatment is notable and substantially better than the historical data with Pembronizumab monotherapy, where 12-month OS and median OS were 51% and 12.3 months, respectively.

Speaker Change: The responses observed in these patients had been durable as reflected in the 12 month OS and median OS which is shown on the next slide.

Speaker Change: Slide 11.

Matteo Levisetti: For patients treated with Q101 and pembrolizumab as first-line treatment, the median PFS of 5.8 months compares favorably to the median PFS of 3.2 months that was observed in the pembrolizumab arm of the Keynote 48 trial. Importantly, the 12-month OS of 90%... And the median OS of 21.8 months observed in patients with CPS greater than or equal to 1, treated with combination treatment, is notable and substantially better than the historical data with Pembrolizumab monotherapy, where 12-month OS and median OS were 51 percent and 12.3 months respectively.

Speaker Change: For patients treated with Q1 O one and pepper Lizardman as first line treatment. The median PFS of five eight months compares favorably to the median PFS of $3. Two months that was observed in the pepper lithium at arm <unk>.

Speaker Change: 48 trial in.

Speaker Change: Importantly, the 12 month OS at 90% and the median OS at 21, eight months observed in patients with Cps greater than or equal to one treated with combination treatment is notable and substantially better than the historical data with Pep Elysium Bad monotherapy, we're 12 months OS.

Speaker Change: And median OS were 51% and $12 three months respectively.

Matteo Levisetti: These enhanced survival metrics, which continue to be followed, are particularly evident when looking at the patients with both low and high PD-L1 expression, as shown on slide 12. Consistent with the enhanced ORR observed in patients with low PDL1 expression, treated with Q101 and Pembronizumab, these patients are demonstrating favorable metrics of survival. In CPS, low patients treated with Q101 and Pembronizumab, the 12-month OS of 82% and the median OS of 21.8 months is importantly notable given the historical values of 44% and 10.8 months observed for Pembronizumab in the Keynote 48 study. The benefit to CPS high patients is also noteworthy with 12 month OS of 100 percent, an immediate OS that has not yet been reached in patients with CPS greater than or equal to 20 treated with Q101 and Pembrolyzumab compared to the historical values of 56 percent and 14.8 months respectively.

Matteo Levisetti: These enhanced survival metrics, which continue to be followed, are particularly evident when looking at the patients with both low and high PD-L1 expression, as shown on slide 12, consistent with the enhanced ORR observed in patients with low PD-L1 exposure, treated with Q101 and pembrolizumab. These patients are demonstrating favorable metrics of survival. CPS low patients treated with Q101 and pembrolizumab, the 12-month OS of 82%, and the median OS of 21.8 months is importantly notable given the historical values of 44% and 10.8 months observed for pembrolizumab in the Keynote 48 study.

Speaker Change: These enhanced survival metrics, which continued to be followed are particularly evident when looking at the patients with both low and high PD lone expression.

As shown on slide 12.

Consistent with the enhanced or are observed in patients with low PDL one expression.

Speaker Change: Treated with Q1 and one in parallelism that these patients are demonstrating favorable metrics of survival and Cps low patients treated with Q1 O. One in timberlands Ya man, the 12 month OS of 82% and the median OS at 21 eight months is importantly, notable given the historical values are for.

Speaker Change: <unk>, 4% and $10 eight months observed for Pep religion met in the keynote 48 study.

Matteo Levisetti: The benefit to CPS high patients is also noteworthy with 12-month OS of 100% and a median OS that has not yet been reached in patients with CPS greater than or equal to 20 treated with Q101 and pembrolizumab compared to the historical values of 56% in 14.8 months respectively. As a reminder, these maturing data from the combination trial appear to be following what we observed in the monotherapy second line plus setting, where Q101 demonstrated significant prolongation of survival as shown in the following slide, slide 13.

Speaker Change: The benefit to Cps high patients is also noteworthy with 12 months or so 100% and median OS that has not yet been reached in patients with cps greater than or equal to 20 treated with Q1 O. One in parallelism that compared to the historical values of $56.

Speaker Change: In 2000 14.8 months respectively.

Matteo Levisetti: As a reminder, these maturing data from the combination trial appeared to be following what we observed in the monotherapy second line plus setting, where Cue 101 demonstrated significant prolongation of survival, as shown in the following slide, slide 13. As shown on the left, the median OS observed in patients treated with Cue 101 monotherapy at 2 mg per kg was 24.8 months and 20.8 months for those treated with Cue 101 and a dose of 4 mg per kg. The survival observed in these patients is remarkable when compared to the median OS observed in the second line with checkpoint inhibitors, where median OS of 7.5 and 8.4 months were observed for Nevilleumab and Pembrolyzumab, respectively.

Speaker Change: As a reminder, these maturing data from the combination trial appeared to be following what we observed in the monotherapy second line plus setting where Q1 O. One demonstrated significant prolongation of survival as shown in the following slide slide 13.

Operator: Good day, and welcome to the Cue Biopharma Second Quarter 2024 earnings call.

Operator: Good day, and welcome to the Cue Biopharma Second Quarter 2024 earnings call. All participants will be in a listen-only mode. Should you need assistance, please signal conference specialists by pressing the star key followed by zero.

Operator: All participants will be in a listen-only mode.

Matteo Levisetti: As shown on the left, the median OS observed in patients treated with Q101 monotherapy at 2 mg per kg was 24.8 months. 20.8 months for those treated with Q101 at a dose of 4 mg per kick. The survival observed in these patients is remarkable when compared to the median OS observed in the second line with checkpoint inhibitors, where median OS of 7.5 and 8.4 months were observed for nivolumab and pembrolizumab respectively. We believe this enhancement of survival to be mediated by the durable and selective expansion of targeted tumor-specific T-cells like Q101.

Speaker Change: As shown on the left the median OS observed in patients treated with Q1 O. One monotherapy at two Megs per King was $24 eight months and 28 months for those treated with Q1 O. One at a dose of four megs per kit.

Operator: Should you need assistance, please signal conference specialists by pressing the star key followed by zero.

Operator: After today's presentation, there will be an opportunity to ask questions.

Operator: After today's presentation, there will be an opportunity to ask questions. To ask a question, you may press star than one on your touch-tone phone. And to withdraw your question, please press star than two. Please note this event is being recorded.

Operator: To ask a question, you may press star than one on your touch-tone phone.

Operator: And to withdraw your question, please press star than two.

Speaker Change: The survival observed in these patients is remarkable when compared to the median OS observed in the second line with checkpoint inhibitors, where median OS at seven five and eight four months were observed for Nivola map and pepper lithium mad respectively.

Operator: Please note this event is being recorded.

Daniel Passeri: I would now like to turn the conference over to our chief executive officer, Mr. Dan Passeri.

Dan Passeri: I would now like to turn the conference over to our chief executive officer, Mr. Dan Passeri. Please go ahead, sir. Okay, thank you, and good afternoon, everyone.

Daniel Passeri: Please go ahead, sir.

Daniel Passeri: Okay, thank you, and good afternoon, everyone.

Daniel Passeri: As a reminder, this presentation and discussion is being recorded and will be available on our website for the next 30 days.

Dan Passeri: As a reminder, this presentation and discussion is being recorded and will be available on our website for the next 30 days. Also, please be aware that the slides accompanying today's update may be advanced directly by those listening in, and we will notify you on what slide we're on throughout the presentation.

Matteo Levisetti: We believe this enhancement of survival to be mediated by the durable and selective expansion of targeted tumor-specific T-cells by Cue 101. In totality, our data suggests that Cue 101 increases the number of patients benefiting checkpoint inhibitors and appears to substantially improve survival in these patients. We continue to monitor and carefully follow the patient's remaining on treatment as well as in survival follow-up and look forward to providing an update that sits in November. The data continues to mature over time, and we believe the observations to date, particularly pertaining to what appears to be a substantial enhancement of survival, will place Cue 101 and, by implication, the Cue 101 series in a favorable and competitive position to potentially become a new standard of care.

Speaker Change: We believe this enhancement of survival to be mediated by the durable and selective expansion targeted tumor specific T cells by Q1 O. One.

Daniel Passeri: Also, please be aware that the slides accompanying today's update may be advanced directly by those listening in, and we will notify you on what slide we're on throughout the presentation.

Matteo Levisetti: In totality, our data suggests that Q101 increases the number of patients benefiting from checkpoint inhibition, and appears to substantially improve survival in these patients. We continue to monitor and carefully follow the patients remaining on treatment as well as in survival follow-up and look forward to providing an update at CIDC in November. The data continues to mature over time, and we believe the observations to date, particularly pertaining to what appears to be a substantial enhancement of survival, will place Q101, and by implication the Q100 series, in a favorable and competitive position to potentially become a new standard of care.

Speaker Change: In totality, our data suggests that Q1 O one increases the number of patients benefiting from checkpoint inhibition.

Speaker Change: In appearance has substantially improved survival in these patients.

Daniel Passeri: Joining me on today's call is Dr. Anish Suri, our president and chief scientific officer, and Dr. Mateo Levisetti, our chief medical officer.

Dan Passeri: Joining me on today's call is Dr. Anish Suri, our president and chief scientific officer, and Dr. Mateo Levisetti, our chief medical officer. Shown here on slide two. This presentation and overview may contain some forward-looking statements and any forward-looking statements made during this call represents the company's views only as of today, August 19, 2024.

Speaker Change: We continue to monitor and carefully followed the patients remaining on treatment as well as in survival follow up and look forward to providing an update at cincy in November.

Daniel Passeri: Shown here on slide two.

Daniel Passeri: This presentation and overview may contain some forward-looking statements and any forward-looking statements made during this call represents the company's views only as of today, August 19, 2024.

Speaker Change: The data continues to mature over time, and we believe the observations to date, particularly pertaining to what appears to be a substantial enhancement of survival will place Q1 O one and by implication the cue 100 series and a favorable and competitive position to potentially become a new standard of care.

Daniel Passeri: I'd like to begin the call by providing you with some context pertaining to our recent announcement focused upon near-term developments with our autoimmune programs and associated corporate restructuring.

Dan Passeri: I'd like to begin the call by providing you with some context pertaining to our recent announcement focused upon near-term developments with our autoimmune programs and associated corporate restructuring. I'll begin with a brief synopsis of the objectives underlying these measures, and just to underscore, we carefully assessed our strategic positioning and evaluated various options for optimizing probabilities of success within the challenges and constraints of the current capital market conditions. The measures recently implemented aim to reduce our capital requirements while also achieving enhanced productivity through what we consider to be basically a balanced business model focusing upon accessing capital and additional resources through a series of anticipated strategic partnerships.

Matteo Levisetti: Moving on to the Cue 102 program, which is being explored in patients with WT1-expressing tumors, including colon, pancreatic, gastric, and ovarian cancers, Cue 102 has been well tolerated to date, and no DLTs have been observed. Preliminary and emerging data show dose-dependent increases in exposure and activation and expansion of WT1-specific T-cells. Patients and all foreign vacations have been treated at the expansion dose of four migs per take and remain on treatment for an active follow-up. As previously reported, we've observed anti-tumor activity in gastric and ovarian patients, as well as durable disease control in several tumor types, including pancreatic cancer.

Matteo Levisetti: Moving on to the Q102 program, which is being explored in patients with WT1-expressing tumors, including colon, pancreatic, gastric, and ovarian cancer. Q102 has been well tolerated to date and no DLTs have been observed. Preliminary and emerging data shows dose-dependent increases in exposure and activation and expansion of WT1. Patients in all four indications have been treated at the expansion dose of four migs per TIG and remain on treatment or in active follow-up. As previously reported, we've observed antitumor activity in gastric and ovarian patients, as well as durable disease control in several tumor types, including pancreatic.

Speaker Change: Moving on to the Q1 or two program, which is being explored in patients with WT, one expressing tumors, including colon pancreatic gastric and ovarian cancers Q1, or two has been well tolerated to date and no DLT as had been observed.

Daniel Passeri: I'll begin with a brief synopsis of the objectives underlying these measures, and just to underscore, we carefully assessed our strategic positioning and evaluated various options for optimizing probabilities of success within the challenges and constraints of the current capital market conditions. The measures recently implemented aim to reduce our capital requirements while also achieving enhanced productivity through what we consider to be basically a balanced business model focusing upon accessing capital and additional resources through a series of anticipated strategic partnerships.

Speaker Change: Preliminary and emerging data showed dose dependent increases in exposure and activation and expansion of WT one specific T cells.

Speaker Change: Patients in all four indications had been treated at expansion dose for Migs per keg and remain on treatment or in active follow up is.

Speaker Change: As previously reported we've observed antitumor activity in gastric and ovarian patients as well as durable disease control in several tumor types, including pancreatic cancer.

Daniel Passeri: These data continue to mature, and we look forward to presenting updated data at CITSI in November. But that I will now turn the call back over to Dan.

Matteo Levisetti: These data continue to mature, and we look forward to presenting updated data at CITSE in November. With that, I will now turn the call back over to Dan. Yeah, thanks, Matteo. As conveyed throughout this update call and shown on the next slide, slide 14, We continue to make significant progress across our platform with programs in both oncology and autoimmune disease. We've demonstrated the ability to selectively modulate targeted T cells, providing what we believe to be a superior therapeutic approach in both oncology and autoimmune disease treatment.

Speaker Change: These data continue to mature and we look forward to presenting updated data at <unk> in November.

Daniel Passeri: Furthermore, we've taken measures for our clinical data to further mature to enhance competitive positioning, particularly relating to patient survival data, enabling near-term cost savings and delaying the launch of a capital intensive trial towards registration. This path provides a higher probability of success as more mature data should bolster the veracity of our mechanistic advantages for establishing the potential of a new standard of care for cancer patients.

Dan Passeri: Furthermore, we've taken measures for our clinical data to further mature to enhance competitive positioning, particularly relating to patient survival data, enabling near-term cost savings and delaying the launch of a capital intensive trial towards registration. This path provides a higher probability of success as more mature data should bolster the veracity of our mechanistic advantages for establishing the potential of a new standard of care for cancer patients.

Dan: With that I will now turn the call back over to Dan Dan.

Daniel Passeri: Dan. Yeah, thanks, Mateo. As conveyed throughout this update call and shown on the next slide, slide 14, we continue to make significant progress across our platform with programs in both oncology and autoimmune disease. We've demonstrated the ability to selectively modulate targeted T-cells, providing what we believe to be a superior therapeutic approach in both oncology and autoimmune disease treatment. We continue to generate data from our two lead oncology programs, Q101 and Q102, and believe the data will continue to strengthen and bolster our position as a potential new standard of care, particularly supported by ongoing data generation pertaining to what appears to be highly meaningful and remarkable survival enhancement.

Dan Dan: Yeah. Thanks Matteo.

Speaker Change: As conveyed throughout this update call and shown on the next slide slide 14.

Speaker Change: We continue to make significant progress across our platform with programs in both oncology and autoimmune disease, we've demonstrated the ability to selectively modulate targeted T cells, providing what we believe to be a superior therapeutic approach in both oncology and autoimmune disease treatment.

Anish Suri: The selective engagement while avoiding systemic activation results in a significant reduction in cytokine release and related toxicities, which should favor patient safety while preserving efficacy.

Anish Suri: We believe the Q500 series of biologics are likely positioned as the best-in-class T-cell engagers for B-cell depletion and could address a very large segment of autoimmune patients across many indications.

Daniel Passeri: As shown in slide number three, we believe we've developed a breakthrough proprietary therapeutic approach to establish a new standard of care for treating both cancer and autoimmune diseases by restoring immune balance to the patient's immune system.

Dan Passeri: As shown in slide number three, we believe we've developed a breakthrough proprietary therapeutic approach to establish a new standard of care for treating both cancer and autoimmune diseases by restoring immune balance to the patient's immune system. As Mateo will elaborate upon shortly, our data from the ongoing Q101 Phase 1 B trial clearly demonstrates evidence of substantial prolongation of survival and patients treated with Q101 monotherapy in the second line plus setting, and Emerging Data from the Combination Trial in Frontline with Catrutas, Pembrolyzumab, that also appears to be following a similar pattern, as what we saw with the Monotherapy Trial.

Anish Suri: In summary, there are three key takeaway messages.

Matteo Levisetti: We continue to generate data from our two lead oncology programs, Q101 and Q102, and believe the data will continue to strengthen and bolster our position as a potential new standard of care, particularly supported by ongoing data generation pertaining to what appears to be highly meaningful and remarkable survival impacts. We believe these observations support the premise that our approach is selectively activating and expanding tumor-specific T cells, providing a durable anti-cancer effect, resulting in enhanced survival.

Speaker Change: We continue to generate data from our two lead oncology programs Q1 O. One in Q1 O two and believe the data will continue to strengthen and bolster our position as a potential new standard of care, particularly supported by ongoing data generation pertaining to what appears to be highly meaningful in <unk>.

Anish Suri: First, due to the shared core structural framework, the clinical de-risking and validation of immunostats in oncology via Q101 and Q102, including lack of clinically relevant immunogenicity, bolsters and supports the clinical application of Q500 series for B-cell depletion in autoimmunity.

Anish Suri: Second, selective harnessing of antiviral memory T-cells to kill B-cells circumvents the safety risk associated with systemic T-cell activation, as noted with PAN T-cell engagers.

Anish Suri: And third, data demonstrating comparable killing while avoiding high levels of pro-inflammatory cytokine production positions the Q500 series to achieve desirable efficacy while not compromising patient safety, which is of highest clinical relevance when considering therapeutic applications in autoimmune diseases.

Daniel Passeri: As Mateo will elaborate upon shortly, our data from the ongoing Q101 Phase 1 B trial clearly demonstrates evidence of substantial prolongation of survival and patients treated with Q101 monotherapy in the second line plus setting, and Emerging Data from the Combination Trial in Frontline with Catrutas, Pembrolyzumab, that also appears to be following a similar pattern, as what we saw with the Monotherapy Trial.

Speaker Change: Remarkable survival enhancement.

Daniel Passeri: We believe these observations support the premise that our approach is selectively activating and expanding to a specific T-cells, providing a durable anti-cancer effect, resulting in an enhanced survival. We believe we have the potential of establishing a new standard of care in the battle against cancer, as well as autoimmune disease. Importantly, as oncology data continue to mature, we have recently taken measures to prioritize our near-term focus in resource deployment upon near-term development milestones in our autoimmune programs, including lead selection and advancement towards the clinic and our partnership with ONO for Q401, as well as positioning Q501 for strategic partnering to further extend our capital runway, enhanced and to enhance our capacity.

Speaker Change: We believe these observations support the premise that our approach is selectively activating and expanding tumor specific T cells, providing a durable anti cancer effect, resulting in enhanced survival.

Daniel Passeri: We believe we have the potential of establishing a new standard of care in the battle against cancer as well as autoimmune disease, and Portland, as oncology, data continue to mature. We have recently taken measures to prioritize our near-term focus and resource deployment upon near-term development milestones in our autoimmune programs, including lead selection and advancement towards a clinic in our partnership with Ono for Q401, as well as positioning Q501 for strategic partnering to further extend our capital runway enhance and to enhance our capacity.

Speaker Change: We believe we have the potential of establishing a new standard of care in the battle against cancer as well as autoimmune disease importantly.

Matteo Levisetti: With that background and update, I'll turn the call over to Matteo to describe the maturing clinical data from the ongoing oncology trials.

Speaker Change: As oncology.

Speaker Change: Data continue to mature.

Matteo Levisetti: Matteo?

Daniel Passeri: We believe this data to be quite remarkable, underscoring what we believe to be the true competitive positioning of our approach.

Dan Passeri: We believe this data to be quite remarkable, underscoring what we believe to be the true competitive positioning of our approach. As such, it's our intention with the measures taken to enable clinical data to further develop and mature in support of our foundational platform, that we believe can induce effective and long lasting anti-tumor activity, or can be harnessed to rebalance the aberrant immune responses to address autoimmune disease.

Speaker Change: We have recently taken measures to prioritize our near term focus and resource deployment upon near term development milestones in our autoimmune programs, including lead selection and advancement towards the clinic and our partnership with Ono for Q4 hundred one as well as positioning Q 501 for strategic partnering to <unk>.

Matteo Levisetti: Thanks, Aneesh.

Matteo Levisetti: Good afternoon to everyone listening in on today's call.

Matteo Levisetti: The maturing clinical data from the ongoing Q101 trial continues to demonstrate highly encouraging and robust metrics of clinical benefit for patients newly diagnosed with recurrent metastatic HPV-positive head and neck cancer treated in combination with pembrolizumab and for heavily pretreated recurrent metastatic HPV-positive head and neck cancer patients treated with monotherapy. The latest data continues to bolster prior observations, further enhancing our confidence in Q101 as a potential new standard of care therapeutic to improve outcomes for patients battling HPV-positive head and neck cancer.

