Q1 2026 Allogene Therapeutics Inc Earnings Call

May 13, 2026

Operator 2: Hello, thank you for standing by. Welcome to Allogene Therapeutics Q1 2026 conference call. After the speaker's presentation, there will be a question and answer session. To ask a question during the session, you will need to press star one one on your telephone. You will hear an automated message advising your hand is raised. To withdraw your question, please press star one one again. Please be aware that today's conference call is being recorded. I would now like to turn the call over to

Operator: Hello, thank you for standing by. Welcome to Allogene Therapeutics Q1 2026 conference call. After the speaker's presentation, there will be a question and answer session. To ask a question during the session, you will need to press star one one on your telephone. You will hear an automated message advising your hand is raised. To withdraw your question, please press star one one again. Please be aware that today's conference call is being recorded. I would now like to turn the call over to

Speaker #1: To ask a question during the session, you will need to press star 11 on your telephone; you will then hear an automated message advising your hand is raised.

Speaker #1: To withdraw your question, please press star 11 again. Please be aware that today's conference call is being recorded. I would now like to turn the call over to Christine Cassiano, Chief Corporate Affairs and Brand Strategy Officer.

David Chang: Christine Cassiano, Chief Corporate Affairs and Brand Strategy Officer. Ms. Cassiano, please go ahead.

Operator: Christine Cassiano, Chief Corporate Affairs and Brand Strategy Officer. Ms. Cassiano, please go ahead.

Speaker #1: Ms. Cassiano, please go ahead.

Speaker #2: Thank you, Operator, and welcome, everyone, to Allogene's conference call. After the market closed, Allogene issued a press release that provided a business update and financial results for the first quarter of 2026.

Christine Cassiano: Thank you, operator, and welcome everyone to Allogene's conference call. After the market closed, Allogene issued a press release that provided a business update and financial results for Q1 2026. This press release and today's webcast are available on our website. Following our prepared remarks, we will host a Q&A session and will aim to keep the call to under an hour. I am joined today by Dr. David Chang, President and Chief Executive Officer, Dr. Zachary Roberts, Executive Vice President of Research and Development and Chief Medical Officer, and Geoffrey Parker, Chief Financial Officer. During today's call, we will be making certain forward-looking statements.

Speaker #2: This press release and today's webcast are available on our website. Following our prepared remarks, we will host a Q&A session and will aim to keep the call to under an hour.

Speaker #2: I am joined today by Dr. David Chang, President and Chief Executive Officer; Dr. Zachary Roberts, Executive Vice President of Research and Development and Chief Medical Officer; and Geoff Parker, Chief Financial Officer.

Speaker #2: During today's call, we will be making certain forward-looking statements. These may include statements regarding the success and timing of our ongoing and planned clinical trials, data presentations, regulatory filings, future research and development efforts, manufacturing capabilities, the safety and efficacy of our product candidates, commercial market forecasts, potential treatment settings, and financial guidance, among other things.

Christine Cassiano: These may include statements regarding the success and timing of our ongoing and planned clinical trials, data presentations, regulatory filings, future research and development efforts, manufacturing capabilities, the safety and efficacy of our product candidates, commercial market forecasts, potential treatment settings, and financial guidance, among other things. These forward-looking statements are based on current information, assumptions, and expectations that are subject to change. A description of potential risks can be found in our press release and latest SEC disclosure documents. You are cautioned not to place undue reliance on these forward-looking statements, and Allogene disclaims any obligation to update these statements. I'll now turn the call over to David.

Speaker #2: These forward-looking statements are based on current information, assumptions, and expectations that are subject to change. A description of potential risks can be found in our press release and latest SEC disclosure documents.

Speaker #2: Your caution not to place undue reliance on these forward-looking statements in Allogene disclaims any obligation to update these statements. I'll now turn the call over to David.

Speaker #3: Thank you, Christine. As we move through 2026, next-generation cell therapy is shifting from promise to proof. The field is increasingly being defined by differentiated clinical evidence rather than platform ambition alone.

David Chang: Thank you, Christine. As we move through 2026, next-generation cell therapy is shifting from promise to proof. The field is increasingly being defined by differentiated clinical evidence rather than platform ambition alone. At Allogene, our lead program, cema-cel is built around the clear objective to establish a differentiated development path. That strategy is now translating into data that provides support for our approach. Our second program, ALLO-329 in autoimmune indications, is built on the same principle of product differentiation enabled by our understanding of CAR T design and the biology of allogeneic rejection. While these two programs are at different stages of development, the evidence emerging to date is consistent and aligned with the design principles behind each.

Speaker #3: At Allogene, our lead program stem cell is built around a clear objective: to establish a differentiated development path. That strategy is now translating into data that provides support for our approach.

Speaker #3: Our second program, Allogene 3290 and autoimmune indications, is built on the same principle of product differentiation enabled by our understanding of CAR-T design and the biology of allogeneic rejection.

Speaker #3: While these two programs are at different stages of development, the evidence emerging to date is consistent and aligned with the design principles behind each.

David Chang: Starting with ALPHA3, we have taken an innovative approach of treating patients with cell in the first-line consolidation setting for large B-cell lymphoma with a primary goal of improving the cure rates. The key to achieving this goal is democratizing access by breaking the barriers that have historically limited the use of CAR T therapy and by enabling cell to be delivered in the outpatient setting. We are very pleased with what we've seen in the recently announced interim futility analysis from the ALPHA3 trial. In this 24 patient analysis, cell achieved a 58.3% MRD clearance rate compared with 16.7% in the observation arm, representing a 41.6% absolute difference. While preliminary, this differential exceeded threshold of MRD clearance reported in other trials that led to groundbreaking clinical outcomes.

Speaker #3: Starting with Alpha 3, we have taken an innovative approach of treating patients with stem cell in the first-line consolidation setting for large B-cell lymphoma with a primary goal of improving the cure rates.

Speaker #3: The key to achieving this goal is democratizing access by breaking the barriers that have historically limited the use of CAR-T therapy and by enabling stem cell to be delivered in the outpatient setting.

Speaker #3: We are very pleased with what we've seen in the recently announced interim fertility analysis from the Alpha 3 trial. In this 24-patient analysis, stem cell achieved a 58.3% MRD clearance rate compared with 16.7% in the observation arm, representing a 41.6% absolute difference.

Speaker #3: While preliminary, this differential exceeded the threshold of MRD clearance reported in other trials that led to groundbreaking clinical outcomes. We also observed a rapid and substantial reduction in circulating tumor DNA, or ctDNA, in the stem cell arm, while the opposite trend was seen in the observation arm, where ctDNA levels increased.

David Chang: We also observed a rapid and substantial reduction in circulating tumor DNA or ctDNA in the cema-cel arm, while the opposite trend was seen in the observation arm, where the ctDNA levels increased. Together, these early findings provide evidence consistent with the biological activity of cema-cel in the first-line consolidation setting as we advance ALPHA3 towards the next key milestone, the interim EFS analysis in mid-2027. Importantly, as we consider use in the outpatient community setting, this early biomarker efficacy signal was accompanied by a favorable safety profile. We observed no CRS, ICANS, or treatment-related hospitalizations, enabling the majority of patients to be managed in the outpatient setting. These results reflect the trial that was designed to lead, not follow. Under Zach's leadership, ALPHA3 was built around MRD testing as a point of intervention rather than passive observation, an approach that moved beyond conventional trial design.

Speaker #3: Together, these early findings provide evidence consistent with the biological activity of stem cell in the first-line consolidation setting as we advance Alpha 3 towards the next key milestone, the interim EFS analysis in mid-2027.

Speaker #3: Importantly, as we consider use in the outpatient community setting, this early biomarker efficacy signal was accompanied by a favorable safety profile. We observed no CRS, ICANS, or treatment-related hospitalization enabling the majority of patients to be managed in the outpatient setting.

Speaker #3: These results reflect the trial that was designed to lead not follow. Under Zach's leadership, Alpha 3 was built around MRD testing as a point of intervention rather than passive observation.

Speaker #3: An approach that moved beyond conventional trial design. We set out to test that forward-looking thesis, and these early data reaffirm my conviction that we are not only in the right path but ahead of the curve.

David Chang: We set out to test that forward-looking thesis. These early data reaffirm my conviction that we are not only in the right path but ahead of the curve. Taken together, we believe these data provide compelling support for a different paradigm, one where cell can be used earlier, made readily available, delivered broadly, and potentially integrated into routine care beyond specialized centers. Turning to ALLO-329, the program is progressing through early clinical development in autoimmune indications with the RESOLUTION basket trial advancing efficiently through dose escalation. This progress embodies the same discipline and forward-looking development approach that underpins ALPHA3. ALLO-329 incorporates the Dagger technology, which is designed to overcome premature rejection of allogeneic CAR T cells. This technology has previously been validated as part of our ALLO-316 program in the metastatic solid tumor setting.

Speaker #3: Taken together, we believe these data provide compelling support for a different paradigm. One where stem cell can be used earlier, made readily available, delivered broadly, and potentially integrated into routine care beyond specialized centers.

Speaker #3: Turning to ALLO-3290, the program is progressing through early clinical development in autoimmune indications, with a resolution basket trial advancing efficiently through dose escalations.

Speaker #3: This progress embodies the same disciplined and forward-looking development approach that underpins Alpha 3. Allogene 3290 incorporates the dagger technology, which is designed to overcome premature rejection of allogeneic CAR-T cells.

Speaker #3: This technology has previously been validated as part of our Allogene 316 program in the metastatic solid tumor setting. However, autoimmune disease represents a fundamentally different clinical context with distinct biology and the different threshold for safety and tolerability.

David Chang: However, autoimmune disease represents a fundamentally different clinical context with distinct biology and a different threshold for safety and tolerability. With that in mind, we designed a structured and stepwise clinical approach beginning at a conservative dose level to establish clear understanding of tolerability before progressing to therapeutic dose levels. Patients treated to date are within this initial dosing range as we evaluate both dose and lymphodepletion strategy. Our focus is on characterizing how the therapy behaves in patients by establishing a tolerability profile that supports continued development while also assessing early signs of activity. Within this framework, we are very pleased with the pace of enrollment and are beginning to observe initial signs of clinical activity coupled with favorable tolerability.

Speaker #3: With that in mind, we designed a structured and stepwise clinical approach beginning at a conservative dose level to establish clear understanding of tolerability before progressing to a therapeutic dose levels.

Speaker #3: Patients treated to date are within this initial dosing range as we evaluate both dose and lymphodepletion strategy. Our focus is on characterizing how the therapy behaves in patients by establishing a tolerability profile that supports continued development while also assessing early signs of activity.

Speaker #3: Within this framework, we are very pleased with the pace of enrollment and the beginning to observe initial signs of clinical activity coupled with favorable tolerability.

David Chang: While still early, these findings are highly encouraging and have important implications for the overall dosing paradigm, which includes not only the dose of Dagger-enabled ALLO-329, but also the required lymphodepletion regimen. As the program progresses, we expect continued dose escalation and patient follow-up to further establish the activity, tolerability, and mechanistic profile of ALLO-329. We look forward to providing a further update in Q4. With that, I will turn it over to Zach to walk through the data in more detail.

Speaker #3: Whilst they're early, these findings are highly encouraging and have important implications for the overall dosing paradigm, which includes not only the dose of dagger-enabled Allogene 3290 but also the required lymphodepletion regimen.

Speaker #3: As the program progresses, we expect continued dose escalation and patient follow-up to further establish the activity, y, tolerability, and mechanistic profile of Allogene 3290.

Speaker #3: We look forward to providing a further update in the fourth quarter. With that, I will turn it over to Zach to walk through the data in more detail.

Speaker #4: Thanks, David. I'll start with Alpha 3 and then turn to Allogene 3290. Alpha 3 was designed around a clear clinical hypothesis that intervening at the point of molecularly detectable disease before clinical relapse can meaningfully alter the course of disease.

Zachary Roberts: Thanks, David. I'll start with ALPHA3 and then turn to ALLO-329. ALPHA3 was designed around a clear clinical hypothesis that intervening at the point of molecularly detectable disease before clinical relapse can meaningfully alter the course of disease. When we initiated the study, MRD was emerging as a prognostic tool in LBCL. Our objective was to move MRD beyond risk assessment and into a treatment decision point. Across oncology, we are now seeing the shift in approaching a potential breakout moment. A case in point is the IMvigor011 trial, which evaluated TECENTRIQ in muscle-invasive bladder cancer. In the trial, patients who were in remission but remained MRD positive after the standard first-line procedure of complete surgical resection were randomized to TECENTRIQ or placebo, with TECENTRIQ demonstrating improvement in both disease-free and overall survival.

Speaker #4: When we initiated the study, MRD was emerging as a prognostic tool in LBCL. Our objective was to move MRD beyond risk assessment and into a treatment decision point.

Speaker #4: Across oncology, we are now seeing the shift in approaching a potential breakout moment. A case in point is the InVigor 11 trial, which evaluated Tecentriq in muscle-invasive bladder cancer.

Speaker #4: In the trial, patients who were in remission but remained MRD positive after the standard first-line procedure of complete surgical resection were randomized to Tecentriq or placebo with Tecentriq demonstrating improvement in both disease-free and overall survival.

Speaker #4: The results of this trial could establish MRD as a clinically actionable endpoint following standard first-line treatment. If approved for this indication, Tecentriq would become the first therapy for which treatment initiation is guided by an ultrasensitive ctDNA MRD assay rather than clinical progression a defining moment for the field.

Zachary Roberts: The results of this trial could establish MRD as a clinically actionable endpoint following standard first-line treatment. If approved for this indication, TECENTRIQ would become the first therapy for which treatment initiation is guided by an ultrasensitive ctDNA MRD assay rather than clinical progression, a defining moment for the field. Against this backdrop, ALPHA3 is positioned at the forefront of how this new paradigm could evolve in large B-cell lymphoma as the first pivotal trial designed to use MRD positivity as the trigger for CAR T therapy. The ALPHA3 study is enrolling patients who have responded to first-line therapy but remain MRD positive and therefore at high risk of relapse. Patients are randomized to treatment with cema-cel or observation. We partnered with Foresight, now a wholly owned subsidiary of Natera, to utilize their CLARITY MRD assay, enabling a highly sensitive and dynamic view of disease burden over time.

Speaker #4: Against this backdrop, Alpha 3 is positioned at the forefront of how this new paradigm could evolve in large B-cell lymphoma as the first pivotal trial designed to use MRD positivity as the trigger for CAR-T therapy.

Speaker #4: The Alpha 3 study's enrolling patients who have responded to first-line therapy but remain MRD positive and therefore at high risk of relapse. Patients are randomized to treatment with stem cell or observation.

Speaker #4: We partnered with Forsythe, now a wholly owned subsidiary of Natera. To utilize their Claroty MRD assay, enabling a highly sensitive and dynamic view of disease burden over time.

Speaker #4: This enhanced sensitivity—detecting disease at or even below 1 in a million, or 10 to the minus 6—is central to the design of the Alpha 3 study and how we interpreted our interim futility data.

Zachary Roberts: This enhanced sensitivity, detecting disease at or even below 1 in a million or 10 to the minus 6, is central to the design of ALPHA3 study and how we interpreted our interim futility data. At the interim analysis, we evaluated the first 24 patients enrolled in the ongoing 2 arms, a single dose of cema-cel versus observation. We observed a 58.3% MRD clearance rate in the cema-cel arm compared to a 16.7% in the observation arm, representing a 41.6 percentage point absolute difference. We also saw a rapid and substantial reduction in circulating tumor DNA. At the day 45 time point, the median ctDNA level decreased by nearly 98% in the cema-cel arm, while the median ctDNA level increased by more than 26% in the observation arm.

Speaker #4: At the interim analysis, we evaluated the first 24 patients enrolled in the ongoing two arms, a single dose of stem cell versus observation. We observed that 58.3% MRD clearance rate in the stem cell arm compared to a 16.7% in the observation arm, representing a 41.6 percentage point absolute difference.

Speaker #4: We also saw a rapid and substantial reduction in circulating tumor DNA, at the day 45 time point, the median ctDNA level decreased by nearly 98% in the stem cell arm while the median ctDNA level increased by more than 26% in the observation arm.

Speaker #4: The Alpha 3 interim futility analysis rests on the assumption that MRD clearance foreshadows clinical benefit. This hypothesis is supported by a growing body of evidence in various clinical settings, including in LBCL, linking MRD clearance in the range of 25% to 30% with meaningful reductions in EFS events.