Matteo Levisetti: As previously and consistently stated, we believe Q101's unique mechanism of action, as evidenced by the data generated to date, enables effective and tolerated dosing and selective expansion of the targeted tumor-specific T cells.

Matteo Levisetti: Pembrolizumab is approved as the current standard of care treatment of first-line patients with recurrent metastatic head and neck cancer that have tumors with a combined positive score, or CPS score, of greater than or equal to 1%, which is a measure of PDL expression. The approval of pembrolizumab in this setting was based on a median overall survival of 12.3 months and with an objective response rate of 19%, as observed in the Keynote 48 study.

Daniel Passeri: As such, it's our intention with the measures taken to enable clinical data to further develop and mature in support of our foundational platform, that we believe can induce effective and long lasting anti-tumor activity, or can be harnessed to rebalance the aberrant immune responses to address autoimmune disease.

Speaker Change: Further extend our capital runway enhance and to enhance our capacity.

Daniel Passeri: As a reminder, we've retained a 50% co-development and co-marketing right to Q401, which has the potential application to multiple autoimmune diseases with multi-billion dollar market potential. Through various proactive measures taken, we've extended our runway to mid-2025, reduced our going-fold cash burn from approximately 40 million per year to approximately 30 million per year, and importantly, additional partnering will further enhance our cash position with upfront milestone payments, as well as reduce our operational cash burn requirements through sponsored full-time equivalent supports. Through these measures, we believe we'll be increasingly capable of sustaining operational continuity through partnerships and other means of support.

Daniel Passeri: As a reminder, we've retained a 50% co-development and co-marketing right to Q401, which has the potential application to multiple autoimmune diseases with multi-billion dollar market potential. Through various proactive measures taken, we've extended our runway to mid-2025, reduced our going-forward cash burn from approximately $40 million per year to approximately $30 million per year.

As a reminder, we've retained a 50% co development and co marketing right to Q4 hundred one which has the potential application to multiple autoimmune diseases with multibillion dollar market potential.

Daniel Passeri: We've also made significant progress with our lead autoimmune disease program Q401, being developed in collaboration with our partner, Ono Pharmaceutical, to address multiple autoimmune and inflammatory diseases, such as rheumatoid arthritis, graft versus host disease, lupus inflammatory bowel disease, psoriasis, multiple sclerosis amongst others, representing large multi-billion dollar market potential, addressing significant unmet medical need. Through this partnership, we've made impressive progress to date and moving towards selection of a lead candidate, which we anticipate in the first quarter of the coming year.

Dan Passeri: We've also made significant progress with our lead autoimmune disease program Q401, being developed in collaboration with our partner, Ono Pharmaceutical, to address multiple autoimmune and inflammatory diseases, such as rheumatoid arthritis, graft versus host disease, lupus inflammatory bowel disease, psoriasis, multiple sclerosis amongst others, representing large multi-billion dollar market potential, addressing significant unmet medical need. Through this partnership, we've made impressive progress to date and moving towards selection of a lead candidate, which we anticipate in the first quarter of the coming year.

Speaker Change: Through various proactive measures taken we've extended our runway to mid 2025 reduced our going forward cash burn from approximately $40 million per year to approximately $30 million per year, and importantly, additional partnering will further enhance our cash position with upfront milestone payments as well.

Daniel Passeri: And importantly, additional partnering will further enhance our cash position with upfront milestone payments as well as reduce our operational cash burn requirements through sponsored full-time equivalent support. Through these measures, we believe we'll be increasingly capable of sustaining operational continuity through partnerships and other means of support. As a result of these measures, combined with the ongoing progress with our maturing data across our programs, We believe we're very well positioned to realize a series of upcoming risk-reducing and value-driving milestones as we continue towards the goal of establishing a new standard of care for treating both cancer and autoimmune disease with our approach to restore health by restoring immune balance. With that, I'd now like to open the call up to questions. Operator?

Speaker Change: As reduce our operational cash burn requirements through sponsored fulltime equivalents supports.

Speaker Change: Through these measures, we believe will be increasingly capable of sustaining operational continuity through partnerships and other means of support.

Daniel Passeri: As a result of these measures, combined with the ongoing progress with our maturing data across our programs, we believe we're very well positioned to realize a series of upcoming risk-reducing and value-driving milestones as we continue to, as the goal of establishing a new standard of care for treating both cancer and autoimmune disease with our approach to restore health by restoring immune balance.

Daniel Passeri: Our collaboration with Ono has been highly productive and supportive, resulting in a growing body of promising data, demonstrating the ability of Q401 to generate and expand regulatory T-cells, or T-regs, fostering disease control, and several disease models tested to date.

Dan Passeri: Our collaboration with Ono has been highly productive and supportive, resulting in a growing body of promising data, demonstrating the ability of Q401 to generate and expand regulatory T-cells, or T-regs, fostering disease control, and several disease models tested to date. As a reminder, QBIO Pharma has retained an option to a 50% U.S. Co-development co-marketing right to Q401. Turning to 501, this program continues to advance and progress forward with a potential of eliminating auto reactive B-cells with a highly selective and well-tolerated biologic.

Speaker Change: As a result of these measures combined with the ongoing progress with our maturing data across our programs. We believe we're very well positioned to realize a series of upcoming risk, reducing and value driving milestones as we continue towards the goal of establishing a new standard of care for treating both cancer and autoimmune disease.

Daniel Passeri: As a reminder, QBIO Pharma has retained an option to a 50% U.S. Co-development co-marketing right to Q401.

Speaker Change: With our approach to restore health by restoring immune balance.

Matteo Levisetti: As presented at ASCO in June, following combination treatment with Q101, the objective response rate of 46%, as shown on slide 10, observed in patients with CPS greater than or equal to 1 represents a greater than doubling compared to the historical ORR of 19% observed with Pembrolizumab monotherapy.

Operator: With that, I'd now like to open the call up to questions, Operator.

Speaker Change: With that I'd now like to open the call up to questions operator.

Speaker Change: Yeah.

Daniel Passeri: Turning to 501, this program continues to advance and progress forward with a potential of eliminating auto reactive B-cells with a highly selective and well-tolerated biologic. This program has the promise of addressing multiple B-cell mediated autoimmune diseases, such as lupus, myostenia gravus, showgrens disease, and myocytus, amongst others, representing significant unmet medical needs with large multi-billion dollar market potential.

Operator: Thank you. We will now begin the question and answer session. To ask a question, please press star, then one on your touch-tone phone. If you're using a speaker phone, please pick up your handset before pressing the keys.

Operator: Thank you. We will now begin the question and answer session. To ask a question, please press star then 1 on your touch-tone phone. If you're using a speakerphone, please pick up your handset before pressing the keys.

Speaker Change: Thank you we will now begin the question and answer session.

Matteo Levisetti: As shown on the waterfall plot, out of 24 valuable patients, we have observed significant tumor reductions across many of these patients, including confirmed partial responses in 10 patients and a confirmed complete response in one patient. Importantly, four patients remain on treatment, including one with stable disease, that exhibits a reduction in their target lesions of minus 28%.

Matteo Levisetti: Notably, for patients with low CPS scores, or scores of 1 to 19, an ORR of 50% was observed with Q101 and Pembrolizumab, which represents a greater than tripling of the historical ORR of approximately 15% observed with Pembrolizumab alone. In totality, our data suggests that not only does Q101 appear, to demonstrably enhance the response rate of PD-1 inhibition, but also does by substantially enhancing responses in patients that are traditionally less likely to respond.

Speaker Change: Ask a question. Please press Star then one on your Touchtone phone.

Speaker Change: If youre using a speakerphone please pick up your handset before pressing the keys.

Operator: If at any time your question has been addressed, and you would like to withdraw your question, please press star then 2. And at this time, we'll pause momentarily to assemble our office. And the first question will come from Stephen Wiley with Stiefel. Please go ahead. Yeah, good afternoon.

Operator: If any time your question has been addressed and you would like to withdraw your question, please press star then two, and at this time, we'll pause momentarily to assemble our roster.

Dan Passeri: This program has the promise of addressing multiple B-cell mediated autoimmune diseases, such as lupus, myostenia gravus, showgrens disease, and myocytus, amongst others, representing significant unmet medical needs with large multi-billion dollar market potential. Furthermore, the same mechanism of action that we would be seeing in B-cell oblation for autoimmune disease may be deployed to address B-cell malignancies, such as B-cell lymphoma, with presently assessing strategic partnering alternatives for furthering the development of this promising program, and look forward to providing updates as to become available.

Speaker Change: If any time your question has been addressed and you would like to withdraw. Your question. Please press Star then two and at this time, we'll pause momentarily to assemble our roster.

Matteo Levisetti: This is particularly important since patients, with low CPS scores represent approximately 50% of all patients that are CPS positive and eligible for treatment with Pembrolizumab in the frontline setting.

Matteo Levisetti: The responses observed in these patients have been durable, as reflected in the 12-month OS, and median OS, which is shown on the next slide, slide 11.

Speaker Change: Okay.

Stephen Willey: In the first question, we'll come from Stephen Wiley with Steeple. Please go ahead. Yeah, good afternoon. Thanks for taking the questions. On each of Dan, I was just wondering if you could speak to maybe what you know at this point about the trafficking capacity of Q5O. 101. And then also just what's your estimate of CMV zero positivity in the general population? I know it's correlated to age. I think it tends to be lower in males versus females, but just wondering kind of what your general estimate of this would be and whether you would need to screen for CMV positivity in the context of a based on those escalation trial.

Matteo Levisetti: For patients treated with Q101 and Pembrolizumab as first-line treatment, the median PFS of 5.8 months compares favorably to the median PFS of 3.2 months that was observed in the Pembrolizumab arm of the Keynote 48 trial.

Speaker Change: And the first question will come from Stephen Wiley with Stifel. Please go ahead.

Matteo Levisetti: Importantly, the 12-month OS of 90% and the median OS of 21.8 months observed in patients, with CPS greater than or equal to 1 treated with combination treatment is notable and substantially better than the historical data with Pembrolizumab monotherapy, where 12-month OS and median OS were 51% and 12.3 months, respectively.

Matteo Levisetti: These enhanced survival metrics, which continue to be followed, are particularly evident, when looking at the patients with both low and high PD-L1 expression, as shown on slide 12. Consistent with the enhanced ORR observed in patients with low PD-L1 expression treated, with Q101 and Pembrolizumab, these patients are demonstrating favorable metrics of survival.

Matteo Levisetti: In CPS low patients treated with Q101 and Pembrolizumab, the 12-month OS of 82% and the median OS of 21.8 months is importantly notable given the historical values of 44% and 10.8 months observed for Pembrolizumab in the Keynote 48 study.

Stephen Wiley: Yeah. Good afternoon, thanks for taking the questions.

Matteo Levisetti: As a reminder, these maturing data from the combination trial appear to be following what, we observed in the monotherapy second line plus setting where Q101 demonstrated significant prolongation of survival as shown in the following slide, slide 13. As shown on the left, the median OS observed in patients treated with Q101 monotherapy, at 2 mg per kg was 24.8 months, and 20.8 months for those treated with Q101 at a dose of 4 mg per kg.

Matteo Levisetti: The benefit to CPS high patients is also noteworthy with 12-month OS of 100% and a median OS, that has not yet been reached in patients with CPS greater than or equal to 20 treated with Q101 and pembrolizumab compared to the historical values of 56% in 14.8 months, respectively.

Matteo Levisetti: The survival observed in these patients is remarkable when compared to the median OS, observed in the second line with checkpoint inhibitors, where median OS of 7.5 and 8.4 months were observed for nivolumab and pembrolizumab, respectively. We believe this enhancement of survival to be mediated by the durable and selective expansion, of targeted tumor-specific T cells by Q101. In totality, our data suggests that Q101 increases the number of patients benefiting, from checkpoint inhibition and appears to substantially improve survival in these patients.

Daniel Passeri: Furthermore, the same mechanism of action that we would be seeing in B-cell oblation for autoimmune disease may be deployed to address B-cell malignancies, such as B-cell lymphoma, with presently assessing strategic partnering alternatives for furthering the development of this promising program, and look forward to providing updates as to become available.

Stephen Willey: Thanks for taking the questions. Anish or Dan, I was just wondering if you.., speak to maybe what you know at this point about the trafficking capacity of Q501. And then also, just what's your estimate of CMV zero positivity in the general population? I know it's correlated to age. I think it tends to be lower in males versus females.

nishu Dan: So nishu Dan was just wondering if you.

Stephen Wiley: I could speak to maybe what you know at this point about the traffic and capacity.

Speaker Change: Q five O.

Speaker Change: One.

Speaker Change: And then also just whats your estimated CMP zero positivity in the general population I know, it's correlated to age.

Daniel Passeri: We have positioned ourselves with a growing portfolio of highly promising drug candidates in both oncology and autoimmune disease, all of which represent significant market opportunities addressing major unmet medical needs.

Dan Passeri: We have positioned ourselves with a growing portfolio of highly promising drug candidates in both oncology and autoimmune disease, all of which represent significant market opportunities addressing major unmet medical needs. We believe we've de-risked and validated our therapeutics platform with the existing data sets from our Q101 and Q102 programs, and have established foundational pre-clinical data pertaining to our autoimmune programs with potential to rebalance the patient's immune system to restore health. We've implemented a cash-efficient business model enabling a reduction of capital requirements with an emphasis on validating net-term partner infrastructures.

Speaker Change: Tends to be lower than males versus females.

Anish Suri: I'm just wondering kind of what your general estimate of this would be and whether you would need to screen for CMV positivity, face-on. Yeah, so both very good questions, Steve. CME is an example we presented, but just to make the point, Steve, we have made. Cue 500 molecules with SARS-CoV-2 and EBV and other viral epitopes as well. So we presented the case with CMV. In the particular case of CMV, zero positivity, anywhere around 65 to 70 percent.

Speaker Change: I'm just wondering kind of what are your general estimate of this would be and whether you would need to screen for CMV positivity of the context.

Speaker Change: Phase one dose escalation trial.

Daniel Passeri: We believe we've de-risked and validated our therapeutics platform with the existing data sets from our Q101 and Q102 programs, and have established foundational pre-clinical data pertaining to our autoimmune programs with potential to rebalance the patient's immune system to restore health.

Daniel Passeri: Yeah. So, both very good questions, Steve. CMV is an example we presented, but just to make the point, Steve, we have made Q500 molecules with SARS-CoV-2 and EBV and other viral epitopes as well. So we presented the case with CMV. In the particular case of CMV, zero positivity anywhere around 65 to 70% in our experience when we've screened donors for SARS-CoV-2 at this point in time in the history of mankind, virtually a hundred percent. A hundred percent have been SARS-CoV-2 for obvious reasons. From the trafficking, we are now doing in vivo studies, but with immunostats in general, Steve, we had published a paper in Nature Methods with Hinaplu several years back, where we used immunopath imaging to make the point that immunostats could penetrate solid tumour tissue as well as an infectious model and directly engage the relevant antigen specific.

Matteo Levisetti: We continue to monitor and carefully follow the patients remaining on treatment as well, as in survival follow-up and look forward to providing an update at CITSE in November.

Speaker Change: Yeah, So both very good questions Steve.

Matteo Levisetti: The data continues to mature over time, and we believe the observations to date, particularly, pertaining to what appears to be a substantial enhancement of survival, will place Q101 and, by implication, the Q100 series in a favorable and competitive position to potentially become a new standard of care.

Matteo Levisetti: Moving on to the Q102 program, which is being explored in patients with WT1-expressing tumors, including colon, pancreatic, gastric, and ovarian cancers, Q102 has been well-tolerated to date, and no DLTs have been observed. Preliminary and emerging data shows dose-dependent increases in exposure and activation and expansion, of WT1-specific T cells. Patients in all four indications have been treated at the expansion dose of 4 mg per, kg and remain on treatment or in active follow-up.

Speaker Change: <unk> as an example, we presented but just to make the point, Steve we have made to.

Matteo Levisetti: As previously reported, we've observed antitumor activity in gastric and ovarian patients, as well as durable disease control in several tumor types, including pancreatic cancer.

Matteo Levisetti: These data continue to mature, and we look forward to presenting updated data at CITSE, in November.

Daniel Passeri: With that, I will now turn the call back over to Dan.

Speaker Change: <unk> 500 molecules with Sars Scooby Doo.

Speaker Change: E P V and other viral epitopes as well so we presented the case with CMV.

Daniel Passeri: We've implemented a cash-efficient business model enabling a reduction of capital requirements with an emphasis on validating net-term partner infrastructures.

Speaker Change: Particular cases of CMV.

Positivity anywhere to around 65, 2% to 70%.

Anish Suri: In our experience, when we've screened donors for SARS-CoV-2 at this point in time, History of Mankind, virtually 100% have been SARS-CoV-2, for obvious reasons. From the trafficking, we are now doing in vivo studies, but with immunostats in general, Steve, we had published a paper in Nature, methods with Hedaplu several years back where we used immunopet imaging to make the point, that immunostats could penetrate solid tumor tissue as well as an infectious model and directly engage the relevant antigen-specific T cells.

Our experience when we screen donors for solder supposed to do at this point in time.

Anish Suri: I'm going to now turn the call over to Anish who will describe the core attributes and advantages of our approach to treating autoimmune disease as well as provide some additional context on our underlying platform developments for both oncology and autoimmune disease.

Dan Passeri: I'm going to now turn the call over to Anish who will describe the core attributes and advantages of our approach to treating autoimmune disease as well as provide some additional context on our underlying platform developments for both oncology and autoimmune disease. After Anish, Matteo will provide further updates on the Q101 and one on two clinical trials and highlight the importance of the maturing data sets with particular attention to the survival metrics that are emerging.

Speaker Change: The history of mankind, virtually 100% of being sorry was positive.

Speaker Change: For obvious reasons.

Speaker Change: From the trafficking, we're now doing in vivo studies, but with immuno stats in general Steve We had published a paper in nature.

Anish Suri: After Anish, Matteo will provide further updates on the Q101 and one on two clinical trials and highlight the importance of the maturing data sets with particular attention to the survival metrics that are emerging.

Speaker Change: Methods with hit up Blue several years back where we used immuno pet imaging to make the point.

Speaker Change: That immuno stats, good penetrates solid tumor tissue as well as an infectious model indirectly engage the relevant antigen specific T cells and we believe the same should hold truthful.

Anish Suri: I'll then return for a brief summary before opening the call up to question Anish. Thanks, Dan, and good afternoon to all listening in on today's call. I'll start by briefly summarizing our platform and the significant potential of our approach for restoring immune balance for treating cancers and autoimmune diseases. As described previously, the immunostat platform enables selective modulation of disease relevant immune cells while avoiding broad perturbations of the immune system. This approach allows us to maximize efficacy while preserving patient safety.

Daniel Passeri: We believe that same should hold true for the 500 series where you can have extravacation and local engagement to essentially be able to recognize the eSus that are bound by these molecules. Okay, that's helpful.

Anish Suri: And we believe the same should hold true. 500 series where you can have extravasation and loppling, to essentially.., be able to, recognized. Charles de la Pound.

Anish Suri: I'll then return for a brief summary before opening the call up to question Anish.

Speaker Change: 500 series, where you can have extravasation and local engagement.

Anish Suri: Thanks, Dan, and good afternoon to all listening in on today's call.

Speaker Change: To essentially be able to.

Speaker Change: Recognize the pieces that are bound by these molecules.

Anish Suri: I'll start by briefly summarizing our platform and the significant potential of our approach for restoring immune balance for treating cancers and autoimmune diseases. As described previously, the immunostat platform enables selective modulation of disease relevant immune cells while avoiding broad perturbations of the immune system. This approach allows us to maximize efficacy while preserving patient safety.

Stephen Willey: Okay, that's helpful. And then, um, maybe just a key one on one question. So, um, I understand that you guys are obviously, kind of pausing things for now, allowing the survival data to mature, but I guess in the context of, front line head and neck right now and what is capable with temporal monotherapy. I think that appears to be the subject of, increasing debate as a function, primarily, I guess, the leak tent data.

Speaker Change: Okay. That's helpful and then.

Daniel Passeri: And then maybe just a key one or one question. So I understand that you guys are obviously kind of pausing things for now and allowing them. It's a survival data to mature, but I guess in the context of frontline head and neck right now, and what is capable with pember amount of therapy, I think that appears to be the subject of some increasing debate as a function of primarily, I guess, the leap 10 data. So just curious, if you think a more mature survival statistic could help attract strategic interest and just curious if you can share anything in terms of the conversations that you've had thus far with potentially interested parties in terms of how they're thinking about what pember amount of therapy historically is capable of.