Zachary Roberts: The ALPHA3 interim futility analysis rests on the assumption that MRD clearance foreshadows clinical benefit. This hypothesis is supported by a growing body of evidence in various clinical settings, including in LBCL, linking MRD clearance in the range of 25% to 30% with meaningful reductions in EFS events. The magnitude of the difference we just announced exceeds that range. While these external datasets support the relationship between MRD clearance and clinical outcomes, the impact on EFS and durability will ultimately be determined through our planned interim and primary EFS analyses. From a safety and treatment administration perspective, we observed no CRS, ICANS, or treatment-related hospitalizations, enabling the majority of patients to be managed entirely in the outpatient setting. We believe this encouraging tolerability profile is a function of treating patients earlier when disease burden is low, which is inherent to the ALPHA3 design.

Speaker #4: The magnitude of the difference we just announced exceeds that range. While these external data sets support the relationship between MRD clearance and clinical outcomes, the impact on EFS and durability will ultimately be determined through our planned interim and primary EFS analyses.

Speaker #4: From a safety and treatment administration perspective, we observed no CRS, ICANS, or treatment-related hospitalizations enabling the majority of patients to be managed entirely in the outpatient setting.

Speaker #4: We believe this encouraging tolerability profile is a function of treating patients earlier, when disease burden is low, which is inherent to the Alpha3 design.

Speaker #4: If the safety profile observed in the interim futility analysis bears out in the study overall, it could mark an important shift towards outpatient CAR-T administration and enable stem cell treatment in community practices where most patients with LBCL receive care.

Zachary Roberts: If the safety profile observed in the interim futility analysis bears out in the study overall, it could mark an important shift towards outpatient CAR T administration and enable cema-cel treatment in community practices where most patients with LBCL receive care. As ALPHA3 progresses, interest in the study is growing. First and foremost, we are seeing robust engagement from existing clinical sites, resulting in high rates of patient screening. At the same time, new sites are expressing significant interest in joining the study, further reinforcing its momentum. From an execution standpoint, the trial continues to scale. We are now enrolling across more than 60 sites with global expansion underway. We recently announced regulatory approval in Australia and South Korea, where site activations and patient screening have begun. We anticipate the Asia Pacific region to expand the study footprint to over 80 sites worldwide. These are not incremental additions.

Speaker #4: As Alpha 3 progresses, interest in the study is growing. First and foremost, we are seeing robust engagement from existing clinical sites, resulting in high rates of patient screening.

Speaker #4: At the same time, new sites are expressing significant interest in joining the study, further reinforcing its momentum. From an execution standpoint, the trial continues to scale.

Speaker #4: We are now enrolling across more than 60 sites with global expansion underway. We recently announced regulatory approval in Australia and South Korea where site activations and patient screening have begun.

Speaker #4: We anticipate the Asia-Pacific region to expand the study footprint to over 80 sites worldwide. These are not incremental additions. Australia and South Korea offer established clinical research infrastructure, experienced investigators, and highly efficient healthcare systems.

Zachary Roberts: Australia and South Korea offer established clinical research infrastructure, experienced investigators, and highly efficient healthcare systems. This expansion reflects both strong global investigator interest and the operational discipline required to execute at scale. We are also seeing meaningful participation from community cancer centers, which contributed approximately one-third of screening and cell treatments in our interim futility analysis. This is an important early proof point up for the feasibility of broader administration as we look to move beyond specialized centers and into broader clinical practice. Let me now turn to ALLO-329, which as a first-in-human phase I trial, has a different objective at this stage of development. The program is supported by robust preclinical data recently published in Nature Communications, supporting the design of ALLO-329. These data demonstrated an optimized CD70 CAR engineered to protect allogeneic CAR T cells from rejection by eliminating alloreactive host T cells.

Speaker #4: This expansion reflects both strong global investigator interest and the operational discipline required to execute at scale. We are also seeing meaningful participation from community cancer centers, which contributed approximately one-third of screening and stem cell treatments in our interim futility analysis.

Speaker #4: This is an important early proof point for the feasibility of broader administration as we look to move beyond specialized centers and into broader clinical practice.

Speaker #4: Let me now turn to ALLO-329, which, as a first-in-human Phase 1 trial, has a different objective at this stage of development. The program is supported by robust preclinical data recently published in Nature Communications, supporting the design of ALLO-329.

Speaker #4: These data demonstrated an optimized CD70 CAR engineered to protect allogeneic CAR-T cells from rejection by eliminating alloreactive host T cells. In those studies, co-expression of CD70 and CD19 CARs drove sustained CAR-T cell persistence, elimination of pathogenic B cells, and activated CD70-positive T cells in humanized SLE models, with corresponding reductions in autoantibody production.

Zachary Roberts: In those studies, co-expression of CD70 and CD19 CARs drove sustained CAR T cell persistence, elimination of pathogenic B cells, and activated CD70-positive T cells in humanized SLE models, and corresponding reductions in autoantibody production. Importantly, the Dagger technology, which eliminates allo-reactive host T cells, has been clinically validated by our third clinical program and first CD70 targeting program, ALLO-316, with recently reported outcome data further supporting the approach and reinforcing our plans to advance the program in the near future. At this stage of development, our focus for ALLO-329 is to define a tolerability profile that supports continued dose escalation while generating early evidence that ALLO-329 can achieve meaningful biological activity in autoimmune disease consistent with its differentiated dual targeting mechanism. The RESOLUTION Basket trial, which includes patients with systemic lupus erythematosus with and without nephritis, scleroderma, and inflammatory myositis, continues to progress through dose escalation.

Speaker #4: Importantly, the Dagger technology, which eliminates alloreactive host T cells, has been clinically validated by our third clinical program and first CD70-targeting program, ALLO-316, with recently reported outcome data further supporting the approach and reinforcing our plans to advance the program in the near future.

Speaker #4: At this stage of development, our focus for Allo329 is to define a tolerability profile that supports continued dose escalation while generating early evidence that Allo329 can achieve meaningful biological activity in autoimmune disease, consistent with its differentiated dual targeting mechanism.

Speaker #4: The resolution basket trial, which includes patients with systemic lupus erythematosus with and without nephritis, scleroderma, and inflammatory myositis, continues to progress through dose escalation.

Zachary Roberts: Nine patients have already been treated since the study started enrollment in November 2025, with three patients at dose level 1 of 20 million cells and three patients at dose level 2 of 40 million cells, both following lymphodepletion with cyclophosphamide, and three patients at dose level 1 with no lymphodepletion. Importantly, the doses evaluated so far are substantially lower than those being explored in other CAR T approaches in autoimmune disease, including autologous programs testing approximately 100 million cells and some allogeneic approaches evaluating doses above 1 billion cells. Even at these lower doses of ALLO-329, both with and without cyclophosphamide, investigators have reported signs of clinical activity. While these observations are preliminary and dose exploration continues, investigators have been very encouraged by these early signals, facilitating strong patient interest in participating in the study. This reflects a consistent approach across our programs.

Speaker #4: Nine patients have already been treated since the study started enrollment in November 2025, with three patients at dose level one of 20 million cells and three patients at dose level two of 40 million cells, both following lymphodepletion with cyclophosphamide, and three patients at dose level one with no lymphodepletion.

Speaker #4: Importantly, the doses evaluated so far are substantially lower than those being explored in other CAR-T approaches in autoimmune disease, including autologous programs, testing approximately 100 million cells, and some allogeneic approaches evaluating doses above 1 billion cells.

Speaker #4: Even at these lower doses of Allo329, both with and without cyclophosphamide, investigators have reported signs of clinical activity. While these observations are preliminary and dose exploration continues, investigators have been very encouraged by these early signals facilitating strong patient interest in participating in the study.

Speaker #4: This reflects a consistent approach across our programs, and with Alpha 3, we designed the study to intervene earlier in disease treatment based on MRD. With Allo329, we are applying that same forward-looking discipline to autoimmune disease, prioritizing mechanism, durability, scalability, and long-term usability from the outset.

Zachary Roberts: In ALPHA3, we designed the study to intervene earlier in disease treatment based on MRD. With ALLO-329, we are applying that same forward-looking discipline to autoimmune disease, prioritizing mechanism, durability, scalability, and long-term usability from the outset. As we continue dose escalation and patient follow-up, our goal is to build a data set that integrates clinical activity with mechanistic understanding and supports a path towards durable outcomes. We expect to provide a comprehensive update in Q4. Across both programs, our focus remains consistent, designing studies with clear hypotheses, executing with discipline, and allowing the data to define the role of allogeneic CAR T. With that, I'll turn it over to Jeff.

Speaker #4: As we continue dose escalation and patient follow-up, our goal is to build the dataset that integrates clinical activity with mechanistic understanding and supports a path towards durable outcomes.

Speaker #4: We expect to provide a comprehensive update in the fourth quarter. Across both programs, our focus remains consistent: designing studies with clear hypotheses, executing with discipline, and allowing the data to define the role of allogeneic CAR-T.

Speaker #4: With that, I'll turn it over to Jeff.

Speaker #1: Thank you, Zach. As we execute against our key clinical milestones in 2026, we remain focused on maintaining a strong financial position that supports continued progress across our portfolio.

Geoffrey Parker: Thank you, Zach. As we execute against our key clinical milestones in 2026, we remain focused on maintaining a strong financial position that supports continued progress across our portfolio. As of 31 March, we had $266.9 million in cash equivalents, and investments. In April, we strengthened that position through a public offering that generated approximately $200.4 million in gross proceeds, extending our cash runway into Q1 2029. R&D expenses for Q1 were $32 million, including $2.7 million of non-cash stock-based compensation, reflecting continued investment in our clinical programs. G&A expenses for Q1 were $14.1 million, including $5.6 million in non-cash stock-based compensation.

Speaker #1: As of March 31st, we had $266.9 million in cash, cash equivalents, and investments. In April, we strengthened that position through a public offering that generated approximately $200.4 million in gross proceeds, extending our cash runway into the first quarter of 2029.

Speaker #1: R&D expenses for the first quarter were 32 million dollars, including 2.7 million dollars of non-cash stock-based compensation, reflecting continued investment in our clinical programs.

Speaker #1: GNA expenses for the first quarter were 14.1 million dollars, including 5.6 million dollars in non-cash stock-based compensation. Net loss for the first quarter was 42.6 million dollars, or 18 cents per share, including non-cash stock-based compensation expense of 8.3 million dollars.

Geoffrey Parker: Net loss for Q1 was $42.6 million or $0.18 per share, including non-cash stock-based compensation expense of $8.3 million. Based upon our current forecast for the overall timing of the ALPHA3 program, we are modestly increasing our guidance for operating cash expense in 2026 from approximately $150 million to $165 million. GAAP operating expenses are also expected to slightly increase from approximately $210 million to $225 million, including estimated non-cash stock-based compensation expense of approximately $35 million. These estimates exclude any impact from potential business development activities. Overall, we believe we are well-positioned to execute on our strategy with the capital and flexibility needed to reach our next set of milestones. We'll now open the call for questions.

Geoffrey Parker: Net loss for Q1 was $42.6 million or $0.18 per share, including non-cash stock-based compensation expense of $8.3 million. Based upon our current forecast for the overall timing of the ALPHA3 program, we are modestly increasing our guidance for operating cash expense in 2026 from approximately $150 to 165 million. GAAP operating expenses are also expected to slightly increase from approximately $210 to 225 million, including estimated non-cash stock-based compensation expense of approximately $35 million. These estimates exclude any impact from potential business development activities. Overall, we believe we are well-positioned to execute on our strategy with the capital and flexibility needed to reach our next set of milestones. We'll now open the call for questions.

Speaker #1: Based upon our current forecast for the overall timing of the Alpha 3 program, we are modestly increasing our guidance for operating cash expense in 2026 from approximately $150 million to $165 million.

Speaker #1: GAAP operating expenses are also expected to slightly increase from approximately 210 million dollars to 225 million dollars, including estimated non-cash stock-based compensation expense of approximately 35 million dollars.

Speaker #1: These estimates exclude any impact from potential business development activities. Overall, we believe we are well positioned to execute on our strategy with the capital and flexibility needed to reach our next set of milestones.

Speaker #1: We'll now open the call for questions.

Speaker #2: Thank you, as a reminder to ask a question, please press star 11 on your telephone and wait for your name to be announced. To withdraw your question, please press star 11 again.

Operator 2: Thank you. As a reminder, to ask a question, please press star one one on your telephone and wait for your name to be announced. To withdraw your question, please press star one one again. Please stand by while we compile the Q&A roster

Operator: Thank you. As a reminder, to ask a question, please press star one one on your telephone and wait for your name to be announced. To withdraw your question, please press star one one again. Please stand by while we compile the Q&A roster

Speaker #2: Please stand by while we compile the Q&A roster. And our first question comes from Michael Yee of UBS. Your line is open.

Operator 1: Our first question comes from Michael Yee of UBS. Your line is open.

Operator: Our first question comes from Michael Yee of UBS. Your line is open.

Michael Yee: Hey, guys. Congrats on the progress to date and the updated autoimmune color. Maybe two quick ones. One is, can you talk a little bit more specifically about some of the initial signs of activity or B-cell reductions? What does that mean? To what degree, maybe there are differences in B-cell reductions for the lymphodepletion cohort compared to any of the different cohorts with different lymphodepletion. If I may get a question on, obviously, the lead DLBCL program. Since the announcement of your MRD negativity interim, how have you seen perhaps enrollment, engagement, and feedback and things of that nature? Maybe just talk a little bit about how things have progressed since that positive interim. Thank you.

Speaker #3: Hey, guys. Congrats on the progress to date, and the updated autoimmune color. Maybe two quick ones. One is, can you talk a little bit more specifically about some of the initial signs of activity or B-cell reductions?

Speaker #3: What does that mean? And to what degree maybe there were differences in B-cell reductions for the lymphodepletion cohort compared to any of the different cohorts with different lymphodepletion?

Speaker #3: And if I may get a question on, obviously, the lead deal BCL program. Since the announcement of your MRD negativity interim, how have you seen perhaps enrollment engagement and feedback and things of that nature, maybe just talk a little bit about how things have progressed since that positive interim.

Speaker #3: Thank you.

Speaker #4: Hey, Mike. Zach here. Thanks for the questions. So on the 329 question, we are we'll be saving the details to sort of pertain to your question until the Q4 update other than to say that the encouraging signs that we referred to are coming from the cohorts that we've highlighted in both with and without LV.

Zachary Roberts: Hey, Michael Yee. Zachary Roberts here. Thanks for the questions. On the 329 question, we'll be saving the details, sort of pertinent to your question until the Q4 update, other than to say that the encouraging signs that we refer to are coming from the cohorts that we've highlighted in, both at with and without LD. We will be continuing to enroll patients according to the protocol design with and without cyclophosphamide and expect to show a more complete update in Q4. So far, so good, and we're really thrilled with the patients coming into the study very briskly. The second question around has the IA1A results stimulated increased activity in ALPHA3? I will say that they have.

Speaker #4: So we will be continuing to enroll patients according to the protocol design with and without cyclophosphamide and expect to show a more complete update in Q4.

Speaker #4: But so far, so good, and we're really thrilled with the patients coming into the study very briskly. The second question around, has the IA1A results stimulated increased activity in Alpha 3?

Speaker #4: I will say that they have. It in these early days, these first couple of weeks since the announcement went out, that has come in the form of new sites coming and asking to participate in Alpha 3, even sites that said early on that they didn't have room in their portfolio before the IA1A data was available.

Zachary Roberts: It in these early days, these first couple of weeks since the announcement went out, that has come in the form of new sites, coming and asking to participate in ALPHA3. Even sites that said early on that they didn't have room in their portfolio before the IA1A data was available. Now they're coming back and saying that they really do wanna participate. That kind of qualitative change is already underway. We will be watching very carefully for a quantitative uptick in the screening and enrollment pace, except to I will say that, you know, that has been going very well in the last few months. We're optimistic, but so far, we're pretty happy with the way things are going.

Speaker #4: Now they're coming back and saying that they really do want to participate. So that kind of qualitative change is already underway. We will be watching very carefully for a quantitative uptick in the screening and enrollment pace except to, I will say that that has been going very well in the last few months.

Speaker #4: So we're optimistic, but so far we're pretty happy with the way things are going.

Speaker #3: Great. Thank you.

Michael Yee: Great. Thank you.

Operator 1: Thank you. Our next question comes from Tyler Van Buren of TD Cowen. Your line is open.

Operator: Thank you. Our next question comes from Tyler Van Buren of TD Cowen. Your line is open.

Speaker #2: Thank you. And our next question comes from Tyler Van Buren of TD Cowan. Your line is open.

Speaker #1: Hey, guys. Congrats on the progress. I have have a couple of 329 questions as well. Since you mentioned favorable tolerability, can you discuss conceptually what sort of safety profile you hope to achieve with Allo 329 over the long term?