Speaker Change: Just the keyword of one question so.

Speaker Change: I understand that you guys are obviously kind.

Speaker Change: Kind of pausing things for now.

Speaker Change: Allowing the survival data to mature, but I guess in the context of <unk>.

Anish Suri: As Dan indicated previously and as summarized on slide three, we have now clinically validated immunostats via the Q100 series that selectively and safely delivers the potent cytokine IL-2 along with the TCR activating signal to preferentially activate tumor-specific T cells while sparing all other irrelevant T cells. This selective stimulation allows for the generation of a therapeutic index for IL-2 which has alluded many others trying to develop IL-2-based cancer therapies.

Anish Suri: As Dan indicated previously and as summarized on slide three, we have now clinically validated immunostats via the Q100 series that selectively and safely delivers the potent cytokine IL-2 along with the TCR activating signal to preferentially activate tumor-specific T cells while sparing all other irrelevant T cells. This selective stimulation allows for the generation of a therapeutic index for IL-2 which has alluded many others trying to develop IL-2-based cancer therapies. In over 120 patients dozed, we have demonstrated a remarkable increase in efficacy with favorable tolerability.

Speaker Change: Frontline head in that right now and what it's capable of timber mono therapy, I think that appears to be the subject of increasing debate is approaching.

Speaker Change: Primarily I guess 10 data so.

Stephen Willey: Just curious, you know, if you think, you know, a more mature survival statistic could help attract strategic interest and just curious if you can share anything in terms of the conversation, potentially interested parties, you know, how they're thinking about, what Pembro Monotherapy has stored. Sure. Thanks, Steve. Dan.

Speaker Change: Just curious.

Speaker Change: If you think more mature survival statistics could help attract strategic interest and just curious if you can share anything in terms of the conversations that you've had thus far with.

Anish Suri: In over 120 patients dozed, we have demonstrated a remarkable increase in efficacy with favorable tolerability.

Speaker Change: Potentially interested parties in terms of.

Anish Suri: Mateo will provide further details on the latest clinical data that continue to demonstrate impressive benefit for patients being treated with Q101 and Q102.

Anish Suri: Mateo will provide further details on the latest clinical data that continue to demonstrate impressive benefit for patients being treated with Q101 and Q102. On the autoimmune front, we have focused on two distinct and highly promising approaches to reset immune balance. Q101 is a novel by specific that stimulates the generation and expansion of regulatory T cells. Regulatory T cells or T-regs possess the ability to dampen and control or reactive lymphocytes hence are an important cell type to maintain immune homeostasis and health.

Speaker Change: They're thinking about.

Speaker Change: Yeah.

Speaker Change: Remember a monotherapy historically is capable.

Daniel Passeri: Sure, thanks, Steve. This is Dan. So it's an important question. We've had dialogue with multiple potential partners on the data sets that we've had historically. When we look at the monotherapy data, I mean, we've actually had the comment of the data looks so promising that how do they know that we haven't biased by selecting healthy patients. And that's one of the reasons we emphasize the randomized strategy for the phase two. I think what's really important here, when you look at the landscape of competing molecules, different kinase inhibitors, et cetera, in this space, we think the survival data is in a really differentiate and truly position.

Daniel Passeri: Dan?

Speaker Change: Sure. Thanks, Steve This is.

Daniel Passeri: Yeah.

Anish Suri: On the autoimmune front, we have focused on two distinct and highly promising approaches to reset immune balance. Q101 is a novel by specific that stimulates the generation and expansion of regulatory T cells. Regulatory T cells or T-regs possess the ability to dampen and control or reactive lymphocytes hence are an important cell type to maintain immune homeostasis and health.

Daniel Passeri: So it's an important question. We've had dialogue with multiple, potential partners, on the data sets that we've had historically. When we look at the monotherapy data, I mean, we've actually had the comment of the data looks so promising that how do they know that we haven't biased by selecting healthy patients? And that's one of the reasons we emphasize the randomized, strategy for the phase two. I think what's really important here when you look at the, landscape of competing molecules, different kinase inhibitors, et cetera, in this space, we think the survival data is gonna really differentiate and truly position Q with an advantage, and a competitive advantage, in terms of the durability of triggering an immune response.

Speaker Change: Dan.

Daniel Passeri: Thanks, Matteo.

Daniel Passeri: As conveyed throughout this update call and shown on the next slide, slide 14, we continue, to make significant progress across our platform with programs in both oncology and autoimmune disease. We've demonstrated the ability to selectively modulate targeted T cells, providing what, we believe to be a superior therapeutic approach in both oncology and autoimmune disease treatment.

Speaker Change: So it's an important question we've had dialogue with multiple.

Daniel Passeri: We continue to generate data, from our two lead oncology programs, Q101 and Q102, and believe the data will continue to strengthen and bolster our position as a potential new standard of care, particularly supported by ongoing data generation pertaining to what appears to be highly meaningful and remarkable survival enhancement. We believe these observations support the premise, that our approach is selectively activating and expanding tumor-specific T cells, providing a durable anti-cancer effect resulting in enhanced survival.

Speaker Change: Potential partners.

On the datasets that we've had historically.

When we look at the monotherapy data I mean, we've actually had the comment of the data looks so promising that how do they know that we havent biased by selecting healthy patients and that's one of the reasons, we emphasize the randomized.

Anish Suri: Q101 has been partnered with ONO Pharmaceuticals and this collaboration continues to move forward strongly.

Anish Suri: Q101 has been partnered with ONO Pharmaceuticals and this collaboration continues to move forward strongly. In addition to Q101, we've also made significant progress developing Q501 from the Q500 series to enable T cell mediated depletion of B cells. This approach has the potential to deliver CAR-T-like efficacy in a biologic while preserving patient safety which offers significant differentiation from other competing approaches. Both Q101 and Q500 series are designed to address large patient populations across numerous autoimmune and inflammatory diseases with a multi-billion dollar market potential.

Speaker Change: Our strategy for the phase two.

Daniel Passeri: We believe we have the potential of establishing, a new standard of care in the battle against cancer as well as autoimmune disease.

Daniel Passeri: Importantly, as oncology data continue to mature, we have recently taken measures to prioritize our near-term focus and resource deployment upon near-term development milestones in our autoimmune programs, including lead selection and advancement towards a clinic in our partnership with Ono for Q401, as well as positioning Q501 for strategic partnering to further extend our capital runway enhance and to enhance our capacity.

Speaker Change: I think what's really important here when you look at the.

Anish Suri: In addition to Q101, we've also made significant progress developing Q501 from the Q500 series to enable T cell mediated depletion of B cells. This approach has the potential to deliver CAR-T-like efficacy in a biologic while preserving patient safety which offers significant differentiation from other competing approaches.

Speaker Change: Landscape of competing molecules different kinase inhibitors et cetera. In this space. We think the survival data is going to really differentiate and truly position Q.

Daniel Passeri: As a reminder, we've retained a 50% co-development, and co-marketing right to Q401, which has the potential application to multiple autoimmune diseases with multi-billion dollar market potential. Through various proactive measures taken, we've extended our runway to mid-2025, reduced our going forward cash burn from approximately 40 million per year to approximately 30 million per year. And importantly, additional partnering, will further enhance our cash position with upfront milestone payments, as well as reduce our operational cash burn requirements through sponsored full-time equivalent supports. Through these measures, we believe we'll be, increasingly capable of sustaining operational continuity through partnerships and other means of support.

Daniel Passeri: As a result of these measures, combined with the ongoing progress with our maturing data across our programs, we believe we're very well positioned to realize a series of upcoming risk-reducing and value-driving milestones as we continue towards the goal of establishing a new standard of care for treating both cancer and autoimmune disease with our approach to restore health by restoring immune balance.

Daniel Passeri: With that, I'd now like to open the call up to questions.

Daniel Passeri: Q with an advantage and a competitive advantage in terms of durability of triggering an immune response. So that survival data, as it continues to mature, I think what we've seen in monotherapy is very impressive. What we're seeing emerge with the combination appears to be following suit. And I think that's going to be dispositive in the long run. I think ultimately a randomized study is basically far more convincing because you're going directly against Pembro as a single agent. But it is an important topic, and it is being watched. And we do have ongoing dialogue with companies on 101.

Speaker Change: With an advantage and a competitive advantage in terms of the durability of triggering an immune response, so that survival data as it continues to mature I think what we've seen in monotherapy is very impressive what we're seen emerge with the combination appears to be following suit.

Daniel Passeri: So that survival data, as it continues to mature, I think what we've seen in monotherapy is very impressive. What we're seeing emerge with the combination appears to be following suit, and I think that's gonna be dispositive in the long run. I think, ultimately, a randomized study is basically far more convincing, because you're going directly against PEMBRO as a single agent.

Anish Suri: Both Q101 and Q500 series are designed to address large patient populations across numerous autoimmune and inflammatory diseases with a multi-billion dollar market potential. We will expand on both programs in the next few slides.

Speaker Change: And I think that's going to be just positive in the long run I think ultimately a randomized study as you know on basically far more convincing because you're going directly against.

Anish Suri: We will expand on both programs in the next few slides. The next slide, slide 4, exemplifies the unique attributes of Q101 in induction and expansion of T-regs. Q101 is a bi-specific composed of the two key cytokines IL-2 and TG of beta that are known to convert peripheral CD4 T cells into T-regs as well as expand pre-existing natural T-regs. This ability to induce new populations of T-regs provides Q101 with the prospects of significant superiority over other approaches deploying IL-2 variants to focus on only the pre-existing natural.

Anish Suri: The next slide, slide 4, exemplifies the unique attributes of Q101 in induction and expansion of T-regs. Q101 is a bi-specific composed of the two key cytokines IL-2 and TG of beta that are known to convert peripheral CD4 T cells into T-regs as well as expand pre-existing natural T-regs. This ability to induce new populations of T-regs provides Q101 with the prospects of significant superiority over other approaches deploying IL-2 variants to focus on only the pre-existing natural.

Speaker Change: <unk> as a single agent, but it is an important topic and it is being watched.

Reni Benjamin: But it is an important topic, and it is being watched, and we do have ongoing dialogue with companies on 101. Alright, thanks for taking the questions. The next question will come from Ren Benjamin with Citizens JMP. Please go ahead. Hey, good afternoon, guys.

Speaker Change: And we do have ongoing dialogue with companies on one on one.

Operator: Operator?

Stephen Willey: Alright, thanks for taking the questions. Yeah.

Reni Benjamin: Thanks for taking the questions. So thanks for the update on 101 in combination with Keytruda and as in the monotherapy. I guess my first question would be how to think about these results, given the current landscape and in particular, you know, kind of the developing landscape given the provocative data we saw at ASCO from Marist, some of the others, you know, that are also in this space. And just as a follow-up to that, you know, I'm kind of curious, I don't think it was mentioned in the earlier comments, can you provide any sort of an update on the neoadjuvants? Sure. Matteo, why don't you take that question for both of them? Yeah, no, I will.

Alright, thanks for taking my questions.

Speaker Change: Yep.

Reni Benjamin: The next question will come from Reni Benjamin with Citizens' JMP. Please go ahead. Hey, good afternoon, guys. Thanks for taking the questions. So thanks for the update on one-on-one incommination with Petrua and the monotherapy. I guess my first question would be how to think about these results, given the current landscape. And in particular, kind of the developing landscape, given the provocative data we saw it ask out from Maris and some of the others that are also in the space. And just as a follow-up to that, I'm kind of curious. I don't think it was mentioned in the earlier comments.

Speaker Change: The next question will come from Ren Benjamin with citizens JMP. Please go ahead.

Operator: Thank you.

Operator: We will now begin the question and answer session.

Matteo Levisetti: And again, just to follow up on the prior question, again, I think this really, you know, the data from the LEAP-10 trial underscores the importance of looking at early survival metrics, specifically, like a 12-month, okay, survival, and also median OS as it matures. And so, if you actually look at the PEMBRO Mono dataset from LEAP-10, the 12-month survival is 59%, okay? If we look at the Q101 combination data, our current 12-month survival is 90%. And if you look at CPS-High, it's 100% of patients are alive at 12 months.

Ren Benjamin: Hey, good afternoon, guys. Thanks for taking the questions.

Operator: To ask a question, please press star then one, on your touch-tone phone. If you're using a speakerphone, please pick up your handset before pressing the keys. If at any time your question has been addressed, and you would like to withdraw your question, please press star then two.

Operator: And the first question will come from Steven Wiley

Operator: And at this time, we'll pause momentarily, to assemble our roster.

Ren Benjamin: So thanks for the update on <unk> hundred one in combination and Keytruda in combination with Keytruda and that the monotherapy I guess, Mike My first question would be how to think about these results.

Anish Suri: T-Rex.

Anish Suri: T-Rex. As shown in slide 4, we believe the mechanism of action of Q401 to enhance T-Rex is qualitatively and quantitatively superior to IL-2 Mutine's targeting CD25, which is the high affinity subunit of the IL-2 receptor expressed on regulatory T cells. Slide 5 highlights data sets that show superiority of Q401 over an IL-2 Mutine analog currently in clinical development for T-Rex generation. As shown on the left side of this slide, in an in vitro human emilar assay, which is an in vitro model for graft-versus-horse disease, Q401 induces differentiation and expansion of T-Rex.

Anish Suri: As shown in slide 4, we believe the mechanism of action of Q401 to enhance T-Rex is qualitatively and quantitatively superior to IL-2 Mutine's targeting CD25, which is the high affinity subunit of the IL-2 receptor expressed on regulatory T cells.

Operator: with Stiefel.

Matteo Levisetti: And so with regards to the question now of the evolving landscape, and with, I guess, in particular, Maris' compound to Potosemtet Mab, again, it's really important to look at the data that they've shared with regards to their survival. And so in the second line setting and beyond, they reported a survival of 11.5 months, with Q101 mono, we're currently at, you know, 20.8 months, and even 20, almost five months in the 2 Mg per kg cohort.

Stephen Willey: Please go ahead.

Speaker Change: Given the current landscape and in particular cobre.

Speaker Change: Developing landscape given the provocative data we saw at Astro from Maris with some some of the others.

Stephen Willey: Yeah, good afternoon.

Stephen Willey: Thanks for taking the questions.

Anish Suri: Slide 5 highlights data sets that show superiority of Q401 over an IL-2 Mutine analog currently in clinical development for T-Rex generation.

Stephen Willey: Aneesha, Dan, was just wondering if you could speak, to maybe what you know at this point about the trafficking capacity of Q501.

Speaker Change: We're also in the space.

Speaker Change: And just as a follow up to that you.

Speaker Change: You know.

Anish Suri: As shown on the left side of this slide, in an in vitro human emilar assay, which is an in vitro model for graft-versus-horse disease, Q401 induces differentiation and expansion of T-Rex.

Speaker Change: I'm kind of curious I don't think it was mentioned in the.

Speaker Change: The earlier comments can you provide any sort of an update on the neo adjuvant study.

Matteo Levisetti: Can you provide any sort of an update on the neo-agent study? Sure. Matteo, why don't you take the question? Yeah, no, I will. And again, just to follow up on the prior question. Again, I think this really, you know, the data from the Lead 10 trial underscores the importance of looking at early median OS as it matures. And so you actually look at the Pembro Mono data set from lead 10, the 12-month survival is 59 percent. If we look at the Q101 combination data, our current 12-month survival is 90 percent. And if you look at CPS high, it's 100 percent of patients are alive at 12 months.

Mitch: Sure Mitch.

Anish Suri: In contrast, a T-Rex-directed IL-2 Mutine is unable to achieve these effects.

Anish Suri: In contrast, a T-Rex-directed IL-2 Mutine is unable to achieve these effects. The bottom left panel confirms that both IL-2 and TGF beta signals are needed for T-Rex generation either alone is unable to achieve this effect. As shown on the right side, and as previously discussed, short-term administration of Q401 results in long-term protection from auto-munity, in this case auto-mium gas tritis. In our ongoing collaboration with ONO Pharmaceuticals, we have further extended the In vivo efficacy with Q401 in several other disease models where we have noted a significant increase in T-Rex accompanied by a notable decrease in pro-inflammatory cytokines.

Speaker Change: Why don't you take that question both of them.

Mitch: Yeah, No I will end and again just to follow up on on the prior question.

Anish Suri: The bottom left panel confirms that both IL-2 and TGF beta signals are needed for T-Rex generation either alone is unable to achieve this effect.

Mitch: Again, I think that's really.

Mitch: The data from the elite 10 trial underscores the importance of looking at early survival metrics specifically.

Anish Suri: As shown on the right side, and as previously discussed, short-term administration of Q401 results in long-term protection from auto-munity, in this case auto-mium gas tritis.

A 12 month, Okay survival and also a median OS as it matures.

Anish Suri: In our ongoing collaboration with ONO Pharmaceuticals, we have further extended the In vivo efficacy with Q401 in several other disease models where we have noted a significant increase in T-Rex accompanied by a notable decrease in pro-inflammatory cytokines.

Mitch: And so if you actually look at the Pembroke Mono data set probably 10 to 12 months survival is 59% okay.

Mitch: If we look at the Q1 O. One combination data our current 12 month survival is 90%, Okay and if you look at Cps high it's 100% of patients are alive at 12 months, Okay and.

Anish Suri: Let's now move to slide 6 to provide an overview and update on the Q500 series for B-cell depletion.

Anish Suri: Let's now move to slide 6 to provide an overview and update on the Q500 series for B-cell depletion. The primary goal behind the design of the Q500 T-cell engages was to achieve T-cell mediated depletion of B-cells while avoiding the adverse effects of systemic immune activation and broad engagement of all T-cells. Our approach enables the potential to achieve cartilic efficacy while avoiding the safety pitfalls of pan-T-cell engages. By design, the Q500 series immunostats bind to CD-19 on B-cells and effectively paint the B-cells with a viral epitope, such as CMV.

Anish Suri: The primary goal behind the design of the Q500 T-cell engages was to achieve T-cell mediated depletion of B-cells while avoiding the adverse effects of systemic immune activation and broad engagement of all T-cells.

Matteo Levisetti: Okay. And so, with regards to the question now of the evolving landscape, in particular, Maris has compounded to FEMTED MAB. Again, it's really important to look at the data that they've shared with regards to their survival. And so, in the second line setting and beyond, they reported a survival of 11.5 months. Okay. With Q101 Mono, we're currently at, you know, 20.8 months and even 20 almost five months in the two-meg per key cohort. So, although in the second line plus, they reported a response rate of 37 percent. Their survival is about half as long, okay, as Q monotherapy, where we observed a response rate of 5 percent.

Mitch: And so with regards to the question now of the evolving landscape.

And with I guess.

Mitch: In particular.

Speaker Change: Merisis compounds.

Speaker Change: But <unk> Mab again, it's really important to look at the data that they've they've shared it with regards to their survival, okay and so in the second line setting and beyond they reported a survival of 11 five months okay.

Anish Suri: Our approach enables the potential to achieve cartilic efficacy while avoiding the safety pitfalls of pan-T-cell engages.

Matteo Levisetti: So, although in the second line plus, they reported a response rate of 37%, their survival is about half as long, okay, as Q monotherapy, where we observed a response rate of 5%. And again, this is fully consistent with patterns of clinical benefit that have been now well-defined in immunotherapy. So, if we look at ChimTrac, recently approved for uveal melanoma, really modest response rate, but a clear survival benefit led to its approval.

Anish Suri: By design, the Q500 series immunostats bind to CD-19 on B-cells and effectively paint the B-cells with a viral epitope, such as CMV. These B-cells are then readily recognized and killed by the memory antiviral T-cells as shown in the slide.

With Q1 O one mono we're currently at.

Anish Suri: These B-cells are then readily recognized and killed by the memory antiviral T-cells as shown in the slide. Engaging virus-specific T-cells or VSTs offers several advantages. These are trained K-cells present in high frequency across the human population. They are localized in disease tissue and perform rapid killing of targets. And due to their specificity of virus antigens, the VSTs avoid the risk of potential reactivity against self-tissue or systemic immune activation as would be with pan-T-cell engages.

Speaker Change: 28 months and even 'twenty almost five months in the two Meg per kg cohort. So although in the second line plus they reported a response rate of 37% their survival is about half as long, okay. As Q monotherapy, where we observed a response rate of 5%.

Anish Suri: Engaging virus-specific T-cells or VSTs offers several advantages.

Anish Suri: These are trained K-cells present in high frequency across the human population. They are localized in disease tissue and perform rapid killing of targets.