Tyler Van Buren: Hey, guys. Congrats on the progress. I have a couple 329 questions as well. Since you mentioned favorable tolerability, can you discuss conceptually what sort of safety profile you hope to achieve with ALLO-329 over the long term? With respect to the update in the Q4, can you give us any sense of what that might entail and kinda help put goalposts around what we should expect with that update?

Speaker #1: And then with respect to the update in the fourth quarter, can you give us any sense of what that might entail and kind of help put goalposts around what we should expect with that update?

David Chang: Hey, Tyler. Thanks for those questions. You know, the safety profile in autoimmune indications, I mean, you know, we want this to be, you know, as clean as, you know, one can get to. I mean, I think that's really the patient population that we're dealing with. I mean, you know, we have seen in ALPHA3 study, even in oncology, in the right clinical setting, you know, CAR T therapy can be well-tolerated. You know, that's kind of profile that we are trying to mirror, where, you know, the treatment can be given as an outpatient, and patient can be managed as an outpatient. That's really the safety profile that we're looking for.

Speaker #5: Hey, Tyler. Thanks for those questions. The safety profile in autoimmune indications I mean, we want this to be as clean as one can get to.

Speaker #5: I mean, I think that's really the patient population that we're dealing with. I mean, we have seen in Alpha 3 study, even in oncology, in the right clinical setting, CAR T therapy can be well tolerated.

Speaker #5: And that's kind of profile that we're trying to mirror where the treatment can be given as an outpatient and patient can be managed as an outpatient.

Speaker #5: So that's really the safety profile that we're looking for. And so far, after completing both 20 and 40 million cell dose levels with cyclophosphamide lymphodepletion, I feel very encouraged that if the safety profile holds out, this can be very interesting finding.

David Chang: So far, after completing both 20 and 40 million cell dose levels with cyclophosphamide lymphodepletion, I feel very encouraged that if the safety profile holds out, this can be very interesting finding. With respect to your second question about how to set up the expectations for the Q4. So far, let's keep in mind in terms of the pace of enrollment that Zach had talked about. We dosed first patient back in November 2023 and May, so within 6 months. Dose escalation study where we have to wait about 1 month after first patient is dosed before we can fill up the rest of the cohort.

Speaker #5: With respect to your second question about how to set up the expectations for the fourth quarter, I mean, so far, let's keep in mind in terms of the pace of enrollment that Zach had talked about.

Speaker #5: We dosed first patient back in November of last year, and May. So within six months, dose about a month after first patient is dosed before we can fill up the rest of the cohort.

David Chang: Even with that kind of, preset barriers in how fast we can enroll, we enrolled nine patients. That is a pretty remarkable support that we are getting from various physicians involved in the autoimmune trial. We are highly encouraged. This autoimmune, the way that the clinical responses are being measured is different than in oncology. When the investigators are calling us and telling us that they're seeing that they would not have expected to see in any setting, that I would view as a highly encouraging early signs.

Speaker #5: With even with that kind of sort of preset barriers in how fast we can enroll, we enrolled nine patients. That is a pretty remarkable support that we are getting from various physicians involved in the autoimmune trial.

Speaker #5: So we are highly encouraged and this autoimmune, obviously, the way that the clinical responses are being measured is different than in oncology. But when the investigators are calling us and telling us that they're seeing that they would not have expected to see in any setting, I mean, that I would view as a highly encouraging early signs.

Speaker #2: Thank you. And our next question comes from Buren Amin of Piper Sandler. Your line is open.

Operator 1: Thank you. Our next question comes from Biren Amin of Piper Sandler. Your line is open.

Operator: Thank you. Our next question comes from Biren Amin of Piper Sandler. Your line is open.

Biren Amin: Yeah. Hi, guys. Thanks for taking my questions. Maybe just to stay on ALLO-329, given your reporting data in Q4, should we expect data across the 20 and 40 million cell doses in the Q4, or could we get higher cell doses? That's the first question. Second question, what would be the patient composition across SLE, myositis, and scleroderma in the Q4 update? Lastly, on the trial itself, recently in April, I think there was a change that was recorded on ClinicalTrials.gov where you increased target enrollment to 66 patients from 54 patients. Could you maybe just talk about that change and what drove that? Thank you.

Speaker #3: Yeah. Hi, guys. Thanks for taking my questions. Maybe just to stay on Allo 329, given your reporting data in Q4, should we expect data across the 20 and 40 million cell doses in the fourth quarter?

Speaker #3: Or could we get higher cell doses? So that's the first question. Second question, what would be the patient composition across SLE myositis and sclerosis in the Q4 update?

Speaker #3: And then lastly, on the trial itself, recently in April, I think there was a change that was recorded on ct.gov where you increased target enrollment to 66 patients from 54 patients.

Speaker #3: Could you maybe just talk about that change and what drove that? Thank you.

Speaker #5: Yeah. Buren, as your first question, I'm also realizing that was Tyler's last question, which I did not fully answer. So in the fourth quarter, obviously, at this point, we have completed 20 and 40 million, and we are continuing to dose escalation.

David Chang: Yeah, Biren, as to your first question, I am also realizing that was Tyler's last question, which I did not fully answer. In the fourth quarter, obviously at this point, we have completed in 20 and 40 million, and we are continuing the dose escalation. By the fourth quarter, you know, update comes, you know, included patient in that will be more than just 20 and 40 million. We are hoping that we can include, certainly the next dose level and possibly even in a higher dose, depending on how the pace of enrollment is maintained. Also, when I am talking about the cell dose levels, certainly, I am talking about both with CY and without cyclophosphamide. Zach, maybe you can cover the patient composition.

Speaker #5: By the fourth quarter, update comes. Included patient in that will be more than just 20 and 40 million. We're hoping that we can include certainly the next dose level and possibly even higher dose depending on how the pace of enrollment is maintained.

Speaker #5: And also when I'm talking about the cell dose levels, certainly I'm talking about both width side and without cyclophosphamide. And Zach, maybe you can cover the patient composition.

Speaker #4: Yeah. So Buren, we're seeing patients come from all of the indications that I listed previously. So lupus, inflammatory myopathies, and scleroderma. It's still too early to say whether the early signs of efficacy that we are seeing as segregated to one patient group or another.

Zachary Roberts: Yeah. Baron, we're seeing patients come from all of the indications that I listed previously, so lupus, inflammatory myopathies, and scleroderma. It's still too early to say whether the early signs of efficacy that we are seeing is segregated to one patient group or another. We're not gonna be making any changes to the basket style design of the protocol. As we continue to enroll patients, we expect a mix, and that mix will be presented in Q4. Then the ClinicalTrials.gov change that occurred, I actually have to say I don't know why we made that change.

Zachary Roberts: Yeah. Biren, we're seeing patients come from all of the indications that I listed previously, so lupus, inflammatory myopathies, and scleroderma. It's still too early to say whether the early signs of efficacy that we are seeing is segregated to one patient group or another. We're not gonna be making any changes to the basket style design of the protocol. As we continue to enroll patients, we expect a mix, and that mix will be presented in Q4. Then the ClinicalTrials.gov change that occurred, I actually have to say I don't know why we made that change.

Speaker #4: So we're not going to be making any changes to the basket style design of the protocol. So as we continue to enroll patients, we expect a mix, and that mix will be presented in Q4.

Speaker #4: And then the ct.gov change that occurred, I actually have to say I don't know why we made that small change. Yeah. Administrative change. Sometimes we have to go through and we have to make little clerical changes to the ct.gov.

David Chang: It's administrative change.

Zachary Roberts: Yeah, administrative change. Sometimes we have to go through and we have to make little clerical changes to ClinicalTrials.gov. There's not been any changes to the study design that would have warranted that change.

Speaker #4: There have not been any changes to the study design that would have warranted that change.

Speaker #2: Thank you. And our next question comes from Salvine Richter of Goldman Sachs. Your line is open.

Operator 1: Thank you. Our next question comes from Salveen Richter of Goldman Sachs. Your line is open.

Operator: Thank you. Our next question comes from Salveen Richter of Goldman Sachs. Your line is open.

Salveen Richter: Good afternoon. Thanks for taking my question. For cema-cel, could you speak to the feedback you're hearing from the community practices to date post the recent data? Then for the ongoing ALLO-329 RESOLUTION study, can you expand upon progress on site activation and patient enrollment and how that's playing out, just given some competition in the field for other autoimmune CAR T programs? Thank you.

Speaker #6: Good afternoon. Thanks for taking my question. For stem cell, could you speak to the feedback you're hearing for the from the community practices to date post the recent data?

Speaker #6: And then for the ongoing Allo 329 resolution study, can you expand upon progress on site activation and patient enrollment and how that's playing out just given some competition in the fields for other autoimmune CAR T programs?

Speaker #6: Thank you.

Zachary Roberts: Salveen, it's Zach. As far as how the community practices are reacting to the interim data from cema-cel, I would echo what I said a moment ago that the feedback has been really overwhelmingly and uniformly positive. As just to give another little anecdote on that, in the couple of literal days after that announcement was made, that same week, we were on the phone with a couple of large community network practices that have already a couple of sites on the study seeking to expand their footprint within their practices and add additional sites. We believe that the interim analysis data is being viewed by the community practices and academic practices alike as potentially something very, very interesting and practice-changing.

Speaker #4: Salvine and Zach, so as far as how the community practices are reacting to the interim data from stem cell, I would echo what I said a moment ago: the feedback has been really overwhelmingly and uniformly positive.

Speaker #4: As just to give another little anecdote on that, in the couple of literal days after that announcement was made that same week, we were on the phone with a couple of large community network practices that already have a couple of sites on the study, seeking to expand their footprint within their practices and add additional sites.

Speaker #4: So, we believe that the interim analysis data is being viewed by the community practices and academic practices alike as potentially something very, very interesting and practice-changing.

David Chang: Yeah. Also, I would say it makes a lot of sense. When you think about, you know, this is giving the community physicians something to offer to patients rather than referring them to a tertiary or cell therapy centers. Two, I think, you know, during the course of treating patients, they are realizing that treatment is relatively hassle-free.

Speaker #5: And also, I would say it makes a lot of sense. And when you think about this is giving the community physicians something to offer to patients, rather than referring them to a tertiary or cell therapy think during the course of treating patients, they are realizing that treatment is relatively hassle-free.

David Chang: You know, what we have shared, you know, with the interim futility findings, is the early safety profile. It was very clean, which also makes, you know, managing patient after the CAR T infusion, extremely smooth. I mean, these are definitely early findings, but these are the things that, you know, I believe is making the community physicians being quite interested in participating in the ALPHA3 study.

Speaker #5: And what we have shared with the interim fertility findings is the early safety profile, it was very clean, which also makes managing patient after the CAR T infusion extremely smooth.

Speaker #5: I mean, these are definitely early findings, but these are the things that I believe is making the community physicians being quite interested in participating in the Alpha 3 study.

Speaker #4: And then your second question, Salvine, about site activation and enrollment in 329. We are approaching the target number of sites that we sought to activate for ALLO-329.

Zachary Roberts: Your second question, Salveen, about site activation and enrollment in ALLO-329. We are approaching the target number of sites that we sought to activate for ALLO-329. I can't say exactly what the number is on ClinicalTrials.gov, but we expect that to be completed here very shortly, within the next few weeks, maybe a couple of months. That's gone very well. We've actually ended up getting quite a bit more traction even in that competitive space that you highlighted. We've got some really excellent marquee sites already listed on ClinicalTrials.gov and a few more in the can ready to come out. They are really being super productive on the patient screening and enrollment as we highlighted previously.

Speaker #4: I can't say exactly what the number is on ct.gov, but we expect that to be completed here very shortly within the next few weeks, maybe a couple of months.

Speaker #4: That's gone very well. We've actually ended up getting quite a bit more traction, even in that competitive space that you highlighted. We've got some really excellent marquee sites already listed on CT.gov, and a few more in the can ready to come out.

Speaker #4: And then they are really being super productive on the patient screening and enrollment as we highlighted previously. So we could not be happier with how Allo 329 is going operationally.

Zachary Roberts: we could not be happier with how ALLO-329 is going operationally.

Speaker #5: And the mixture of the patients in this basket study is essentially excellent.

David Chang: The mixture of the patients in this basket study is, you know, essentially is, you know, is excellent.

Zachary Roberts: Yeah.

Speaker #2: Thank you. And our next question comes from Samantha Seminkau of Citi. Your line is open.

Operator 1: Thank you. Our next question comes from Samantha Semenkow of Citi. Your line is open.

Operator: Thank you. Our next question comes from Samantha Semenkow of Citi. Your line is open.

Samantha Semenkow: Good afternoon. Thanks very much for taking the question. Another one on ALLO-329. I'm wondering if you could just talk a little bit about your thoughts on dosing going forward. You know, you mentioned some early clinical signals that you're seeing in these first nine patients. I'm wondering, do you think the 20 million dose is too low or subtherapeutic? Curious your thoughts there. How are you thinking about dosing going forward? Are there any adjustments you're planning to make to the dose escalation? Thanks very much.

Speaker #7: Good afternoon. Thanks very much for taking the question. Another one on 329. I'm wondering if you could just talk a little bit about your thoughts on dosing going forward.

Speaker #7: You mentioned some early clinical signals that you're seeing in these first nine patients. I'm wondering, do you think the 20 million dose is too low or subtherapeutic?

Speaker #7: Curious your thoughts there. And how are you thinking about dosing going forward? Are there any adjustments you're planning to make to the dose escalation?

Speaker #7: Thanks very much.

Zachary Roberts: Hey, Sam. With respect to the question around the doses that we've tried so far, you know, in the tenets of a phase I dose escalation study, you're really gated by safety. I wanna echo what David said a moment ago, that safety is paramount here, and we wanna make sure that we maintain the safety profile that would make this therapy attractive to patients and doctors with autoimmune disease. We're gonna keep going up until we start to bump up against the toxicity that we think would be prohibitive. Whether you call it subtherapeutic or room to go, I'm more of a room to go type of guy. We're gonna keep dose escalating. Your other question is, do we see any need to make any adjustments?

Speaker #4: Hey, Sam. So with respect to the question around the doses that we've tried so far, we in the tenets of phase one dose escalation study, you really gated by safety.

Speaker #4: And I want to echo what David said a moment ago: that safety is paramount here, and we want to make sure that we maintain the safety profile that would make this therapy attractive to patients and doctors with autoimmune disease.

Speaker #4: And so we're going to keep going up until we start to bump up against that toxicity that we think would be prohibitive. So whether you call it subtherapeutic or room to go, I'm more of a room-to-go type of guy.

Speaker #4: And so we're going to keep dose escalating. And then your other question is, do we see any need to make any adjustments? At this point, we do not.

Zachary Roberts: At this point, we do not. We still have some doses to go up, and we're hopeful that we'll start to see, you know, really compelling activity here in these next dose or the dose after that, and we can maintain that safety profile. Look forward to that Q4 update.

Speaker #4: We still have some doses to go up. And we're hopeful that we'll start to see really compelling activity here in these next dose or the dose after that, and we can maintain that safety profile.

Speaker #4: So look forward to that Q4 update.

Speaker #2: Thank you. And our next question comes from Roger Song of Jefferies. Your line is open.

Operator 1: Thank you. Our next question comes from Roger Song of Jefferies. Your line is open.

Operator: Thank you. Our next question comes from Roger Song of Jefferies. Your line is open.

Chacha: Hi, this is Chacha on for Roger. Thanks so much for taking our question. I have two. One is, can you just give us some more color on what your current cash runway covers? My second question is on ALLO-329. Can you tell us more about the decision factors that are driving the optionality for the fludarabine addition? I know you mentioned with the option of adding this. Can you just explain the gating factors for why we add or why we don't? Thanks.

[Analyst] (Jefferies): Hi, this is Chacha on for Roger. Thanks so much for taking our question. I have two. One is, can you just give us some more color on what your current cash runway covers? My second question is on ALLO-329. Can you tell us more about the decision factors that are driving the optionality for the fludarabine addition? I know you mentioned with the option of adding this. Can you just explain the gating factors for why we add or why we don't? Thanks.

Speaker #8: Hi, this is Chacha on for Roger. Thanks so much for taking our question. I have two. So, one is: can you just give us some more color on what your current cash runway covers?

Speaker #8: And then on my second question is on also Allo 329. Can you tell us more about the decision factors that are driving the optionality for the fludarabine addition?

Speaker #8: I know you mentioned the option of adding this. Can you just explain the gating factors for why we would add it or why we wouldn't?

Speaker #8: Thanks.

Speaker #9: Hi. This is Jeff. On the cash runway, as we discussed in the script, our current cash runway based on the addition of the capital added in the recent financing, the $200 million financing takes us into the first quarter of 2029.