Matteo Levisetti: And again, this is fully consistent with patterns of clinical benefit that have been now well-defined in immunotherapy. So if we look at TEMTRAC, recently approved for UVIL melanoma, really modest response rate, but a clear survival benefit led to its approval. And so back to Potosimab now in the they actually only reported data on about half of the patients that were treated with very minimal follow-up. So, with the follow-up median follow-up, if you looked at the swimmer plot about four months. So again, I would just, you know, use caution and clearly hear the data; you know, needs to mature.

Speaker Change: And again this is fully consistent with patterns of clinical benefit that that had been now well defined immunotherapy. So if we look at him track recently approved for for for Uveal melanoma.

Anish Suri: And due to their specificity of virus antigens, the VSTs avoid the risk of potential reactivity against self-tissue or systemic immune activation as would be with pan-T-cell engages.

Speaker Change: Really modest response rate, but a clear survival benefit led to its approval.

Anish Suri: Importantly, and as shown in slide 7, VSTs in this case, CMV-specific memory T-cells can achieve the same degree of killing of B-cells as pan-T-cell engages, in this case an anti-CD-19, anti-CD-3 by specific molecule.

Anish Suri: Importantly, and as shown in slide 7, VSTs in this case, CMV-specific memory T-cells can achieve the same degree of killing of B-cells as pan-T-cell engages, in this case an anti-CD-19, anti-CD-3 by specific molecule. Note here that the killing is specific to the engagement of CMV T-cells since a Q500 molecule expressing an HIV epitope is unable to mediate B-cell killing since HIV-specific T-cells are largely absent in most individuals. Slide 8 further exemplifies the difference in safety and side-up and production between Q501 and pan-T-cell engages.

Matteo Levisetti: And so back to Pitocimab now in the front-line setting, you know, they, at ASCO, reported some, you know, very preliminary data. They actually only reported data on about half of the patients that were treated, with very minimal follow-up. So with the follow-up, median follow-up, if you looked at the swimmer plot, about four months.

Speaker Change: And so back to <unk> now in the frontline setting.

Speaker Change: They are at ESCO reported some some very preliminary data.

Anish Suri: Note here that the killing is specific to the engagement of CMV T-cells since a Q500 molecule expressing an HIV epitope is unable to mediate B-cell killing since HIV-specific T-cells are largely absent in most individuals.

Speaker Change: They actually only reported data on or about half of the patients that were treated.

Speaker Change: With very minimal follow upset with the follow up a median follow up if you'd looked at their swimmer plot about four months. So again I would just yeah. You know you use caution and clearly here the data.

Matteo Levisetti: So again, I would just use caution. And clearly here, the data needs to mature. And as I mentioned before, we have maturing metrics, both at 12-month OS and median OS, that are established. So that's real data.

Anish Suri: Slide 8 further exemplifies the difference in safety and side-up and production between Q501 and pan-T-cell engages.

Needs to mature and as I mentioned before we have maturing metrics. Both at 12 months and median O S them better establish so that's real data and we'll have to see what happens going forward with that and perhaps.

Matteo Levisetti: And as I mentioned before, we have maturing metrics both at 12 month OS and median OS that are established. So that's real data, and we'll have to see what happens. I'm going forward with Potosian app. And perhaps, you know, one could hypothesize, it will be similar to different inhibitors of these pathways for which they're inevitably pop up bypass pathways, and hence the advantages of engaging the immune system and inducing expansion of a durable anti-tumored T-cell population.

Anish Suri: Due to the high selective engagement, the Q501 molecule does not result in copious production of inflammatory cytokines such as interferon gamma and TNF as shown here.

Anish Suri: Due to the high selective engagement, the Q501 molecule does not result in copious production of inflammatory cytokines such as interferon gamma and TNF as shown here. In contrast, a pan-T-cell engage a molecule due to its anti-CD-3 binding to all T-cells results in significantly high levels of cytokine released which ultimately compromises patient safety and drug tolerability.

Matteo Levisetti: And we'll have to see what happens going forward with Pitocinab. And perhaps one could hypothesize it'll be similar to different inhibitors of these pathways for which there inevitably pop up bypass pathways, and hence the advantages of engaging the immune system and inducing expansion of a durable anti-tumor T-cell population. I'm sorry, Ren.

Anish Suri: In contrast, a pan-T-cell engage a molecule due to its anti-CD-3 binding to all T-cells results in significantly high levels of cytokine released which ultimately compromises patient safety and drug tolerability.

Speaker Change: Perhaps you know one could hypothesize it'll be similar to different inhibitors of these pathways.

Speaker Change: For which there inevitably pop up bypass pathways and hence the advantages of engaging the immune system and inducing expansion.

Anish Suri: The following slide, slide 9, highlights some of the notable points of differentiation between Q500, CARTI approaches, and Pan-T cell-engaging molecules.

Anish Suri: The following slide, slide 9, highlights some of the notable points of differentiation between Q500, CARTI approaches, and Pan-T cell-engaging molecules. Note that all three approaches involve T cell mediated killing of target B cells, but it's only the Q500 series that can selectively engage, trained memory killer T cells, and redirect them to kill B cells. The selective engagement while avoiding systemic activation results in a significant reduction in cytokine release and related toxicities which it favors patient safety while preserving efficacy. We believe the Q500 series of biologics are likely positioned as the best in class T cell engages for B cell depletion and could address a very large segment of autoimmune patients across many indications.

Speaker Change: But durable anti tumor T cell population.

Matteo Levisetti: I think there was one other question about the new adjuvant, if I recall, and so that study is progressing well. The investigators at Washington University are very close to completing enrollment in Schedule B, where patients are getting two doses of 101, and we're getting tissue pre- and post-treatment. Again, the preliminary data that we've seen looks very encouraging. The investigators really, I know, have the intent of submitting this for publication in a very high-level journal, and so when this will become public and shared really depends on how they choose to proceed. Got it.

Matteo Levisetti: Sorry, Reni, there's one other question about the new adjuvant, if I recall. And so, that study is progressing well. The investigators at Washington University are very close to completing enrollment in schedule B, where patients are getting two doses of 101, and we're getting tissue pre- and post-treatment. You know, again, this is the preliminary data that we've seen looks very encouraging. The investigators really, I think, I know have the intent of submitting this for publication in a very high level journal. And so, you know, when this will become public and shared really depends on how they choose to proceed.

Speaker Change: Got it and just alright random one other question about the new adjuvant, if I recall and so that study is progressing well the investigators at Washington University or very close to completing enrollment in schedule B, where patients are getting two doses of <unk>.

Anish Suri: Note that all three approaches involve T cell mediated killing of target B cells, but it's only the Q500 series that can selectively engage, trained memory killer T cells, and redirect them to kill B cells.

Anish Suri: The selective engagement while avoiding systemic activation results in a significant reduction in cytokine release and related toxicities which it favors patient safety while preserving efficacy.

Speaker Change:

Speaker Change: And we're getting a tissue pre and post treatment.

Speaker Change: And this is the preliminary data that we've seen looks very encouraging.

Anish Suri: We believe the Q500 series of biologics are likely positioned as the best in class T cell engages for B cell depletion and could address a very large segment of autoimmune patients across many indications.

The investigators really I think have had I do have the intent of submitting this for for publication in a very high level journal and so when this will become public and sure it really depends on how they choose to proceed.

Anish Suri: In summary, there are three key takeaway messages. First, due to the shared core structural framework, the clinical de-risking and validation of amino-stats in oncology via Q101 and Q102, including lack of clinically relevant immunogenicity, bolsters, and supports the clinical application of Q500 series for B cell depletion in auto immunity.

Anish Suri: In summary, there are three key takeaway messages. First, due to the shared core structural framework, the clinical de-risking and validation of amino-stats in oncology via Q101 and Q102, including lack of clinically relevant immunogenicity, bolsters, and supports the clinical application of Q500 series for B cell depletion in auto immunity. Second, selective harnessing of anti-viral memory T cells to kill B cells circumvents the safety risk associated with systemic T cell activation as noted with anti-cell engages.

Anish Suri: And third, data demonstrating comparable killing while avoiding high levels of pro-inflammatory cytokine production positions the Q500 series to achieve desirable efficacy while not compromising patient safety, which is of highest clinical relevance when considering therapeutic applications in autoimmune diseases.

Stephen Willey: And then also, just what's your estimate of CMV-0 positivity in the general population?

Matteo Levisetti: Got it.

Reni Benjamin: And then just maybe a final question, on kind of funding and your current cash position and the like. Can you maybe help us understand how you plan on bridging the gap between now and kind of initial milestone payments expected from the ONO opt-in versus selection of lead candidates and the like? How do you see that kind of unfolding?

Daniel Passeri: And then just maybe a final question on kind of funding and your current cash position. Like, can you maybe help us understand how you plan on bridging the gap between now and kind of initial milestone payments expected from the owner opt in versus selection of lead candidates and the like? How do you see that kind of unfolding? Thanks. Yeah, thanks. Thanks, Ren, as a Dan. That's an important question. One thing I want to emphasize, you know, we were very prudent and deliberate, and basically looking at that question in a very dynamic way. The one thing we have not chosen to do historically is with the cost of capital, as the small cap biotech sector has, you know, basically been compressed in terms of valuations.

Speaker Change: Got it.

Speaker Change: Just maybe a final question.

Speaker Change: On on kind of funding and your current cash position like can you maybe help us understand how you plan on bridging the gap between now and kind of initial milestone payments expected from the Oh no opt in versus selection of lead candidates in the and the like how do you how do you see that kind of.

Anish Suri: Second, selective harnessing of anti-viral memory T cells to kill B cells circumvents the safety risk associated with systemic T cell activation as noted with anti-cell engages.

Anish Suri: And third, data demonstrating comparable killing while avoiding high levels of pro-inflammatory cytokine production positions the Q500 series to achieve desirable efficacy while not compromising patient safety, which is of highest clinical relevance when considering therapeutic applications in autoimmune diseases.

Speaker Change: Unfolding.

Daniel Passeri: Thanks. Yeah, thanks. Thanks, Ren. This is Dan.

Speaker Change: Yeah. Thanks. Thanks, Brent This is Dan that's an important question.

Stephen Willey: I know it's correlated to age.

Stephen Willey: I think it tends to be lower in males versus females, but just wondering kind of what your, general estimate of this would be and whether you would need to screen for CMV positivity in the context of a base-1 dose escalation trial.

Speaker Change: One thing I want to emphasize we were very prudent and deliberate and.

Daniel Passeri: It's an important question. One thing I want to emphasize, you know, we were very prudent and deliberate and basically looking at that question in a very dynamic way. The one thing we have not chosen to do historically is with the cost of capital, as the small cap biotech sector has, you know, basically been compressed in terms of valuations. We have not chosen to go out and do a, you know, massively dilutive financing.

Basically we're looking at that question in a very dynamic way. The one thing we have not chosen to do historically with the cost of capital as the small cap biotech sector has basically been compressed in terms of valuations we have not chosen to go out and do a massively.

Mateo Levisetti: With that background and update, I'll turn the call over to Mateo to describe the mature and clinical data from the ongoing oncology trials.

Mateo Levisetti: With that background and update, I'll turn the call over to Mateo to describe the mature and clinical data from the ongoing oncology trials. Mateo? Thanks, Anish.

Mateo Levisetti: Mateo?

Daniel Passeri: We have not chosen to go out and do a massively dilutive financing. So, we've taken a look at a business model where we have programs that are all kind of moving over time. We have a partnered program right now, 401 with ONO. And if one looks back at that, it was actually a really nice design. They're helping; they're subsidizing basically the preclinical development, working very closely with us. They're supporting our scientists. And that has resulted in a really good high quality body of data going forward to select a lead candidate that then with the objective of getting into the clinic, we have a 50% opt-in there.

Mateo Levisetti: Thanks, Anish.

Mateo Levisetti: Good afternoon to everyone listening in on today's call.

Mateo Levisetti: Good afternoon to everyone listening in on today's call. The maturing clinical data from the ongoing Q101 trial continues to demonstrate highly encouraging and robust metrics of clinical benefit for patients newly diagnosed with recurrent metastatic HPV-positive head neck cancer treated in combination with Pemberlizumet. And for heavily pre-treated recurrent metastatic HPV-positive head neck cancer patients treated with monotherapy. The latest data continues to bolster prior observations. Further enhancing our confidence in Q101 as a potential new standard of care therapeutic to improve outcomes for patients battling HPV-positive head neck cancer.

Mateo Levisetti: The maturing clinical data from the ongoing Q101 trial continues to demonstrate highly encouraging and robust metrics of clinical benefit for patients newly diagnosed with recurrent metastatic HPV-positive head neck cancer treated in combination with Pemberlizumet.

Speaker Change: Dilutive financing so we've taken a look at our business model, where we have.

Daniel Passeri: So we've taken a look at a business model where we have programs that are all kind of moving over time. We have a partnered program right now, 401 with Ono. And if one looks back at that, it was actually a really nice design.

Speaker Change: Programs that are all kind of moving over time, we have a partnered program right now 401 with Ono.

And if one looks back at that it was actually a really nice design, they're helping their subsidizing basically the preclinical development.

Mateo Levisetti: And for heavily pre-treated recurrent metastatic HPV-positive head neck cancer patients treated with monotherapy.

Daniel Passeri: They're helping, they're subsidizing basically the preclinical development, working very closely with us, they're supporting scientists. And that has resulted in a really good, a high-quality body of data going forward to select a lead candidate that then with the objective of getting into the clinic, we have a 50% opt-in there. Even with the 50% opt-in, we'll receive milestones. So if, Those milestones get triggered, they help subsidize the development of that program. We have 501 in late-stage discussions with several companies. The objective there is to consummate a transaction where we have an upfront. We have additional support of our scientists that are going to be committed to that program. That reduces our burn rate.

Mateo Levisetti: The latest data continues to bolster prior observations. Further enhancing our confidence in Q101 as a potential new standard of care therapeutic to improve outcomes for patients battling HPV-positive head neck cancer.

Speaker Change: Working very closely with us they're supporting our scientists.

Speaker Change: And that has resulted in a really good.

Speaker Change: High quality body of data going forward to select a lead candidate and then with the objective of getting into the clinic, we have a 50% opt in there even with the 50% opt in we'll receive milestones.

Mateo Levisetti: As previously and consistently stated, we believe Q101's unique mechanism of action as evidenced by the data generated to date enables effective and tolerated dosing and selective expansion of the targeted tumor-specific T-cells.

Mateo Levisetti: As previously and consistently stated, we believe Q101's unique mechanism of action as evidenced by the data generated to date enables effective and tolerated dosing and selective expansion of the targeted tumor-specific T-cells. Pemberlizumet is approved as this current standard of care treatment of first-line patients with recurrent metastatic head neck cancer that have tumors with the combined positive score or CPS score of greater than or equal to 1%, which is a measure of PDL expression.

Daniel Passeri: Even with the 50% opt-in, will receive milestones. So, if those milestones get triggered, they help subsidize the development of that program. We have 501 in late stage discussions with several companies. The objective there is to consummate a transaction where we have an upfront. We have additional support of our scientists that are going to be committed to that program. That reduces our burn rate and then a series of milestones, beginning obviously with lead candidate selection, IND filing. Those milestones overlap with the ONO milestones. You know, are really important to basically give us continuity. So, the measures we've taken for reducing our burn, basically enabling 101 data to mature without going into a very costly phase two.

Speaker Change: So.

Speaker Change: If.

Speaker Change: Those milestones get triggered they help subsidize the development of that program are.

Speaker Change: We have 501 in late stage discussions with several companies.

Mateo Levisetti: Pemberlizumet is approved as this current standard of care treatment of first-line patients with recurrent metastatic head neck cancer that have tumors with the combined positive score or CPS score of greater than or equal to 1%, which is a measure of PDL expression.

Speaker Change: The objective there is to consummate a transaction, where we have an upfront.

Speaker Change: Additional support of our scientists that are going to be committed to that program that reduces our burn rate and then a series of milestones beginning obviously with lead candidate selection IND filing those milestones overlapped with the Oh no milestones are really important to basically give us continuity.

Daniel Passeri: And then a series of milestones, beginning obviously with lead candidate selection, IND filing. Those milestones, overlapped with the ONO milestones, are really important to basically give us continuity. So, the measures we've taken for reducing our burn, basically enabling 101 data to mature without going into a very costly phase two, in just being prudent about what we're focusing on in the near term, focusing on partnering 501 to supplement. So these milestones help extend the runway in a sort of tiered manner.

Mateo Levisetti: The approval of Pemberlizumet in this setting was based on a median overall survival of 12.3 months and with an objective response rate of 19% as observed in the keynote 48 studies.

Mateo Levisetti: The approval of Pemberlizumet in this setting was based on a median overall survival of 12.3 months and with an objective response rate of 19% as observed in the keynote 48 studies. As presented at ASCO in June, following combination treatment with Q101, the objective response rate of 46% as shown on slide 10, observed in patients with CPS greater than or equal to 1, represents a greater than doubling compared to the historical ORR of 19% observed with Pembronizumab monotherapy.

Speaker Change: Alrighty.

Speaker Change: So.

Mateo Levisetti: As presented at ASCO in June, following combination treatment with Q101, the objective response rate of 46% as shown on slide 10, observed in patients with CPS greater than or equal to 1, represents a greater than doubling compared to the historical ORR of 19% observed with Pembronizumab monotherapy.

Speaker Change: The measures we've taken for reducing our burn.

Speaker Change: Basically our enabling 101 data to mature without going into a very costly phase two.

Daniel Passeri: And just being prudent about what we're focusing on in the near term. Focusing on partnering 501 to supplement. So, these milestones help extend the runway in a sort of tiered manner. So, if we do need to raise any capital and not sure right now where we're going to need to, but if we do, it's going to be a modest amount. We're really trying to keep dilution down to a minimum because cost of capital is key. And ultimately what we want to do is hit these milestones, further develop the pipeline, demonstrate further robustness of our clinical competitive positioning.

Speaker Change: And just being prudent about what were focusing on in the near term focusing on partnering fivefold one to supplement. So these milestones help extend the runway and sort of tiered manner. So if we do need to raise any capital and not sure right now where we're going to need to but if we do it's going to be a modest amount.

Mateo Levisetti: As shown on the waterfall plot out of 24 valuable patients, we have observed significant tumor reductions across many of these patients, including confirmed partial responses in 10 patients, and a confirmed complete response in one patient. Importantly, four patients remain on treatment, including one with stable disease that exhibits a reduction in their target lesions of minus 28%.

Mateo Levisetti: As shown on the waterfall plot out of 24 valuable patients, we have observed significant tumor reductions across many of these patients, including confirmed partial responses in 10 patients, and a confirmed complete response in one patient. Importantly, four patients remain on treatment, including one with stable disease that exhibits a reduction in their target lesions of minus 28%. Notably, for patients with low CPS scores, or scores of 1 to 19, an ORR of 50% was observed with Q101 and Pembronizumab, which represents a greater than tripling of the historical ORR of approximately 15% observed with Pembronizumab alone.

Daniel Passeri: So if we do need to raise any capital, and not sure right now where we're going to need to, but if we do, it's going to be a modest amount, we're really trying to keep dilution down to a minimum because cost of capital is key. And ultimately what we want to do is hit these milestones, further develop the pipeline, demonstrate further robustness of our clinical competitive positioning, and ultimately at some point in the future when the stock is a healthy evaluation, cost of capital is onerous.

Speaker Change: We're really trying to keep dilution down to a minimum because cost of capital is key and ultimately we want to do is hit these milestones further develop a pipeline demonstrate further.

Speaker Change: The robustness of our clinical and competitive positioning.

Daniel Passeri: And ultimately, at some point in the future, when the stock is a healthy evaluation, cost of capital is in his own risk. So, I hope that's a clear answer, but it's basically a dynamic analysis, and we have a lot of moving parts here. But it's basically building up. That's why I meant by a balanced business model. Having a stream of capital options coming in with these milestones being triggered and looking at raising capital in a very sort of prudent, pragmatic manner based on cost of capital. in the middle.

Speaker Change: And ultimately at some point in the future when the stock is up a healthy evaluation cost of capital isn't as onerous. So I hope that's a clear answer, but it's basically a dynamic analysis and we have a lot of moving parts here, but it's basically building that's why I met by our balanced business model, having a stream of capital.

Mateo Levisetti: Notably, for patients with low CPS scores, or scores of 1 to 19, an ORR of 50% was observed with Q101 and Pembronizumab, which represents a greater than tripling of the historical ORR of approximately 15% observed with Pembronizumab alone.