Geoffrey Parker: Hi, this is Jeff. On the cash runway, as we discussed in the script, our current cash runway, based on the addition of the capital added in the recent financing, the $200 million financing, takes us into Q1 2029. During that time, you know, we intend to complete the ALPHA3 study. As you know, we anticipate finishing enrollment at the end of 2027. We anticipate an interim analysis on EFS in mid-2027, primary analysis in mid-2028 with the filing of the BLA as quickly as possible, based on the results of those interim or final analysis.

Speaker #9: And during that time, we intend to complete the Alpha 3 study. So as you know, we anticipate finishing enrollment at the end of 2027.

Speaker #9: We anticipate an interim analysis on EFS in mid-2027, primary analysis in mid-2028, with the filing of the BLA as quickly as possible based on the results of those interim or final analyses.

Geoffrey Parker: It really is focused on covering ALPHA3, as well as completing this Phase 1 RESOLUTION study for ALLO-329, as we indicated, having the comprehensive data set in the Q4 of this year.

Speaker #9: So it really is focused on covering ALPHA3 as well as completing this Phase 1 resolution study for 329, as we indicated—having the comprehensive data set in the fourth quarter of this year.

Geoffrey Parker: It really is focused on covering ALPHA3, as well as completing this phase I RESOLUTION study for ALLO-329, as we indicated, having the comprehensive data set in the Q4 of this year.

Speaker #5: Yeah. And let me take the question on the optionality of fludarabine. I think this is just how we try to make the protocol as flexible as possible without predefined idea about when to kick in these optionality.

David Chang: Yeah. Let me take the question on the optionality of fludarabine. I think this is just, you know, how, you know, we try to make the, you know, protocol as flexible as possible, you know, without, you know, predefined, you know, idea about when to kick in these optionality. I mean, it's really looking at the data and then, you know, making the decision. Right now, based on the data, our primary focus is continuing the dose escalation.

Speaker #5: I mean, it's really looking at the data and then making the decision. And right now, based on the data of primary focus is continuing the dose escalation.

Zachary Roberts: I'll just add one other piece of color on that. Honestly, there, in part, this would be driven by the demand to come into the study. By opening additional cohorts, it would allow us to park some patients and to allow patients into the trial. That is another factor that could come into it. Nothing has changed at all about our belief in the Cy or no Cy possibility here. We are continuing with that primary goal.

Speaker #4: And I'll just add one other piece of color on that. And honestly, in part, this would be driven by the demand to come into the study.

Speaker #4: By opening additional cohorts, it would allow us to park some patients to allow patients into the trial. So that is another factor that could come into it.

Speaker #4: But nothing has changed at all about our belief in the psi or no psi possibility here. So we are continuing with that primary goal.

Speaker #2: Thank you. And our next question comes from Matthew Phipps of William Blair. Your line is open.

Operator 1: Thank you. Our next question comes from Matt Phipps of William Blair. Your line is open.

Operator: Thank you. Our next question comes from Matt Phipps of William Blair. Your line is open.

Matt Phipps: Good afternoon. Thanks for taking my question. You know, a lot, it's gonna be on ALLO-329 as well. There's obviously been a lot made about B cell reset after, you know, CAR T with CD19. I was wondering if from your experience with ALLO-316, what the T cell kind of repopulation might have looked like after treatment, if you looked at that. I guess, do you expect maybe some ability to have an immune autoreactive T cell reset following ALLO-329 treatment? Will you have any data on that by Q4? Thank you.

Matt Phipps: Good afternoon. Thanks for taking my question. You know, a lot, it's gonna be on ALLO-329 as well. There's obviously been a lot made about B cell reset after, you know, CAR T with CD19. I was wondering if from your experience with ALLO-316, what the T-cell kind of repopulation might have looked like after treatment, if you looked at that. I guess, do you expect maybe some ability to have an immune autoreactive T-cell reset following ALLO-329 treatment? Will you have any data on that by Q4? Thank you.

Speaker #10: Good afternoon. Thanks for taking my question. It's going to be on 329 as well. There's obviously been a lot made about B-cell reset after CAR-T with C19.

Speaker #10: I was wondering if from your experience with Allo 316, what the T-cell kind of repopulation might have looked like after treatment if you looked at that.

Speaker #10: And I guess, do you expect maybe some ability to have an immune autoreactive T-cell reset following 329 treatment? Will you have any data on that by Q4?

Speaker #10: Thank you.

Zachary Roberts: Matt, a great question. Really insightful, and I think right on point in terms of our understanding of the mechanism of action of ALLO-329. We are really focused on how the B-cell and the T-cell repertoires will change. You know, whether we achieve the reset as defined as just absolute B-cells going all the way down to 0, or whether there's some editing of the repertoire on both the B-cell and the T-cell side. Obviously, B-cells, we expect the chances of those cells going very low or to 0 to be higher because, you know, we're targeting a pan-B-cell marker. In the case of CD70, you're absolutely correct. It's only a subset that are gonna be CD70 positive.

Zachary Roberts: Matt, a great question. Really insightful, and I think right on point in terms of our understanding of the mechanism of action of ALLO-329. We are really focused on how the B-cell and the T-cell repertoires will change. You know, whether we achieve the reset as defined as just absolute B-cells going all the way down to zero, or whether there's some editing of the repertoire on both the B-cell and the T-cell side. Obviously, B-cells, we expect the chances of those cells going very low or to zero to be higher because, you know, we're targeting a pan-B-cell marker. In the case of CD70, you're absolutely correct. It's only a subset that are gonna be CD70 positive.

Speaker #4: Matt, great question. Really insightful. And I think right on point in terms of our understanding of the mechanism of action of Allo 329. We are really focused on how the B-cell and the T-cell repertoires will change.

Speaker #4: And whether we achieve the reset as defined as just absolute B-cells going all the way down to zero or whether there's some editing of the repertoire on both the B-cell and the T-cell side.

Speaker #4: Now, obviously, B-cells, we expect the chances of those cells going very lower to zero to be higher because we're targeting a pan B-cell marker.

Speaker #4: In the case of CD70, you're absolutely correct. It's only a subset that are going to be CD70 positive. Of course, there's going to be a population of alloreactive cells that we expect to be depleted through the dagger effect.

Zachary Roberts: Of course, there's going to be a population of allo-reactive cells that we expect to be depleted through the Dagger effect. There is also known to be CD70 positive pathogenic AID-causing T cells, so clonal populations with specific TCRs that also express CD70. That has actually been one of the main reasons that we designed ALLO-329 the way we did, was try to wipe out that set, that clone or set of clones that may be driving the pathogenesis. We will be analyzing the T cell repertoire as part of the ALLO-329 study. If we've got something to share in Q4, we'll share it.

Speaker #4: But there is also known to be CD70 positive pathogenic AID causing T-cells so clonal populations with specific TCRs that also express CD70. And that is actually been one of the main reasons that we designed 329 the way we did was try to wipe out that set that clone or set of clones that may be driving the pathogenesis.

Speaker #4: And so we will be analyzing the T-cell repertoire as part of the Allo 329 study. And if we've got something to share in Q4, we'll share it.

Speaker #2: Thank you. And our next question comes from Jack Allen of Baird. Your line is open.

Operator 1: Thank you. Our next question comes from Jack Allen of Baird. Your line is open.

Operator: Thank you. Our next question comes from Jack Allen of Baird. Your line is open.

Jack Allen: Great. Thanks so much for taking the questions. Congrats on the progress. I'll keep the theme going with ALLO-329 questions to start, and then I have one on cema-cel as well. On ALLO-329, I was just hoping you'd provide some additional color as it relates to how many doses you could escalate the study in, and, you know, what the next step up might be. I guess logically it looks like 60 million would be a realistic target for the next dose, but how high could you go in that trial? Then on cema-cel, I just wanted to ask about the interim EFS look in mid 2027 and any additional color you can provide around the powering there.

Speaker #10: Great. Thanks so much for taking the questions and congrats on the progress. I'll keep the theme going with the 329 questions to start. And then I have one on semicell as well.

Speaker #10: On 329, I was just hoping you provide some additional color as it relates to how many doses you could escalate the study in and what the next step might be.

Speaker #10: I guess, logically, it looks like 60 million would be a realistic target for the next dose. But how high could you go in that trial?

Speaker #10: And then on Semicell, I just wanted to ask about the interim EFS look in mid-2027, and any additional color you can provide around the powering there.