Daniel Passeri: So I hope that's a clear answer, but it's basically a dynamic analysis, and we have a lot of moving parts here, but it's basically building up, that's why I meant by a balanced business model, having a stream of capital options coming in with these milestones being triggered and looking at raising capital in a very sort of prudent, pragmatic manner based on cost of capital.

Speaker Change:

Mateo Levisetti: In totality, our data suggests that not only does Q101 appear to demonstriply enhance the response rate of PD1 inhibitions, but also does so by substantially enhancing responses in patients that are traditionally less likely to respond.

Mateo Levisetti: In totality, our data suggests that not only does Q101 appear to demonstriply enhance the response rate of PD1 inhibitions, but also does so by substantially enhancing responses in patients that are traditionally less likely to respond. This is particularly important since patients with low CPS scores represent approximately 50% of all patients that are CPS positive and eligible for treatment with Pembronizumab in the front line setting. The responses observed in these patients have been durable, as reflected in the 12-month OS and median OS, which is shown on the next slide, slide 11.

Speaker Change: Options coming in with these milestones being triggered and looking at raising capital in a very sort of prudent pragmatic manner based on cost of capital.

Anish Suri: Yeah.

Daniel Passeri: Great, thanks. Good luck going forward. All right, appreciate it, Reni. Thank you.

Reni Benjamin: Great, thanks and good luck going forward. I appreciate it, Ren. Thank you. The next question will come from Maurice Raycroft with Jeffreys, please go ahead. Hi, congrats on the data update, and thanks for taking my questions. I'll ask one on the Q500 series.

Speaker Change: Great. Thanks, and good luck going forward.

Speaker Change: Alright I appreciate it thank you.

Maurice Raycroft: The next question will come from Mari Raycroft with Jeff Reese. Please go ahead. Hi, congrats on the data update, and thanks for taking my questions. I'll ask one on the Q500 series for Q501. Can you talk more about plans or options for next steps to position this program for partnering? What did enhance potential for BDFU? Got regulator feedback or even key investigator buy-in to help define what the clinical development path to look like? Yeah, very important question. I think obviously the ONO partnership has enhanced our sort of insight on the autoimmune space. We have a very attractive sort of preclinical data set right now.

Anish Suri: So both very good questions, Steve.

Mateo Levisetti: This is particularly important since patients with low CPS scores represent approximately 50% of all patients that are CPS positive and eligible for treatment with Pembronizumab in the front line setting.

Speaker Change: The next question will come from Maury Raycroft with Jefferies. Please go ahead.

Anish Suri: CMV is an example we presented, but just to make the point, Steve, we have made Q500 molecules, with SARS-CoV-2 and EBV and other viral epitopes as well.

Maury Raycroft: Hi, Congrats on the data update and thanks for taking my questions I'll ask one on the Q 500 series Sport Q 501 can you talk more about plans or options for next steps to position this program for partnering.

Maurice Raycroft: For Q501, can you talk more about plans or options for next steps to position this program for partnering? Would it enhance potential for BD if you got regulator feedback or even key investigator buy-in to help define what the clinical development path could look like? Yeah, very important question.

Mateo Levisetti: The responses observed in these patients have been durable, as reflected in the 12-month OS and median OS, which is shown on the next slide, slide 11.

Speaker Change: What does it enhance potential for BD, if you got regular regulator feedback or even key investigator bias to help define what the clinical development path could look like.

Mateo Levisetti: For patients treated with Q101 and Pembronizumab as first line treatment, the median PFS of 5.8 months compares favorably to the median PFS of 3.2 months that was observed in the Pembronizumab arm of the 8 months observed in patients with CPS greater than or equal to 1, treated with combination treatment is notable and substantially better than the historical data with Pembronizumab monotherapy, where 12-month OS and median OS were 51% and 12.3 months respectively.

Mateo Levisetti: For patients treated with Q101 and Pembronizumab as first line treatment, the median PFS of 5.8 months compares favorably to the median PFS of 3.2 months that was observed in the Pembronizumab arm of the 8 months observed in patients with CPS greater than or equal to 1, treated with combination treatment is notable and substantially better than the historical data with Pembronizumab monotherapy, where 12-month OS and median OS were 51% and 12.3 months respectively. These enhanced survival metrics, which continue to be followed, are particularly evident when looking at the patients with both low and high PDL1 expression, as shown on slide 12.

Anish Suri: So we presented the case with CMV.

Anish Suri: In the particular case of CMV, zero positivity, anywhere around 65 to 70%.

Anish Suri: In our experience, when we've screened donors for SARS-CoV-2 at this point in time in the, history of mankind, virtually 100% have been SARS-positive for obvious reasons.

Daniel Passeri: I think, obviously, the ONO partnership has enhanced our sort of insight on the autoimmune space. We have a very attractive sort of preclinical data set right now. We've been in discussions with several potential pharma partners on 501, various stages of diligence and progression, which is highly confident that, based on the feedback we have, it's a differentiated asset. It's very attractive based on basically being a biologic that mirrors what CAR T was able to do with lupus. That's what the intent is. It compares favorably with bispecifics, the CD3, CD19 molecules.

Anish Suri: From the trafficking, we are now doing in vivo studies, but with immunostats in general, Steve, we had published a paper in Nature, Methods with Hitaplu, several years back, where we used immunopet imaging to make the point that immunostats could penetrate solid tumor tissue as well as an infectious model and directly engage the relevant antigen-specific, T cells.

Speaker Change: Very important question.

Anish Suri: And we believe the same should hold true for the 500 series, where you can have extravasation, and local engagement to essentially be able to recognize the T cells that are bound by these molecules.

Speaker Change: I think obviously the Ono partnership has enhanced our sort of insight on the autoimmune space. We have a very attractive set of preclinical data set right now we've been in discussions with several.

Anish Suri: Okay.

Stephen Willey: That's helpful.

Daniel Passeri: We've been in discussions with several potential pharma partners on 501, various stages of diligence and progression. We're just highly confident that, based on the feedback we have, is a differentiated asset. It's very attractive based on basically being a biologic that mirrors what Carti was able to do with lupus. That's what the intent is. It compares favorably with by specifics, the CD3, CD19 molecules. We think the data set presents an opportunity for us to partner in the near term.

Speaker Change: Potential pharma partners on 501, various stages of diligence and progression.

Stephen Willey: And then maybe just a key one-on-one question.

Speaker Change: Highly confident that based on the feedback we have.

Daniel Passeri: So we think the data set presents an opportunity for us to partner in the near term. And in terms of indications with that molecule, we're obviously going to hold off until the assets partnered and we're able to engage in strategic dialogue with the partner on what to focus on in a sort of a series of indications. But I think for that program, we look at partnering as an important means of subsidizing development. But also aim to preserve a cell type, for instance, eosinophils or mast cells, something like that, where we retain control and upside of sort of a number of indications from those cell types.

Speaker Change: It's a differentiated asset is very attractive based on basically being a biologic that mirrors with car T was able to do with Lucas asked what the intent is compares favorably with bi specifics the CD three CD 19 molecules. So we think the dataset presents.

Mateo Levisetti: These enhanced survival metrics, which continue to be followed, are particularly evident when looking at the patients with both low and high PDL1 expression, as shown on slide 12. Consistent with the enhanced ORR observed in patients with low PDL1 expression, treated with Q101 and Pembronizumab, these patients are demonstrating favorable metrics of survival.

Opportunity for us to partner in the near term.

Mateo Levisetti: Consistent with the enhanced ORR observed in patients with low PDL1 expression, treated with Q101 and Pembronizumab, these patients are demonstrating favorable metrics of survival. In CPS, low patients treated with Q101 and Pembronizumab, the 12-month OS of 82% and the median OS of 21.8 months is importantly notable given the historical values of 44% and 10.8 months observed for Pembronizumab in the keynote 48 study. The benefit to CPS High Patients is also noteworthy with 12 month OS of 100 percent, an immediate OS that has not yet been reached in patients with CPS greater than or equal to 20 treated with Q101 and Pembrolyzumab compared to the historical values of 56 percent and 14.8 months respectively.

Daniel Passeri: In terms of indications with that molecule, we're obviously going to hold off until the assets are partnered and we're able to engage in dialogue, strategic dialogue with a partner on what to focus on and a sort of a series of indications. But I think for that program, we look at partnering as an important means of subsidizing development. We'd also aim to preserve a cell type, for instance, eosinophils or mass cells, something like that, where we retain control and upside of sort of a number of indications from those cell types. I hope that answers your question, Mark.

Speaker Change: And in terms of indications with that molecule, we're obviously going to hold off until.

Speaker Change: The assets partnered and we're able to engage in.

Speaker Change: Dialogue strategic dialogue with the with a partner on what to focus on in a sort of a series of indications.

Mateo Levisetti: In CPS, low patients treated with Q101 and Pembronizumab, the 12-month OS of 82% and the median OS of 21.8 months is importantly notable given the historical values of 44% and 10.8 months observed for Pembronizumab in the keynote 48 study.

Speaker Change: But I think.

Speaker Change: For that program as we look at partnering as an important means of subsidizing development would also aim to preserve a cell type for instance, eosinophils or mass sell something like that.

Mateo Levisetti: The benefit to CPS High Patients is also noteworthy with 12 month OS of 100 percent, an immediate OS that has not yet been reached in patients with CPS greater than or equal to 20 treated with Q101 and Pembrolyzumab compared to the historical values of 56 percent and 14.8 months respectively.

Speaker Change: Where we retain control and upside of sort of a number of indications from those so cell types.

Maurice Raycroft: So I hope that answers your question, Mark. Yep, yeah, really helpful. And maybe just to follow up on the financial side as well, I guess, for the ONO opt-in, is there any room to negotiate and potentially accelerate milestones or opt-in potential based on the data that you've generated so far? Or would it not make sense to try to do that at this point?

Speaker Change: I hope that answers your question Mark.

Stephen Willey: So I understand that you guys are obviously kind of pausing things for now and allowing, the survival data to mature, but I guess in the context of frontline head and neck right now and what is capable with Pembro monotherapy, I think that appears to be the subject of some increasing debate as a function of primarily, I guess, the LEAP-10 data.

Daniel Passeri: Yeah, really helpful.

Stephen Willey: So just curious if you think a more mature survival statistic could help attract strategic, interest and just curious if you can share anything in terms of the conversations that you've had thus far with potentially interested parties in terms of how they're thinking about what Pembro monotherapy historically is capable of.

Mark: Yeah, Yeah really helpful and maybe just to follow up on the financial side as well I guess for the Oh, no opt in there any room to negotiate and potentially accelerate milestones or option potential based on the data that you've generated so far or would it not make sense to try to do that at this point.

Daniel Passeri: Maybe just to follow up on the financial side as well, I guess for the ONO opt-in, is there any room to negotiate and potentially accelerate milestones or opt-in potential based on the data that you've generated so far, or would it not make sense to try to do that at this point? Yeah, I don't think it would make sense to try to modify it right now. We've been making really good progress. The partnerships have actually been extremely productive. They've really been an outstandingly supportive partner, and we're aligned on what the next steps are, so I think we're very much seeing things from a similar perspective.

Stephen Willey: Thanks.

Mateo Levisetti: As a reminder, these maturing data from the combination trial appeared to be following what we observed in the Monotherapy Second Line Plus setting, where Cue 101 demonstrated significant prolongation of survival as shown in the following slide, slide 13. As shown on the left, the median OS observed in patients treated with Cue 101 Monotherapy at 2 Migs per Kig was 24.8 months and 20.8 months for those treated with Cue 101 and a dose of 4 Migs per Kig.

Mateo Levisetti: As a reminder, these maturing data from the combination trial appeared to be following what we observed in the Monotherapy Second Line Plus setting, where Cue 101 demonstrated significant prolongation of survival as shown in the following slide, slide 13. As shown on the left, the median OS observed in patients treated with Cue 101 Monotherapy at 2 Migs per Kig was 24.8 months and 20.8 months for those treated with Cue 101 and a dose of 4 Migs per Kig.

Daniel Passeri: Yeah, I don't think it would make sense to try to modify it right now. We've been making really good progress. The partnership's actually been extremely productive. They've really been an outstandingly supportive partner.

Speaker Change: Yes, I don't think it would make sense to try to modify it right now we've been making really good progress. The partnership has actually been extremely productive they've really been an outstandingly supportive partner.

Daniel Passeri: And we're kind of we're aligned on what the next steps are. So I think we're very much seeing things from a similar perspective. Got it.

Speaker Change: And we're kind of we're aligned on what the next steps are so I think we're very much seeing things from a similar perspective.

Daniel Passeri: Got it. Okay, thanks for taking my questions.

Got it okay. Thanks for taking my questions.

Leland Gershell: The next question will come from Lee-Lynn Gershell with Oppenheimer. Please go ahead. Hey, good afternoon. Thanks for the update and taking my questions. Let me just a few for you, Jen or Nish. Looks like you have a good base of preclinical data here for four, one, five, or one.

Daniel Passeri: Sure.

Maurice Raycroft: Okay, thanks for taking my question. The next question will come from Leland Gershell with Oppenheimer. Please go ahead. Hey, good afternoon. Thanks for the update and taking my questions. Maybe just a few for you, Dan or Anish.

Leland <unk>: The next question will come from Leland <unk> with Oppenheimer. Please go ahead.

Mateo Levisetti: The survival observed in these patients is remarkable when compared to the median OS observed in the second line with checkpoint inhibitors, where median OS of 7.5 and 8.4 months were observed for Nevilleumab and Pembrolyzumab respectively.

Mateo Levisetti: The survival observed in these patients is remarkable when compared to the median OS observed in the second line with checkpoint inhibitors, where median OS of 7.5 and 8.4 months were observed for Nevilleumab and Pembrolyzumab respectively. We believe this enhancement of survival to be mediated by the durable and selective expansion of targeted tumor-specific T-cells by Cue 101. In totality, our data suggests that Cue 101 increases the number of patients benefiting checkpoint inhibitors and appears to substantially improve survival in these patients.

Daniel Passeri: Thanks, Steve.

Leland <unk>: Hey, good afternoon, thanks for the update and taking my questions. Let me just.

Daniel Passeri: This is Dan.

Leland <unk>: Hugh.

Hugh: For your 10 or a niche.

Leland Gershell: It looks like you have a good base of preclinical data here for 401, 501. Wanted to know what might be the next set of non-clinical data that we might be looking for that you might have to present to us. And in that, are there any particular studies you're doing that may guide your thought process with respect to the indications that you have prioritized for both those assets?

Speaker Change #102: You have a good base of preclinical data here for.

401 fiber one wanted to know what might be the next set of non clinical data that we might be looking for that you might have to present to us.

Anish Suri: I wanted to know what might be the next set of nonclinical data that we might be looking for, that you might have to present to us, and in that, are there any particular studies you're doing that make guide your thought process with respect to the indications that you prioritize for both of us? Thank you. Yeah, thanks, Leland. This is an issue. So we continue to generate pretty exciting data for both programs and auto-munity with 401 obviously in collaboration with ONO, where we have seen efficacy and activity in several disease models, and in due time collectively and collaboratively will release that in the public domain.

Mateo Levisetti: We believe this enhancement of survival to be mediated by the durable and selective expansion of targeted tumor-specific T-cells by Cue 101. In totality, our data suggests that Cue 101 increases the number of patients benefiting checkpoint inhibitors and appears to substantially improve survival in these patients.

Are there any particular studies are doing that May guide your thought process with respect to the indications.

Speaker Change #103: The indications in the courthouse.

Speaker Change #104: Both those assets. Thank you.

Mateo Levisetti: We continue to monitor and carefully follow the patient's remaining on treatment as well as in survival follow-up and look forward to providing an update that sits in November. The data continues to mature over time, and we believe the observations to date, particularly pertaining to what appears to be a substantial enhancement of survival, will place Cue 101 and by implication the Cue 101 series in a favorable and competitive position to potentially become a new standard of care.

Mateo Levisetti: We continue to monitor and carefully follow the patient's remaining on treatment as well as in survival follow-up and look forward to providing an update that sits in November. The data continues to mature over time, and we believe the observations to date, particularly pertaining to what appears to be a substantial enhancement of survival, will place Cue 101 and by implication the Cue 101 series in a favorable and competitive position to potentially become a new standard of care.

Daniel Passeri: So it's an important question.

Anish Suri: Yeah, thanks Leland, this is Anish. So we continue to generate pretty exciting data for both programs in autoimmunity with 401 obviously in collaboration with Ono, where we have seen, efficacy and activity in several disease models and in due time, collectively and collaboratively will release that in the public domain. In total the data does seem to reflect what I've mentioned, which is a molecule that generates copious amounts of, regular treat T-cells along with Signatures for, halting autoimmune processes, seizing and reversing or minimizing pro-inflammatory cytokine production and related.

Anish: Yeah. Thanks, Nathan this is a niche so we continue to generate pretty exciting data for both programs in order immunity with 41, obviously in collaboration with Ono.

Daniel Passeri: We've had dialogue with multiple potential partners on the data sets that we've had historically.

Daniel Passeri: When we look at the monotherapy data, I mean, we've actually had the comment of the data, looks so promising that how do they know that we haven't biased by selecting healthy patients?

Daniel Passeri: So that survival data as it continues to mature, I think what we've seen in monotherapy is, very impressive.

Daniel Passeri: And that's one of the reasons we emphasize the randomized strategy for the phase two.

Daniel Passeri: I think what's really important here when you look at the landscape of competing molecules, different kinase inhibitors, et cetera, in this space, we think the survival data is going to really differentiate and truly position Q with an advantage and a competitive advantage in terms of the durability of triggering an immune response.

Speaker Change #105: Well we have seen.

Speaker Change #105: Efficacy in activity in several disease models and in due time.

Speaker Change #105: Collectively collaboratively with release that in the public domain.

Anish Suri: In total, the data does seem to reflect what I've mentioned, which is a molecule that generates copious amounts of regulatory T cells along with signatures for halting autoimmune processes, seizing and sort of reversing or minimizing pro-inflammatory cytokine production and related pathologies. For 500, we have, are in the process of in vivo experiments. And again, we hope to sort of release that, as we see, start for the understanding relationship between dosing, B-cell depletion, and so the models that we're categorizing now.

Daniel Passeri: What we're seeing emerge with the combination appears to be following suit.

Speaker Change #105: In total the data does seem to reflect what I've mentioned, which is a molecule that generates copious amounts of <unk>.

Mateo Levisetti: Moving on to the Cue 102 program, which is being explored in patients with WT1 expressing tumors, including colon, pancreatic, gastric, and ovarian cancers, Cue 102 has been well tolerated to date, and no DLTs have been observed. Preliminary and emerging data shows dose-dependent increases in exposure and activation and expansion of WT1-specific T-cells.

Mateo Levisetti: Moving on to the Cue 102 program, which is being explored in patients with WT1 expressing tumors, including colon, pancreatic, gastric, and ovarian cancers, Cue 102 has been well tolerated to date, and no DLTs have been observed. Preliminary and emerging data shows dose-dependent increases in exposure and activation and expansion of WT1-specific T-cells. Patients and all foreign vacations have been treated at the expansion dose of four migs per take and remain on treatment for an active follow-up.

Speaker Change #105: Regulatory T cells, along with <unk>.

Signatures for.

Holding autoimmune processes are seizing and sort of reversing or minimizing prone inflammatory cytokine production.

Speaker Change #105: And related pathologies.

Anish Suri: For 500, we are in the process of in vivo experiments, and again, we hope, will release that as we start further understanding the relationship between.., dosing, B cell depletion, and some of the models that we're characterizing now. So both programs, the intentions are, continue to go through this year to be able to talk about the, Great, thanks Jakey for asking. Again, if you have a question, please press star, then 1. Our next question will come from Ted Tenthoff with Piper Sandler. Please go ahead.

Daniel Passeri: And I think that's going to be dispositive in the long run.

Daniel Passeri: I think ultimately a randomized study is basically far more convincing because you're going directly, against PEMBRO as a single agent.

Speaker Change #105: For 500, we have are in the process of in vivo experiments and again, we hope to see.

Daniel Passeri: But it is an important topic and it is being watched.

Mateo Levisetti: Patients and all foreign vacations have been treated at the expansion dose of four migs per take and remain on treatment for an active follow-up.

Daniel Passeri: And we do have ongoing dialogue with companies on 101.

Speaker Change #105: Released that.

Speaker Change #105: We start for the understanding relationship between.

Speaker Change #105: Dosing b cell depletion.

Operator: The next question will come from Ren Benjamin

Mateo Levisetti: As previously reported, we've observed anti-tumor activity in gastric and ovarian patients, as well as durable disease control in several tumor types, including pancreatic cancer.

Mateo Levisetti: As previously reported, we've observed anti-tumor activity in gastric and ovarian patients, as well as durable disease control in several tumor types, including pancreatic cancer. These data continue to mature, and we look forward to presenting updated data at CITSI in November.

Speaker Change #105: And so the models that we're characterizing now so both programs are the intentions on this as we continue to go through this year to be able to talk about these datasets as they emerge.

Anish Suri: So both programs are the intentions on this, as we continue to go through this year to be able to talk about these data sets as they merge. Thank you very much. Thank you very much, thank you very much.

Operator: with Citizens JMP.

Reni Benjamin: Please go ahead.

Reni Benjamin: Hey, good afternoon, guys.

Speaker Change #106: Alright, thanks for the question.

Operator: Again, if you have a question, please write star, then one.

Mateo Levisetti: These data continue to mature, and we look forward to presenting updated data at CITSI in November.

Reni Benjamin: Thanks for taking the questions.

Ted <unk>: Again, if you have a question. Please press Star then one our next question will come from Ted <unk> with Piper Sandler. Please go ahead.

Ted Tenthoff: Our next question will come from Ted Tenoff, with Piper Sandler. Please go ahead. Great, thank you very much. Thank you to sort of the evolving world of targeting CB-19 to Blake B cells for autoimmune disease.

Reni Benjamin: So thanks for the update on 101 in combination with Keytruda and as in the monotherapy.

Daniel Passeri: But that I will now turn the call back over to Dan.

Dan Passeri: But that I will now turn the call back over to Dan. Dan. Yeah, thanks, Mateo.

Daniel Passeri: Dan.

Daniel Passeri: Yeah, thanks, Mateo.

Ted: Great. Thank you very much.

Daniel Passeri: As conveyed throughout this update call and shown on the next slide, slide 14, we continue to make significant progress across our platform with programs in both oncology and autoimmune disease. We've demonstrated the ability to selectively modulate targeted T-cells, providing what we believe to be a superior therapeutic approach in both oncology and autoimmune disease treatment.

Dan Passeri: As conveyed throughout this update call and shown on the next slide, slide 14, we continue to make significant progress across our platform with programs in both oncology and autoimmune disease. We've demonstrated the ability to selectively modulate targeted T-cells, providing what we believe to be a superior therapeutic approach in both oncology and autoimmune disease treatment. We continue to generate data from our two lead oncology programs, Q101 and Q102, and believe the data will continue to strengthen and bolster our position as a potential new standard of care, particularly supported by ongoing data generation pertaining to what appears to be highly meaningful and remarkable survival enhancement. We believe these observations support the premise that our approach is selectively activating and expanding to a specific T-cells, providing a durable anti-cancer effect, resulting in an enhanced survival.

Reni Benjamin: I guess my first question would be how to think about these results given the current, landscape, and in particular, you know, kind of the developing landscape given the provocative data we saw at ASCO from Marist and some of the others, you know, that are also in this space.

Speaker Change #109: Two sort of evolving.

World of.

Ted Tenthoff: Great, thank you very much, targeting CB19 to Blake B cells for autoimmune disease. How much has the safety, the potential safety profile that you've generated on the ImmuneStop platform from 101 to 102, differentiating from the cell therapies? And is that something that investors are focused on?

Speaker Change #110: Targeting CD 19, AAA T cells for autoimmune disease.

Daniel Passeri: How much is the CT, the potential CT profile that you've generated on the immunostat platform from 101-102 differentiating from the cell therapies? And is that something that investors are focused on? Thanks so much.

How much is the safety potential safety profile that you've generated on our platform.

Speaker Change #111: 101 going to differentiate them from the cell therapy and is that something that investors are focused on thanks. So much.

Daniel Passeri: We continue to generate data from our two lead oncology programs, Q101 and Q102, and believe the data will continue to strengthen and bolster our position as a potential new standard of care, particularly supported by ongoing data generation pertaining to what appears to be highly meaningful and remarkable survival enhancement. We believe these observations support the premise that our approach is selectively activating and expanding to a specific T-cells, providing a durable anti-cancer effect, resulting in an enhanced survival.

Anish Suri: Yeah, Ted, again, very good question, and I think I try to stress that, but the clinical de-risking and vulnerability of immunostats in man. In general, what we've shown with 101-102, we believe has an enormous positive implication on the 500 series of B-cell depletion. Simply, even if you look at from metrics of told mobility from immunogenicity, as you will know, we have not seen any clinically relevant immunogenicity in our 100 series trials with 101-102. We've had patients receiving drug up to two years. So, again, that speaks to the nature of selective TCR engagement; we are this framework.

Anish Suri: Thanks so much. Yeah, Ted, again, very good question. And I think I try to stress that, but the clinical de-risking and vulnerability of immunostats in man, in general, what we've shown with 101 and 102, we believe has an enormous positive implication on the 500 series obesity. Simply, even if you look at the metrics of tolerability from immunogenicity, as you well know, we have not seen any clinically relevant immunogenicity in our 100-series, trials with 101, 102. We've had patients receiving drugs up to two years.

Reni Benjamin: And just as a follow-up to that, you know, I'm kind of curious, I don't think it was, mentioned in the earlier comments.

Ted <unk>: Yeah Ted.

Speaker Change #112: Again, very good question and I think.

Speaker Change #113: Tried to stress that the clinical derisking and fold or ability of immuno stats and Matt in general what we've shown with 101 in one or two we believe has an enormous positive implication on the 500 series B cell depletion simply even if you look at the metrics of Tolerability from Immunogenicity.

Reni Benjamin: Can you provide any sort of an update on the neoadjuvant study?

As you will know we have not seen any clinically relevant immunogenicity in a 100 series of trials with one on one or two we've had patients receiving drug up to two years. So again that that speaks to the nature of selective TCR engagement via this framework.

Daniel Passeri: We believe we have the potential of establishing a new standard of care in the battle against cancer, as well as autoimmune disease.

Dan Passeri: We believe we have the potential of establishing a new standard of care in the battle against cancer, as well as autoimmune disease. Importantly, as oncology data continue to mature, we have recently taken measures to prioritize our near-term focus in resource deployment upon near-term development milestones in our autoimmune programs, including lead selection and advancement towards the clinic and our partnership with ONO for Q401, as well as positioning Q501 for strategic partnering to further extend our capital runway enhanced and to enhance our capacity.

Anish Suri: So, again, that speaks to the nature of selective TCR engagement via this framework. The second is the fact that by virtue of the fact that you're only co-opting a very small percentage of your peripheral T cell repertoire in an individual, and not carpet bombing all T-cells with anti-CD3-based approaches, we refer to as the pan-diesel engagers, we believe should also offer superior safety and tolerability metrics and some of that is evidence from this in vitro assessments of cytokine release that we did where you saw this profound, Production of cytokines by pan-T cell engager molecule, as opposed to Q500 where it was significantly reduced, despite the fact that Q500 shows a very comparable metrics of killing.

Daniel Passeri: Importantly, as oncology data continue to mature, we have recently taken measures to prioritize our near-term focus in resource deployment upon near-term development milestones in our autoimmune programs, including lead selection and advancement towards the clinic and our partnership with ONO for Q401, as well as positioning Q501 for strategic partnering to further extend our capital runway enhanced and to enhance our capacity.

Anish Suri: The second is the fact that by virtue of the fact that you're only co-opting a very small percentage of your peripheral T cell repertoire in an individual and not carpet bombing all T cells with anti-CD-3-based approaches, which we refer to as the panties of engages. We believe should also offer superior safety and told mobility metrics, and some of that is evident from this in vitro assessments of cytokine release that we did, where you saw this profound production of cytokines by panties of engage of molecule. as opposed to Q500 by a significantly reduced, despite the fact that Q500 shows a very comparable matrix of killing efficacy of B cells.

Speaker Change #114: The second is the fact that by virtue of the fact that you're only coopting a very small percentage of your peripheral T cell repertoire in an individual.

Speaker Change #114: And not carpet bombing all of T cells.

With anti CD, three based approaches, which which we refer to as the <unk> T cell engages.

Speaker Change #114: We believe should also offer a superior safety and Tolerability metrics and some of that is.

Daniel Passeri: As a reminder, we've retained a 50% co-development and co-marketing right to Q401, which has the potential application to multiple autoimmune diseases with multi-billion dollar market potential.

Dan Passeri: As a reminder, we've retained a 50% co-development and co-marketing right to Q401, which has the potential application to multiple autoimmune diseases with multi-billion dollar market potential. Through various proactive measures taken, we've extended our runway to mid-2025, reduced our going-fold cash burn from approximately 40 million per year to approximately 30 million per year, and importantly, additional partnering will further enhance our cash position with upfront milestone payments, as well as reduce our operational cash burn requirements through sponsored full-time equivalent supports. Through these measures, we believe we'll be increasingly capable of sustaining operational continuity through partnerships and other means of support.

Speaker Change #114: Evident from this in vitro assessments of cytokine release that we did where you saw this profound.

Production of cytokines by Pan T cell engaging molecules.

Speaker Change #114: As opposed.

Daniel Passeri: Through various proactive measures taken, we've extended our runway to mid-2025, reduced our going-fold cash burn from approximately 40 million per year to approximately 30 million per year, and importantly, additional partnering will further enhance our cash position with upfront milestone payments, as well as reduce our operational cash burn requirements through sponsored full-time equivalent supports. Through these measures, we believe we'll be increasingly capable of sustaining operational continuity through partnerships and other means of support.

Speaker Change #114: Opposed to Q 500, but it was significantly reduced despite the fact that Q 500 chosen very comparable metrics of killing efficacy of BSO. So that's also quite important and thirdly I think we should.

Anish Suri: So that's also quite important.

Anish Suri: So that's also quite important. Thirdly, I think we should sort of reemphasize the fact that, through nature... Your memory antiviral T-cells is something that all of us have harbored from the time we were born, through our life, to provide us protective immunity, are the better, long-lasting killer T cell population at One Harbour.

Anish Suri: Thirdly, I think we should sort of re-emphasize the fact that through nature, your memory anti-viral T cells is something that all of us have harbored from the time we're born through our life to provide us protective immunity. So there's no other better, long-lasting killer T cell population than one harvest, you know, as compared to what these cells offer. So we do think being able to redirect them to kill targets such as B cells provides a very exciting avenue for really harnessing a potential of what nature has already given the individual. Yes, very great.

Speaker Change #114: Would we should we should sort of reemphasize the fact that through nature.

Speaker Change #115: Your memory anti viral T cells is something that all of us have habit from the time, we are born through a life to provide us protective immunity. So theres no other better long lasting killer T cell population that one harvest.

Anish Suri: You know.., compared to what these cells offer. So we do think. And being able to redirect them to kill targets such as B-cells provides a very exciting avenue for really harnessing the potential of what nature has already given them. Levin. Yes, I agree. And obviously a very different manufacturing approach than what we're seeing with the autology.

Speaker Change #115: You know well.

Speaker Change #116: That's compared to what the sales office, so we do think that.

Daniel Passeri: As a result of these measures, combined with the ongoing progress with our maturing data across our programs, we believe we're very well positioned to realize a series of upcoming risk-reducing and value-driving milestones as we continue to as the goal of establishing a new standard of care for treating both cancer and autoimmune disease with our approach to restore health by restoring immune balance.

Dan Passeri: As a result of these measures, combined with the ongoing progress with our maturing data across our programs, we believe we're very well positioned to realize a series of upcoming risk-reducing and value-driving milestones as we continue to as the goal of establishing a new standard of care for treating both cancer and autoimmune disease with our approach to restore health by restoring immune balance.

Speaker Change #117: Being able to redirect them to kill targets such as <unk> provides a very exciting Avenue.

Speaker Change #117: Harnessing the potential of what nature has already given the.

Speaker Change #117: The individual.

Speaker Change #117: Alright, Greg and obviously, they're very different manufacturing approach than what we're seeing with neonatology.

Anish Suri: And obviously a very different manufacturing approach than what we're seeing with your targets is a car key. Oh, that's exactly right. That's exactly right. So just to add to that, the manufacturability is exactly what we've seen with 101-102 and a body-based biologics. The yields are in line with what we've seen at similar stages for immunostats, which are clinically great. Products have yielded in grams per liter with very good shell stability of the GMP product. That's a very important point.

Ted Tenthoff: Oh, that's exactly right. That's exactly right, Ted. So just to add to that, the manufacturability is exactly what we've seen with 101, 102 antibody based biologics. The yields are in line with what we've seen at similar stages for immunostats, which are clinically great products, have yielded in grams per liter with very good shelf stability of the genome.

Greg: Oh, that's right that's exactly right that's exactly right. So just to add to that the manufacturer ability is exactly what we've seen with 111 or two antibody based biologics. The yields are in line with what we've seen at similar stages for immuno stats, which are clinically grade products have yielded in grams per liter with very good shows stability of that.

Operator: With that, I'd now like to open the call up to questions, operator.

Operator: With that, I'd now like to open the call up to questions, operator. Thank you, we will now begin the question and answer session. To ask a question, please press star than one on your touch tone phone. If you're using a speaker phone, please pick up your handset before pressing the keys. If any time your question has been addressed and you would like to withdraw your question, please press star than two, and at this time, we'll pause momentarily to assemble our roster.

Operator: Thank you, we will now begin the question and answer session.

Operator: To ask a question, please press star than one on your touch tone phone. If you're using a speaker phone, please pick up your handset before pressing the keys.

Greg: M P product.

Greg: It's a very important point.

Daniel Passeri: Great. Well, thanks, guys. The credit to you have a progress. Thank you, Ted.

Greg: Thanks, Todd as a credit to your progress.

Operator: If any time your question has been addressed and you would like to withdraw your question, please press star than two, and at this time, we'll pause momentarily to assemble our roster.

Ted <unk>: Thank you Ted.

Matteo Levisetti: Sure.

Operator: This concludes our question and answer session.

Anish Suri: That's very important. Well, thanks, guys. Credit to you. Have a great day. Thank you, Ted. This concludes our question and answer session. I would like to turn the conference back over to Mr. Dan Passeri for any closing remarks. Please go ahead, sir.

Matteo Levisetti: Matteo, why don't you take that question for both of them?

Mr. Dan: This concludes our question and answer session I would like to turn the conference back over to Mr. Dan for theory for any closing remarks. Please go ahead Sir.

Matteo Levisetti: Yeah.

Reni Benjamin: How do you see that kind of unfolding?

Matteo Levisetti: No, I will.

Daniel Passeri: I would like to turn the conference back over to Mr. Dan Pisseri for closing remarks. Please go ahead, sir. Thank you. We just want to thank everyone for listening in. You continued interest in our progress, and we look forward to keeping you updated with the progress we make going forward. So thank you very much, and take care.

Reni Benjamin: Thanks.

Matteo Levisetti: And again, just to follow up on the prior question, again, I think this really, you, know, the data from the LEAP-10 trial underscores the importance of looking at early survival metrics, specifically like a 12-month, okay, survival, and also median OS as it matures.

Daniel Passeri: Yeah.

Matteo Levisetti: And so if you actually look at the PEMBRO Mono dataset from LEAP-10, the 12-month survival, is 59%, okay?

Daniel Passeri: Thanks.

Matteo Levisetti: If we look at the Q101 combination data, our current 12-month survival is 90%, okay?

Daniel Passeri: Thanks, Ren.

Matteo Levisetti: And if you look at CPS-HI, it's 100% of patients are alive at 12 months, okay?

Daniel Passeri: This is Dan.

Matteo Levisetti: And so with regards to the question now of the evolving landscape, and with, I guess, in particular, Maris' compound, Pitocentamab, again, it's really important to look at the data that they've shared with regards to their survival, okay?

Daniel Passeri: It's an important question.

Daniel Passeri: Thank you.

Matteo Levisetti: And so in the second-line setting and beyond, they reported a survival of 11.5 months, okay?

Daniel Passeri: Thank you. We just want to thank everyone for listening in, your continued interest in our progress and we look forward to keeping you updated with the progress we make going forward. So thank you very much and take care. The conference is now concluded. Thank you for attending today's presentation. You may now disconnect, www.mytrendyphone.co.uk END OF THE WORLD, The End and Matteo Levisetti. © BF-WATCH TV 2021, Edward Tenthoff, Reni Benjamin, Stephen Willey, Anish Suri, © BF-WATCH TV 2021

Daniel Passeri: One thing I want to emphasize, you know, we were very prudent and deliberate in basically, looking at that question in a very dynamic way.

Operator: The next question will come from Maurice Raycroft with Jeffries.

Daniel Passeri: We've been making really good progress.

Matteo Levisetti: With Q101 Mono, we're currently at, you know, 20.8 months and even 20, almost, 5 months, in the 2 Mg per kg cohort.

Stephen Willey: In the first question, we'll come from Stephen Wiley with Steeple, please go ahead.

Stephen Willey: In the first question, we'll come from Stephen Wiley with Steeple, please go ahead. Yeah, good afternoon. Thanks for taking the questions. On each or Dan, I was just wondering if you could speak to maybe what you know at this point about the trafficking capacity of Q5O. 101. And then also just what's your estimate of CMV zero positivity in the general population? I know it's correlated to age. I think it tends to be lower in males versus females, but just wondering kind of what your general estimate of this would be and whether you would need to screen for CMV positivity in the context of a based on those escalation trial.

Speaker Change #120: Thank you.

Daniel Passeri: The one thing we have not chosen to do historically is, with the cost of capital, as the small-cap, biotech sector has, you know, basically been compressed in terms of valuations, we have not chosen to go out and do a, you know, massively dilutive financing.

Operator: Please go ahead.

Daniel Passeri: The partnership's actually been extremely productive.

Matteo Levisetti: So although in the second-line plus, they reported a response rate of 37%, their survival, is about half as long, okay, as Q Monotherapy, where we observed a response rate of 5%.

Daniel Passeri: So we've taken a look at a business model where we have programs that are all kind of, moving over time.

Maurice Raycroft: Hi.

Daniel Passeri: They've really been an outstandingly supportive partner.

Matteo Levisetti: And again, this is fully consistent with patterns of clinical benefit that have been now well-defined, in immunotherapy.

Leland Gershell: Thanks for the update and taking my questions.

Dan Dan: I just want to thank everyone for listening in and your continued interest in our progress and we look forward to keeping you updated with the progress we make going forward. So thank you very much and take care.

Daniel Passeri: We have a partnered program right now, 401 with ONO, and if one looks back at that, it, was actually a really nice design.

Maurice Raycroft: Congrats on the data update, and thanks for taking my questions.

Daniel Passeri: And we're aligned on what the next steps are.

Matteo Levisetti: So if we look at Kimtrak, recently approved for uveal melanoma, really modest response, rate, but a clear survival benefit led to its approval.

Leland Gershell: Maybe just a few for you, Dan or Aneesh.

Daniel Passeri: They're helping – they're subsidizing, basically, the preclinical development, working very closely, with us. They're supporting our scientists.

Maurice Raycroft: I'll ask one on the Q500 series.

Daniel Passeri: So,

Matteo Levisetti: And so back to Pitocentamab now in the front-line setting, you know, they, at ASCO, reported, some, you know, very preliminary data. They actually only reported data on about half of the patients that were treated with, very minimal follow-up.

Leland Gershell: It looks like you have a good base of preclinical, data here for 401, 501.

Daniel Passeri: And that has resulted in a really good, high-quality body of data going forward to select a lead, candidate that then – with the objective of getting into the clinic.

Maurice Raycroft: For Q501, can you talk more about plans or options for next steps to, position this program for partnering?

Daniel Passeri: And we look forward to keeping you updated, with the progress we make going forward.

Daniel Passeri: I think we're very much seeing things from a similar perspective.

Matteo Levisetti: So with the follow-up, median follow-up, if you looked at the swimmer plot, about 4 months.

Leland Gershell: I wanted to know what might be the next set of non-clinical data that we might be looking for that you might have to present to us.

Stephen Willey: Yeah, good afternoon.

Daniel Passeri: We have a 50 percent opt-in there.

Maurice Raycroft: Would it enhance potential for BD if you got regulator feedback or even key investigator buy-in to help define what the clinical development path could look like?

Maurice Raycroft: Got it.

Matteo Levisetti: So again, I would just, you know, use caution, and clearly here the data, you know, needs, to mature.

Leland Gershell: And in that, are there any particular studies you're doing that may guide your thought process with respect to the indications that you have prioritized for both those assets?

Daniel Passeri: Even with the 50 percent opt-in, we'll receive milestones. So if those milestones get triggered, they help subsidize the development of that program.

Daniel Passeri: Yeah, very important question.

Maurice Raycroft: Okay.

Stephen Willey: Thanks for taking the questions.

Matteo Levisetti: And as I mentioned before, we have maturing metrics, both at 12-month OS and median OS, that are established.

Leland Gershell: Thank you.

Daniel Passeri: We have 501 in late-stage discussions with several companies.

Daniel Passeri: I think, obviously, the ONO partnership has enhanced our sort of insight on the autoimmune space.

Maurice Raycroft: Thanks for taking my questions.

Matteo Levisetti: So that's real data, and we'll have to see what happens going forward with Pitocinab.

Anish Suri: Yeah.

Daniel Passeri: The objective there is to consummate a transaction where we have an upfront.

Daniel Passeri: We have a very attractive sort of preclinical data set right now.

Operator: The next question will come from Leland Gershall with Oppenheimer.

Matteo Levisetti: And perhaps, you know, one could hypothesize it'll be similar to different inhibitors of, these pathways, for which there inevitably pop up bypass pathways, and hence the advantages of engaging the immune system and inducing expansion of a durable anti-tumor T-cell population.

Daniel Passeri: So thank you very much and take care.

Anish Suri: Thanks, Leland.

Stephen Willey: On each or Dan, I was just wondering if you could speak to maybe what you know at this point about the trafficking capacity of Q5O.

Daniel Passeri: We have additional support of our scientists that are going to be committed to that program.

Daniel Passeri: We've been in discussions with several potential pharma partners on 501, various stages of diligence and progression. We're just highly confident that, based on the feedback we have, it's a differentiated asset.

Operator: Please go ahead.

Matteo Levisetti: I'm sorry, Ren, I think there was one other question about the neoadjuvant, if I recall.

Anish Suri: This is Anish.

Daniel Passeri: That reduces our burn rate.

Daniel Passeri: It's very attractive based on basically being a biologic that mirrors what CAR T was able to do with lupus.

Leland Gershell: Hey, good afternoon.

Matteo Levisetti: And so that study is progressing well.

Anish Suri: So, we continue to generate pretty exciting data for both programs in autoimmunity with, 401, obviously, in collaboration with Ono, where we have seen efficacy and activity in several disease models, and in due time, collectively and collaboratively, we'll release that in the public domain. In total, the data does seem to reflect what I've mentioned, which is a molecule that generates, copious amounts of regulatory T cells along with signatures for halting autoimmune processes, seizing and sort of reversing or minimizing pro-inflammatory cytokine production and related pathologies.

Daniel Passeri: And then a series of milestones, beginning, obviously, with lead candidate selection, IND filing.

Daniel Passeri: That's what the intent is.

Matteo Levisetti: The investigators at Washington University are very close to completing enrollment in, Schedule B, where patients are getting two doses of 101, and we're getting tissue pre-and post-treatment.

Anish Suri: For 500, we have, are in the process of in vivo experiments, and again, we hope to sort, of release that as we start further understanding relationship between dosing B cell depletion and some of the models that we're characterizing now.

Daniel Passeri: Those milestones overlapped with the ONO milestones are really important to basically give us, continuity.

Daniel Passeri: It compares favorably with bi-specifics, the CD3, CD19 molecules.

Matteo Levisetti: You know, again, this is—the preliminary data that we've seen looks very encouraging.

Anish Suri: So, both programs, the intentions are in this, as we continue to go through this year, to, be able to talk about these data sets as they emerge.

Daniel Passeri: So the measures we've taken for reducing our burn, basically enabling 101 data to mature, without going into a very costly phase two, and just being prudent about what we're focusing on in the near term, focusing on partnering 501 to supplement. So these milestones help extend the runway in a sort of tiered manner.

Daniel Passeri: We think the data set presents an, opportunity for us to partner in the near term.

Matteo Levisetti: The investigators really, I think, I know, have the intent of submitting this for publication, in a very high-level journal.

Anish Suri: Great.

Operator: The conference is now concluded.

Daniel Passeri: So if we do need to raise any capital – and I'm not sure right now where we're going, to need to, but if we do, it's going to be a modest amount – we're really trying to keep dilution down to a minimum, because cost of capital is key.

Daniel Passeri: In terms of indications with that molecule, we're obviously going to hold off until the asset's partnered and we're able to engage in strategic dialogue with the partner on what to focus on in sort of a series of indications.

Matteo Levisetti: And so, you know, when this will become public and shared really depends on how they choose, to proceed.

Operator: The conference is now concluded. Thank you for attending today's presentation.

Anish Suri: Thanks for your questions.

Daniel Passeri: And ultimately, what we want to do is hit these milestones, further develop the pipeline, demonstrate further robustness of our clinical competitive positioning, and ultimately, at some point in the future when the stock is a healthier valuation, cost of capital is and is onerous.

Daniel Passeri: But I think for that program, we look at partnering as an important means of subsidizing, development.

Reni Benjamin: Got it.

Speaker Change #121: The conference has now concluded. Thank you for attending today's presentation you may now disconnect.

Operator: Again, if you have a question, please press star, then 1.

Operator: Thank you for attending today's presentation.

Daniel Passeri: So I hope that's a clear answer, but it's basically a dynamic analysis, and we have, a lot of moving parts here, but it's basically building – that's why I meant by a balanced business model.

Daniel Passeri: We'd also aim to preserve a cell type, for instance, eosinophils or mast cells, something like that, where we retain control and upside of sort of a number of indications from those cell types.

Reni Benjamin: And then just maybe a final question on kind of funding and your current cash position, and the like. Can you maybe help us understand how you plan on bridging the gap between now and kind of, initial milestone payments expected from the ONO opt-in versus selection of lead candidates and the like?

Operator: Our next question will come from Ted Tinoff with Piper Sandler.

Daniel Passeri: Having a stream of capital options coming in with these milestones being triggered, and looking at raising capital in a very sort of prudent, pragmatic manner based on cost of capital.

Daniel Passeri: So, I hope that answers your question, Mari.

Operator: Please go ahead.

Reni Benjamin: Great.

Maurice Raycroft: Yep.

Operator: You may now disconnect.

Ted Tinoff: Great.

Operator: You may now disconnect.

Reni Benjamin: Thanks, and good luck going forward.

Maurice Raycroft: Yeah, really helpful.

Ted Tinoff: Thank you very much.

Stephen Willey: 101.

Reni Benjamin: All right.

Daniel Passeri: And maybe just to follow up on the financial side as well, I guess, for the ONO opt-in, is there any room to negotiate and potentially accelerate milestones or opt-in potential based on the data that you've generated so far, or would it not make sense to try to do that at this point?

Ted Tinoff: To sort of the evolving world of targeting CB19 to Blake B cells for autoimmune disease, how much is the safety, the potential safety profile that you've generated on the immunostats platform from 101 and 102 differentiating from the cell therapies, and is that something that investors are focused on?

Daniel Passeri: I appreciate it, Ren.

Daniel Passeri: Yeah, I don't think it would make sense to try to modify it right now.

Ted Tinoff: Thanks so much.

Stephen Willey: And then also just what's your estimate of CMV zero positivity in the general population? I know it's correlated to age.

[music].

Anish Suri: Yeah.

Anish Suri: Ted, again, very good question, and I think I try to stress that, but the clinical de-risking, and vulnerability of immunostats in man, in general, what we've shown with 101 and 102, we believe has an enormous positive implication on the 500 series of B cell depletion.

Anish Suri: Simply, even if you look at the metrics of tolerability from immunogenicity, as you well, know, we have not seen any clinically relevant immunogenicity in our 100 series trials with, 101, 102. We've had patients receiving drug up to two years.

Anish Suri: Again, that speaks to the nature of selective TCR engagement via this framework.

Anish Suri: The second is the fact that by virtue of the fact that you're only co-opting a very small, percentage of your peripheral T cell repertoire in an individual, and not carpet bombing all T cells with anti-CD3 based approaches, which we refer to as the pan-T cell engages, we, believe should also offer superior safety and tolerability metrics, and some of that is evident from this in vitro assessment of cytokine release that we did, where you saw this profound production of cytokines by pan-T cell engager molecules, as opposed to Q500 where it was significantly reduced, despite the fact that Q500 shows very comparable metrics of killing efficacy of B cells.

Anish Suri: So that's also quite important.

Anish Suri: Thirdly, I think we should sort of reemphasize the fact, that through nature, your memory antiviral T cells is something that all of us have harbored from the time we're born through our life to provide us protective immunity.

Anish Suri: So there's no other better, long-lasting, killer T cell population that one harbors, as compared to what these cells offer.

Anish Suri: So we do think being able to redirect them, to kill targets such as B cells provides a very exciting avenue for really harnessing the potential of what nature has already given the individual.

Speaker Change #121: Yes.

Stephen Willey: I think it tends to be lower in males versus females, but just wondering kind of what your general estimate of this would be and whether you would need to screen for CMV positivity in the context of a based on those escalation trial.

Ted Tinoff: Yep, I agree.

Anish Suri: And obviously a very different manufacturing approach, than what we're seeing with the autologous CAR T-exam.

[music].

Anish Suri: Oh, that's exactly right.

Anish Suri: That's exactly right, Ted.

Anish Suri: So just to add to that, the manufacturability is exactly what we've seen with 101, 102 antibody-based biologics.

Anish Suri: The yields are in line with what we've seen, at similar stages for immunostats, which are clinically great. Products have yielded in grams per liter, with very good shelf stability of the GMP product.

Anish Suri: That's a very important point.

Speaker Change #121: Okay.

Ted Tinoff: Great, well, thanks, Ty, as a credit to you for the progress.

Speaker Change #121: Yeah.

Ted Tinoff: Thank you, Ted.

Operator: This concludes our question and answer session.

Speaker Change #121: Sure.

Operator: I would like to turn the conference back over

Speaker Change #121: [music].

Daniel Passeri: to Mr. Dan Passeri for any closing remarks.

Daniel Passeri: Please go ahead, sir.

Daniel Passeri: Thank you.

Daniel Passeri: We just want to thank everyone for listening, and your continued interest in our progress.

Daniel Passeri: Yeah.

Daniel Passeri: So both very good questions, Steve.

Stephen Willey: Yeah. So both very good questions, Steve. CMV is an example we presented, but just to make the point, Steve, we have made Q500 molecules with SARS-CoV-2 and EBV and other viral epitopes as well. So we presented the case with CMV in the particular case of CMV zero positivity anywhere around 65 to 70% in our experience when we've screened donors for SARS-CoV-2 at this point in time in the history of mankind, virtually a hundred percent.

Speaker Change #121: Yes.

Speaker Change #121: Uh huh.

Daniel Passeri: CMV is an example we presented, but just to make the point, Steve, we have made Q500 molecules with SARS-CoV-2 and EBV and other viral epitopes as well.

Speaker Change #121: [music].

Yeah.

Daniel Passeri: So we presented the case with CMV in the particular case of CMV zero positivity anywhere around 65 to 70% in our experience when we've screened donors for SARS-CoV-2 at this point in time in the history of mankind, virtually a hundred percent.

Speaker Change #121: [music].

Daniel Passeri: A hundred percent have been SARS-CoV-2 for obvious reasons.

Stephen Willey: A hundred percent have been SARS-CoV-2 for obvious reasons. From the trafficking, we are now doing in vivo studies, but with immunostats in general, Steve, we had published a paper in nature methods with Hinaplu several years back, where we used immunopath imaging to make the point that immunostats could penetrate solid tumour tissue as well as an infectious model and directly engage the relevant antigen specific. We believe that same should hold true for for the 500 series where you can have extravacation and local engagement to essentially be able to recognize the eSus that are bound by these molecules.

Daniel Passeri: From the trafficking, we are now doing in vivo studies, but with immunostats in general, Steve, we had published a paper in nature methods with Hinaplu several years back, where we used immunopath imaging to make the point that immunostats could penetrate solid tumour tissue as well as an infectious model and directly engage the relevant antigen specific. We believe that same should hold true for for the 500 series where you can have extravacation and local engagement to essentially be able to recognize the eSus that are bound by these molecules.

Stephen Willey: Okay, that's helpful.

Stephen Willey: Okay, that's helpful. And then maybe just a key one or one question. So I understand that you guys are obviously kind of pausing things for now and allowing them. It's a survival data to mature, but I guess in the context of frontline head and neck right now, and what is capable with pember amount of therapy, I think that appears to be the subject of some increasing debate as a function of primarily, I guess, the leap 10 data.

Stephen Willey: And then maybe just a key one or one question.

Stephen Willey: So I understand that you guys are obviously kind of pausing things for now and allowing them.

Stephen Willey: It's a survival data to mature, but I guess in the context of frontline head and neck right now, and what is capable with pember amount of therapy, I think that appears to be the subject of some increasing debate as a function of primarily, I guess, the leap 10 data.

Daniel Passeri: So just curious, if you think a more mature survival statistic could help attract strategic interest and just curious if you can share anything in terms of the conversations that you've had thus far with potentially interested parties in terms of how they're thinking about what pember amount of therapy historically is capable of.

Stephen Willey: So just curious, if you think a more mature survival statistic could help attract strategic interest and just curious if you can share anything in terms of the conversations that you've had thus far with potentially interested parties in terms of how they're thinking about what pember amount of therapy historically is capable of. Sure, thanks, Steve. This is Dan. So it's an important question. We've had dialogue with multiple potential partners on the data sets that we've had historically, when we look at the monotherapy data, I mean, we've actually had the comment of the data looks so promising that how do they know that we haven't biased by selecting healthy patients.

Daniel Passeri: Sure, thanks, Steve.

Daniel Passeri: This is Dan.

Daniel Passeri: So it's an important question.

Daniel Passeri: We've had dialogue with multiple potential partners on the data sets that we've had historically, when we look at the monotherapy data, I mean, we've actually had the comment of the data looks so promising that how do they know that we haven't biased by selecting healthy patients.

Daniel Passeri: And that's one of the reasons we emphasize the randomized strategy for the phase two.

Stephen Willey: And that's one of the reasons we emphasize the randomized strategy for the phase two. I think what's really important here, when you look at the landscape of competing molecules, different kinase inhibitors, et cetera, in this space, we think the survival data is in a really differentiate and truly position. Q with an advantage and a competitive advantage in terms of durability of triggering an immune response. So that survival data as it continues to mature, I think what we've seen in monotherapy is very impressive.

Daniel Passeri: I think what's really important here, when you look at the landscape of competing molecules, different kinase inhibitors, et cetera, in this space, we think the survival data is in a really differentiate and truly position.

Daniel Passeri: Q with an advantage and a competitive advantage in terms of durability of triggering an immune response.

Daniel Passeri: So that survival data as it continues to mature, I think what we've seen in monotherapy is very impressive.

Daniel Passeri: What we're seeing emerge with the combination appears to be following suit.

Stephen Willey: What we're seeing emerge with the combination appears to be following suit. And I think that's going to be dispositive in the long run. I think ultimately a randomized study is basically far more convincing because you're going directly against Pembro as a single agent. But it is an important topic and it is being watched. And we do have ongoing dialogue with companies on 101. Alright, thanks for taking the questions. Yeah.

Daniel Passeri: And I think that's going to be dispositive in the long run.

Daniel Passeri: I think ultimately a randomized study is basically far more convincing because you're going directly against Pembro as a single agent.

Daniel Passeri: But it is an important topic and it is being watched.

Daniel Passeri: And we do have ongoing dialogue with companies on 101.

Stephen Willey: Alright, thanks for taking the questions.

Reni Benjamin: Yeah.

Reni Benjamin: The next question will come from Reni Benjamin with Citizens' JMP.

Reni Benjamin: The next question will come from Reni Benjamin with Citizens' JMP. Please go ahead. Hey, good afternoon, guys. Thanks for taking the questions. So thanks for the update on one-on-one incommination with Petrua and the monotherapy. I guess my first question would be how to think about these results, given the current landscape. And in particular, kind of the developing landscape, given the provocative data, we saw it ask out from Maris and some of the others that are also in the space.

Reni Benjamin: Please go ahead.

Reni Benjamin: Hey, good afternoon, guys.

Reni Benjamin: Thanks for taking the questions.

Reni Benjamin: So thanks for the update on one-on-one incommination with Petrua and the monotherapy.

Reni Benjamin: I guess my first question would be how to think about these results, given the current landscape.

Reni Benjamin: And in particular, kind of the developing landscape, given the provocative data, we saw it ask out from Maris and some of the others that are also in the space.

Reni Benjamin: And just as a follow-up to that, I'm kind of curious.

Reni Benjamin: And just as a follow-up to that, I'm kind of curious. I don't think it was mentioned in the earlier comments. Can you provide any sort of an update on the neo-agent study? Sure. Matteo, why don't you take the question? Yeah, no, I will. And again, just to follow up on the prior question. Again, I think this really, you know, the data from the lead 10 trial underscores the importance of looking at early median OS as it matures.

Reni Benjamin: I don't think it was mentioned in the earlier comments.

Reni Benjamin: Can you provide any sort of an update on the neo-agent study?

Mateo Levisetti: Sure.

Mateo Levisetti: Matteo, why don't you take the question?

Mateo Levisetti: Yeah, no, I will.

Mateo Levisetti: And again, just to follow up on the prior question.

Mateo Levisetti: Again, I think this really, you know, the data from the lead 10 trial underscores the importance of looking at early median OS as it matures.

Mateo Levisetti: And so you actually look at the Pembro Mono data set from lead 10, the 12-month survival is 59 percent.

Reni Benjamin: And so you actually look at the Pembro Mono data set from lead 10, the 12-month survival is 59 percent. If we look at the Q101 combination data, our current 12-month survival is 90 percent. And if you look at CPS high, it's 100 percent of patients are alive at 12 months. Okay. And so with regards to the question now of the evolving landscape in particular, Maris has compounded to FEMTED MAB. Again, it's really important to look at the data that they've shared with regards to their survival.

Mateo Levisetti: If we look at the Q101 combination data, our current 12-month survival is 90 percent.

Mateo Levisetti: And if you look at CPS high, it's 100 percent of patients are alive at 12 months.

Mateo Levisetti: Okay.

Mateo Levisetti: And so with regards to the question now of the evolving landscape in particular, Maris has compounded to FEMTED MAB.

Mateo Levisetti: Again, it's really important to look at the data that they've shared with regards to their survival.

Mateo Levisetti: And so in the second line setting and beyond, they reported a survival of 11.5 months.

Reni Benjamin: And so in the second line setting and beyond, they reported a survival of 11.5 months. Okay. With Q101 Mono, we're currently at, you know, 20.8 months and even 20 almost five months in the two-meg per key cohort. So although in the second line plus, they reported a response rate of 37 percent. Their survival is about half as long, okay, as Q monotherapy where we observed a response rate of 5 percent. And again, this is fully consistent with patterns of clinical benefit that have been now well-defined in immunotherapy.

Mateo Levisetti: Okay.

Mateo Levisetti: With Q101 Mono, we're currently at, you know, 20.8 months and even 20 almost five months in the two-meg per key cohort.

Mateo Levisetti: So although in the second line plus, they reported a response rate of 37 percent.

Mateo Levisetti: Their survival is about half as long, okay, as Q monotherapy where we observed a response rate of 5 percent.

Mateo Levisetti: And again, this is fully consistent with patterns of clinical benefit that have been now well-defined in immunotherapy.

Mateo Levisetti: So if we look at TEMTRAC recently approved for UVIL melanoma, really modest response rate, but a clear survival benefit led to its approval.

Reni Benjamin: So if we look at TEMTRAC recently approved for UVIL melanoma, really modest response rate, but a clear survival benefit led to its approval. And so back to Potosimab now in the they actually only reported data on about half of the patients that were treated with very minimal follow-up. So with the follow-up median follow-up, if you looked at the swimmer plot about four months. So again, I would just, you know, use caution and clearly hear the data, you know, needs to mature.

Mateo Levisetti: And so back to Potosimab now in the they actually only reported data on about half of the patients that were treated with very minimal follow-up.

Mateo Levisetti: So with the follow-up median follow-up, if you looked at the swimmer plot about four months.

Mateo Levisetti: So again, I would just, you know, use caution and clearly hear the data, you know, needs to mature.

Mateo Levisetti: And as I mentioned before, we have maturing metrics both at 12 month OS and median OS that are established.

Reni Benjamin: And as I mentioned before, we have maturing metrics both at 12 month OS and median OS that are established. So that's real data, and we'll have to see what happens. I'm going forward with Potosian app. And perhaps, you know, one could hypothesize, it will be similar to different inhibitors of these pathways for which they're inevitably pop up bypass pathways and hence the advantages of engaging the immune system and inducing expansion of a durable anti-tumored T-cell population.

Mateo Levisetti: So that's real data, and we'll have to see what happens.

Mateo Levisetti: I'm going forward with Potosian app.

Mateo Levisetti: And perhaps, you know, one could hypothesize, it will be similar to different inhibitors of these pathways for which they're inevitably pop up bypass pathways and hence the advantages of engaging the immune system and inducing expansion of a durable anti-tumored T-cell population.

Mateo Levisetti: Sorry, Reni, there's one other question about the new adjuvant, if I recall.

Reni Benjamin: Sorry, Reni, there's one other question about the new adjuvant, if I recall. And so, that study is progressing well. The investigators at Washington University are very close to completing enrollment in schedule B, where patients are getting two doses of 101, and we're getting tissue pre and post treatment. You know, again, this is the preliminary data that we've seen looks very encouraging. The investigators really, I think, I know have the intent of submitting this for publication in a very high level journal.

Mateo Levisetti: And so, that study is progressing well. The investigators at Washington University are very close to completing enrollment in schedule B, where patients are getting two doses of 101, and we're getting tissue pre and post treatment.

Mateo Levisetti: You know, again, this is the preliminary data that we've seen looks very encouraging.

Mateo Levisetti: The investigators really, I think, I know have the intent of submitting this for publication in a very high level journal.

Mateo Levisetti: And so, you know, when this will become public and shared really depends on how they choose to proceed.

Reni Benjamin: And so, you know, when this will become public and shared really depends on how they choose to proceed. Got it. And then just maybe a final question on kind of funding and your current cash position. Like, can you maybe help us understand how you plan on bridging the gap between now and kind of initial milestone payments expected from the owner opt in versus selection of lead candidates and the like? How do you see that kind of unfolding?

Reni Benjamin: Got it.

Reni Benjamin: And then just maybe a final question on kind of funding and your current cash position.

Reni Benjamin: Like, can you maybe help us understand how you plan on bridging the gap between now and kind of initial milestone payments expected from the owner opt in versus selection of lead candidates and the like?

Reni Benjamin: How do you see that kind of unfolding?

Reni Benjamin: Thanks.

Daniel Passeri: Yeah, thanks.

Daniel Passeri: Thanks, Ren, as a Dan.

Reni Benjamin: Thanks. Yeah, thanks. Thanks, Ren, as a Dan. That's an important question. One thing I want to emphasize, you know, we were very prudent and deliberate and basically looking at that question in a very dynamic way. The one thing we have not chosen to do historically is with the cost of capital as the small cap biotech sector has, you know, basically been compressed in terms of valuations. We have not chosen to go out and do a massively dilutive financing.

Daniel Passeri: That's an important question.

Daniel Passeri: One thing I want to emphasize, you know, we were very prudent and deliberate and basically looking at that question in a very dynamic way.

Daniel Passeri: The one thing we have not chosen to do historically is with the cost of capital as the small cap biotech sector has, you know, basically been compressed in terms of valuations.

Daniel Passeri: We have not chosen to go out and do a massively dilutive financing.

Daniel Passeri: So, we've taken a look at a business model where we have programs that are all kind of moving over time.

Reni Benjamin: So, we've taken a look at a business model where we have programs that are all kind of moving over time. We have a partnered program right now, 401 with ONO. And if one looks back at that, it was actually a really nice design. They're helping, they're subsidizing basically the preclinical development, working very closely with us. They're supporting our scientists. And that has resulted in a really good high quality body of data going forward to select a lead candidate that then with the objective of getting into the clinic, we have a 50% opt in there.

Daniel Passeri: We have a partnered program right now, 401 with ONO.

Daniel Passeri: And if one looks back at that, it was actually a really nice design.

Daniel Passeri: They're helping, they're subsidizing basically the preclinical development, working very closely with us. They're supporting our scientists.

Daniel Passeri: And that has resulted in a really good high quality body of data going forward to select a lead candidate that then with the objective of getting into the clinic, we have a 50% opt in there.

Daniel Passeri: Even with the 50% opt in will receive milestones. So, if those milestones get triggered, they help subsidize the development of that program.

Reni Benjamin: Even with the 50% opt in will receive milestones. So, if those milestones get triggered, they help subsidize the development of that program. We have 501 in late stage discussions with several companies. The objective there is to consummate a transaction where we have an upfront. We have additional support of our scientists that are going to be committed to that program. That reduces our burn rate and then a series of milestones beginning obviously with lead candidate selection, IND filing.

Daniel Passeri: We have 501 in late stage discussions with several companies.

Daniel Passeri: The objective there is to consummate a transaction where we have an upfront.

Daniel Passeri: We have additional support of our scientists that are going to be committed to that program.

Daniel Passeri: That reduces our burn rate and then a series of milestones beginning obviously with lead candidate selection, IND filing.

Daniel Passeri: Those milestones overlap with the ONO milestones.

Reni Benjamin: Those milestones overlap with the ONO milestones. You know, are really important to basically give us continuity. So, the measures we've taken for reducing our burn basically enabling 101 data to mature without going into a very costly phase two. And just being prudent about what we're focusing on in the near term. Focusing on partnering 501 to supplement. So, these milestones help extend the runway in a sort of tiered manner. So, if we do need to raise any capital and not sure right now where we're going to need to but if we do it's going to be a modest amount, we're really trying to keep dilution down to a minimum because cost of capital is key.

Daniel Passeri: You know, are really important to basically give us continuity.

Daniel Passeri: So, the measures we've taken for reducing our burn basically enabling 101 data to mature without going into a very costly phase two.

Daniel Passeri: And just being prudent about what we're focusing on in the near term.

Daniel Passeri: Focusing on partnering 501 to supplement.

Daniel Passeri: So, these milestones help extend the runway in a sort of tiered manner.

Daniel Passeri: So, if we do need to raise any capital and not sure right now where we're going to need to but if we do it's going to be a modest amount, we're really trying to keep dilution down to a minimum because cost of capital is key.

Daniel Passeri: And ultimately what we want to do is hit these milestones further develop the pipeline demonstrate further robustness of our clinical competitive positioning.

Reni Benjamin: And ultimately what we want to do is hit these milestones further develop the pipeline demonstrate further robustness of our clinical competitive positioning. And ultimately at some point in the future when the stock is a healthy evaluation cost of capital is in his own risk. So, I hope that's a clear answer but it's basically a dynamic analysis and we have a lot of moving parts here but it's basically building up. That's why I meant by a balanced business model.

Daniel Passeri: And ultimately at some point in the future when the stock is a healthy evaluation cost of capital is in his own risk.

Daniel Passeri: So, I hope that's a clear answer but it's basically a dynamic analysis and we have a lot of moving parts here but it's basically building up.

Daniel Passeri: That's why I meant by a balanced business model.

Daniel Passeri: Having a stream of capital options coming in with these milestones being triggered and looking at raising capital in a very sort of prudent, pragmatic manner based on cost of capital, in the middle.

Reni Benjamin: Having a stream of capital options coming in with these milestones being triggered and looking at raising capital in a very sort of prudent, pragmatic manner based on cost of capital, in the middle. Great, thanks. Good luck going forward. All right, appreciate it, Reni. Thank you.

Daniel Passeri: Great, thanks.

Daniel Passeri: Good luck going forward.

Daniel Passeri: All right, appreciate it, Reni.

Mari Raycroft: Thank you.

Mari Raycroft: The next question will come from Mari Raycroft with Jeff Reese.

Maurice Raycroft: The next question will come from Mari Raycroft with Jeff Reese. Please go ahead. Hi, congrats on the data update, and thanks for taking my questions.

Mari Raycroft: Please go ahead.

Mari Raycroft: Hi, congrats on the data update, and thanks for taking my questions.

Mari Raycroft: I'll ask one on the Q500 series for Q501.

Maurice Raycroft: I'll ask one on the Q500 series for Q501. Can you talk more about plans or options for next steps to position this program for partnering? What did enhance potential for BDFU? Got regulator feedback or even key investigator buy-in to help define what the clinical development path to look like? Yeah, very important question. I think obviously the ONO partnership has enhanced our sort of insight on the autoimmune space. We have a very attractive sort of preclinical data set right now.

Mari Raycroft: Can you talk more about plans or options for next steps to position this program for partnering?

Mari Raycroft: What did enhance potential for BDFU?

Mari Raycroft: Got regulator feedback or even key investigator buy-in to help define what the clinical development path to look like?

Daniel Passeri: Yeah, very important question.

Daniel Passeri: I think obviously the ONO partnership has enhanced our sort of insight on the autoimmune space.

Daniel Passeri: We have a very attractive sort of preclinical data set right now.

Daniel Passeri: We've been in discussions with several potential pharma partners on 501, various stages of diligence and progression.

Maurice Raycroft: We've been in discussions with several potential pharma partners on 501, various stages of diligence and progression. We're just highly confident that based on the feedback we have is a differentiated asset. It's very attractive based on basically being a biologic that mirrors what Carti was able to do with Lupus. That's what the intent is. It compares favorably with by specifics, the CD3, CD19 molecules. We think the data set presents an opportunity for us to partner in the near term.

Daniel Passeri: We're just highly confident that based on the feedback we have is a differentiated asset.

Daniel Passeri: It's very attractive based on basically being a biologic that mirrors what Carti was able to do with Lupus.

Daniel Passeri: That's what the intent is.

Daniel Passeri: It compares favorably with by specifics, the CD3, CD19 molecules.

Daniel Passeri: We think the data set presents an opportunity for us to partner in the near term.

Daniel Passeri: In terms of indications with that molecule, we're obviously going to hold off until the assets partnered and we're able to engage in dialogue, strategic dialogue with a partner on what to focus on and a sort of a series of indications.

Maurice Raycroft: In terms of indications with that molecule, we're obviously going to hold off until the assets partnered and we're able to engage in dialogue, strategic dialogue with a partner on what to focus on and a sort of a series of indications. But I think for that program, we look at partnering as an important means of subsidizing development. We'd also aim to preserve a cell type, for instance, eosinophils or mass cells, something like that, where we retain control and upside of sort of a number of indications from those cell types. I hope that answers your question, Mark. Yeah, really helpful.

Daniel Passeri: But I think for that program, we look at partnering as an important means of subsidizing development.

Daniel Passeri: We'd also aim to preserve a cell type, for instance, eosinophils or mass cells, something like that, where we retain control and upside of sort of a number of indications from those cell types.

Daniel Passeri: I hope that answers your question, Mark.

Mari Raycroft: Yeah, really helpful.

Daniel Passeri: Maybe just to follow up on the financial side as well, I guess for the ONO opt-in, is there any room to negotiate and potentially accelerate milestones or opt-in potential based on the data that you've generated so far, or would it not make sense to try to do that at this point?

Maurice Raycroft: Maybe just to follow up on the financial side as well, I guess for the ONO opt-in, is there any room to negotiate and potentially accelerate milestones or opt-in potential based on the data that you've generated so far, or would it not make sense to try to do that at this point? Yeah, I don't think it would make sense to try to modify it right now. We've been making really good progress. The partnerships have actually been extremely productive. They've really been an outstandingly supportive partner and we're aligned on what the next steps are, so I think we're very much seeing things from a similar perspective. Got it.

Daniel Passeri: Yeah, I don't think it would make sense to try to modify it right now.

Daniel Passeri: We've been making really good progress. The partnerships have actually been extremely productive. They've really been an outstandingly supportive partner and we're aligned on what the next steps are, so I think we're very much seeing things from a similar perspective.

Daniel Passeri: Got it.

Mari Raycroft: Okay, thanks for taking my questions.

Maurice Raycroft: Okay, thanks for taking my questions.

Lee-Lynn Gershell: The next question will come from Lee-Lynn Gershell with Oppenheimer.

Leland Gershell: The next question will come from Lee-Lynn Gershell with Oppenheimer. Please go ahead. Hey, good afternoon. Thanks for the update and taking my questions. Let me just a few for you, Jen or Nish. Looks like you have a good base of preclinical data here for four, one, five, or one.

Lee-Lynn Gershell: Please go ahead.

Lee-Lynn Gershell: Hey, good afternoon.

Lee-Lynn Gershell: Thanks for the update and taking my questions.

Lee-Lynn Gershell: Let me just a few for you, Jen or Nish.

Lee-Lynn Gershell: Looks like you have a good base of preclinical data here for four, one, five, or one.

Lee-Lynn Gershell: I wanted to know what might be the next set of nonclinical data that we might be looking for that you might have to present to us and in that, are there any particular studies you're doing that make guide your thought process with respect to the indications that you prioritize for both of us?

Leland Gershell: I wanted to know what might be the next set of nonclinical data that we might be looking for that you might have to present to us and in that, are there any particular studies you're doing that make guide your thought process with respect to the indications that you prioritize for both of us? Thank you. Yeah, thanks, Leland, this is an issue. So we continue to generate pretty exciting data for both programs and auto-munity with 401 obviously in collaboration with ONO, where we have seen efficacy and activity in several disease models and in due time collectively and collaboratively will release that in the public domain.

Anish Suri: Thank you.

Anish Suri: Yeah, thanks, Leland, this is an issue.

Anish Suri: So we continue to generate pretty exciting data for both programs and auto-munity with 401 obviously in collaboration with ONO, where we have seen efficacy and activity in several disease models and in due time collectively and collaboratively will release that in the public domain.

Anish Suri: In total, the data does seem to reflect what I've mentioned, which is a molecule that generates copious amounts of regulatory T cells along with signatures for halting autoimmune processes, seizing and sort of reversing or minimizing pro-inflammatory cytokine production and related pathologies.

Leland Gershell: In total, the data does seem to reflect what I've mentioned, which is a molecule that generates copious amounts of regulatory T cells along with signatures for halting autoimmune processes, seizing and sort of reversing or minimizing pro-inflammatory cytokine production and related pathologies. For 500, we have, are in the process of in vivo experiments. And again, we hope to sort of release that, as we see, start for the understanding relationship between dosing, b-cell depletion, and so the models that we're catrising now.

Anish Suri: For 500, we have, are in the process of in vivo experiments. And again, we hope to sort of release that, as we see, start for the understanding relationship between dosing, b-cell depletion, and so the models that we're catrising now.

Anish Suri: So both programs are the intentions on this, as we continue to go through this year to be able to talk about these data sets as they merge.

Leland Gershell: So both programs are the intentions on this, as we continue to go through this year to be able to talk about these data sets as they merge. Thank you very much. Thank you very much, thank you very much. Again, if you have a question, please write star, then one.

Anish Suri: Thank you very much.

Edward Tenthoff: Our next question will come from Ted, Tenoff, with Piper Sandler, please go ahead. Great, thank you very much. Thank you to sort of the evolving world of targeting CB-19 to Blake B cells for autoimmune disease.

Anish Suri: Thank you very much, thank you very much.

Operator: Again, if you have a question, please write star, then one.

Ted Tenthoff: Our next question will come from Ted, Tenoff, with Piper Sandler, please go ahead.

Ted Tenthoff: Great, thank you very much.

Ted Tenthoff: Thank you to sort of the evolving world of targeting CB-19 to Blake B cells for autoimmune disease.

Ted Tenthoff: How much is the CT, the potential CT profile that you've generated on the immunostat platform from 101-102 differentiating from the cell therapies?

Edward Tenthoff: How much is the CT, the potential CT profile that you've generated on the immunostat platform from 101-102 differentiating from the cell therapies? And is that something that investors are focused on? Thanks so much. Yeah, Ted, again, very good question, and I think I try to stress that, but the clinical de-risking and vulnerability of immunostats in man. In general, what we've shown with 101-102, we believe has an enormous positive implication on the 500 series of b-cell depletion.

Ted Tenthoff: And is that something that investors are focused on?

Daniel Passeri: Thanks so much.

Daniel Passeri: Yeah, Ted, again, very good question, and I think I try to stress that, but the clinical de-risking and vulnerability of immunostats in man.

Daniel Passeri: In general, what we've shown with 101-102, we believe has an enormous positive implication on the 500 series of b-cell depletion.

Daniel Passeri: Simply even if you look at from metrics of told mobility from immunogenicity, as you will know, we have not seen any clinically relevant immunogenicity in our 100 series trials with 101-102.

Edward Tenthoff: Simply even if you look at from metrics of told mobility from immunogenicity, as you will know, we have not seen any clinically relevant immunogenicity in our 100 series trials with 101-102. We've had patients receiving drug up to two years. So, again, that speaks to the nature of selective TCR engagement, we are this framework. The second is the fact that by virtue of the fact that you're only co-opting a very small percentage of your peripheral T cell repertoire in an individual and not carpet bombing all T cells with anti-CD-3-based approaches, which we refer to as the panties of engages.

Daniel Passeri: We've had patients receiving drug up to two years.

Daniel Passeri: So, again, that speaks to the nature of selective TCR engagement, we are this framework.

Daniel Passeri: The second is the fact that by virtue of the fact that you're only co-opting a very small percentage of your peripheral T cell repertoire in an individual and not carpet bombing all T cells with anti-CD-3-based approaches, which we refer to as the panties of engages.

Daniel Passeri: We believe should also offer superior safety and told mobility metrics, and some of that is evident from this in vitro assessments of cytokine release that we did, where you saw this profound production of cytokines by panties of engage of molecule, as opposed to Q500 by a significantly reduced, despite the fact that Q500 shows a very comparable matrix of killing efficacy of B cells.

Edward Tenthoff: We believe should also offer superior safety and told mobility metrics, and some of that is evident from this in vitro assessments of cytokine release that we did, where you saw this profound production of cytokines by panties of engage of molecule, as opposed to Q500 by a significantly reduced, despite the fact that Q500 shows a very comparable matrix of killing efficacy of B cells. So that's also quite important. Thirdly, I think we should sort of re-emphasize the fact that through nature, your memory anti-viral T cells is something that all of us have harbored from the time we're born through our life to provide us protective immunity.

Daniel Passeri: So that's also quite important.

Daniel Passeri: Thirdly, I think we should sort of re-emphasize the fact that through nature, your memory anti-viral T cells is something that all of us have harbored from the time we're born through our life to provide us protective immunity.

Daniel Passeri: So there's no other better, long-lasting killer T cell population than one harvest, you know, as compared to what these cells offer.

Edward Tenthoff: So there's no other better, long-lasting killer T cell population than one harvest, you know, as compared to what these cells offer. So we do think being able to redirect them to kill targets such as B cells provides a very exciting avenue for really harnessing a potential of what nature has already given the individual. Yes, very great. And obviously a very different manufacturing approach than what we're seeing with your targets is a car key.

Daniel Passeri: So we do think being able to redirect them to kill targets such as B cells provides a very exciting avenue for really harnessing a potential of what nature has already given the individual.

Daniel Passeri: Yes, very great.

Daniel Passeri: And obviously a very different manufacturing approach than what we're seeing with your targets is a car key.

Daniel Passeri: Oh, that's exactly right.

Edward Tenthoff: Oh, that's exactly right. That's exactly right. So just to add to that, the manufacturability is exactly what we've seen with 101-102 and a body based biologics. The yields are in line with what we've seen at similar stages for immunostats, which are clinically great. Products have yielded in grams per liter with very good shell stability of the GMP product. That's a very important point. Great. Well, thanks, guys. The credit to you have a progress. Thank you, Ted.

Daniel Passeri: That's exactly right.

Daniel Passeri: So just to add to that, the manufacturability is exactly what we've seen with 101-102 and a body based biologics.

Daniel Passeri: The yields are in line with what we've seen at similar stages for immunostats, which are clinically great.

Daniel Passeri: Products have yielded in grams per liter with very good shell stability of the GMP product.

Daniel Passeri: That's a very important point.

Daniel Passeri: Great.

Daniel Passeri: Well, thanks, guys.

Daniel Passeri: The credit to you have a progress.

Daniel Passeri: Thank you, Ted.

Operator: This concludes our question and answer session.

Operator: This concludes our question and answer session.

Daniel Passeri: I would like to turn the conference back over to Mr. Dan Pisseri for an closing remarks.

Dan Passeri: I would like to turn the conference back over to Mr. Dan Pisseri for an closing remarks. Please go ahead, sir. Thank you. We just want to thank everyone for listening in. You continued interest in our progress and we look forward to keeping you updated with the progress we make going forward. So thank you very much and take care.

Daniel Passeri: Please go ahead, sir.

Daniel Passeri: Thank you.

Daniel Passeri: We just want to thank everyone for listening in.

Daniel Passeri: You continued interest in our progress and we look forward to keeping you updated with the progress we make going forward.

Daniel Passeri: So thank you very much and take care.

Operator: The conference is now concluded.

Operator: The conference is now concluded.

Operator: Thank you for attending today's presentation.

Operator: Thank you for attending today's presentation.

Operator: You may now disconnect.

Operator: You may now disconnect.