Speaker #4: So Jack, great question. The next dose level that we're going to be looking at is not 60. It's actually 80, 80 million cells. So that cohort is enrolling now.

Zachary Roberts: Jack, great question. The next dose level that we're gonna be looking at is not 60, it's actually 80 million cells. That cohort is enrolling now, following Cy, and then the no Cy cohort is close behind. I'm gonna hold off on saying exactly how many cell doses that we plan to go up, and we'll sort of reveal that at Q4, because I do think that we'll be in that zone by the time we give that update. Stay tuned. 80 million is the next dose cohort that we're working on now. As far as cema-cel, we talked quite a bit about this with the fundraising and the alpha allocation for the IA2.

Speaker #4: Following psi, and then the no psi cohort is close behind. I'm going to hold off on saying exactly how many cell doses that we plan to go up.

Speaker #4: And we'll sort of reveal that at Q4 because I do think that we'll be in that zone by the time we give that update.

Speaker #4: So, stay tuned. But 80 million is the next dose cohort that we're working on now. As far as Semicel, we talked quite a bit about this.

Speaker #4: With the fundraising and the alpha allocation for the IA2, we have not gone into specific detail. The method that we use to allocate the alpha was the O'Brien-Fleming spending function.

Zachary Roberts: You know, we have not gone into specific detail. The method that we used to allocate the alpha was the O'Brien-Fleming spending function, so that will give you some general understanding of the fraction of alpha that's allocated to the IA 2. I will take the opportunity now to reiterate, though, that, you know, the results of the interim analysis 1, does give us the possibility of having a positive outcome in IA 2. That is something we are looking forward to and of course, working feverishly to enroll the study and deliver on those timelines.

Speaker #4: So that will give you some general understanding of the fraction of alpha that's allocated to the IA2. I will take the opportunity now to reiterate, though, that the results of the interim analysis one do give us the possibility of having a positive outcome in IA2.

Speaker #4: And so that is something we are looking forward to. And of course, working feverishly to enroll the study and deliver on those timelines.

Speaker #10: Awesome. Thanks so much for the color.

Jack Allen: Awesome. Thanks so much for the color.

Operator 1: Thank you. Our next question comes from John Newman of Canaccord Genuity. Your line is open.

Operator: Thank you. Our next question comes from John Newman of Canaccord Genuity. Your line is open.

Speaker #2: Thank you. And our next question comes from John Newman of Canaccord Genuity. Your line is open.

Speaker #11: Hi, guys. Thank you for taking the question. I also have one on ALLO-329. The question is, do you expect that the Dagger technology that's targeting CD70-positive T cells could actually give you maybe differential efficacy in some of the cohorts that you're enrolling versus lupus, for example?

John Newman: Hi, guys. Thank you for taking the question. Also have one on ALLO-329. The question is, do you expect that the Dagger® technology that's targeting CD70 positive T cells could actually give you maybe differential efficacy in some of the cohorts that you're enrolling versus lupus, for example, scleroderma and myositis, where it's sort of theorized that there's more T-cell activity? Thanks.

John Newman: Hi, guys. Thank you for taking the question. Also have one on ALLO-329. The question is, do you expect that the Dagger technology that's targeting CD70 positive T-cells could actually give you maybe differential efficacy in some of the cohorts that you're enrolling versus lupus, for example, scleroderma and myositis, where it's sort of theorized that there's more T-cell activity? Thanks.

Speaker #11: Scleroderma, myositis—whether it’s sort of theorized that there’s more T-cell activity. Thanks.

Zachary Roberts: John, great question. As usual, thank you for the insight. The answer is yes. Not just within these rheumatologic disorders where T cells are known to play a role, and there's literature on it, but of course, there are lots and lots of papers and understanding about other therapeutic areas which are even thought to be more dependent on T cell biology. Just to throw out a couple, multiple sclerosis and type 1 diabetes are thought to be, you know, primarily driven by pathogenic T cells. Not only within this initial set do we think we could have some differential efficacy, as you put it, but we also believe it will give us a more plausible pathway into other therapeutic areas where T cells are known to play a larger role than just a straight CD19 product.

Speaker #4: John, great question. As usual, thank you for the insight. And the answer is yes. So, not just within these rheumatologic disorders, where T-cells are known to play a role and there's literature on it, but of course, there are lots and lots of papers and understanding about other therapeutic areas, which are even thought to be more dependent on T-cell biology. Just to throw out a couple: multiple sclerosis and type 1 diabetes.

Zachary Roberts: John, great question. As usual, thank you for the insight. The answer is yes. Not just within these rheumatologic disorders where T-cells are known to play a role, and there's literature on it, but of course, there are lots and lots of papers and understanding about other therapeutic areas which are even thought to be more dependent on T-cell biology. Just to throw out a couple, multiple sclerosis and Type 1 diabetes are thought to be, you know, primarily driven by pathogenic T-cells. Not only within this initial set do we think we could have some differential efficacy, as you put it, but we also believe it will give us a more plausible pathway into other therapeutic areas where T-cells are known to play a larger role than just a straight CD19 product.

Speaker #4: Are thought to be primarily driven by pathogenic T-cells. And so, not only within this initial set do we think we could have some differential efficacy, as you put it, but we also believe it will give us a more plausible pathway into other therapeutic areas where T-cells are known to play a larger role than just a straight CD19 product.

Speaker #11: Great. Thank you.

John Newman: Great. Thank you.

Speaker #2: Thank you. And our next question comes from Renny Benjamin of Citizens. Your line is open.

Operator 1: Thank you. Our next question comes from Reni Benjamin of Citizens. Your line is open.

Operator: Thank you. Our next question comes from Reni Benjamin of Citizens. Your line is open.

Speaker #12: Hey, guys. Thanks for taking the questions. Maybe just starting off with the interim analysis. Now that you've been able to kind of sit on the data with the futility analysis, do you feel that this delta that you're seeing increases the chances of a successful interim mid-2027 versus what you were thinking when you first started the study?

Reni Benjamin: Hey, guys. Thanks for taking the questions. Maybe just starting off with the interim analysis. Now, now that you've been able to, you know, kind of sit on the data with the futility analysis, do you feel that this delta that you're seeing increases the chances of a successful interim mid 2027 versus, you know, what you were thinking when you first started the study? If so, does it make sense to potentially modify the trial design to allocate a little bit more alpha and increase your chances of success there?

Speaker #12: And if so, does it make sense to potentially modify the trial design to allocate a little bit more alpha and increase your chances of success there?

Speaker #12: And then regarding 329, as we kind of look at the landscape, look at autologous therapies and bispecifics, can you maybe just guide us as to what is the clinical sort of efficacy and safety benchmarks you're hoping to hit, hoping to meet so that you can move this program forward?

Reni Benjamin: Regarding ALLO-329, as we kind of look at the landscape, look at autologous therapies and bispecifics, can you maybe just guide us as to what is the clinical sort of efficacy and safety benchmarks you're hoping to hit, hoping to meet so that you can move this program forward? Does this program move forward ideally with a partner, or do you think you do this on your own? Thanks.

Speaker #12: And does this program move forward ideally with a partner, or do you think you do this on your own? Thanks.

Zachary Roberts: Hey, Ren. On the interim analysis, in a, you know, a EFS analysis, you know, without a question, after looking at the MRD clearance differential, we believe the probability, I mean, or the powering for the interim analysis, you know, has gone up quite a bit. I mean, that really, you know, goes down to, we have said that, you know, study was designed to demonstrate, you know, the hazard ratio of 0.5.

Zachary Roberts: Hey, Reni. On the interim analysis, in a, you know, a EFS analysis, you know, without a question, after looking at the MRD clearance differential, we believe the probability, I mean, or the powering for the interim analysis, you know, has gone up quite a bit. I mean, that really, you know, goes down to, we have said that, you know, study was designed to demonstrate, you know, the hazard ratio of 0.5.

Speaker #11: Hi, Ryan. On the interim analysis, an EFS analysis without a question after looking at the MRD clearance differential, we believe the probability or the powering for the interim analysis has gone up quite a bit.

Speaker #11: I mean, that really goes down to we have said that in a study was designed to demonstrate the hazard ratio of 0.5. But the MRD clearance, as we extrapolate based on the existing data, leads us to a potential hazard ratio being much lower than 0.5.

David Chang: The MRD clearance, as we extrapolate, based on the existing data, you know, leads us to a potentially, the hazard ratio being much lower than 0.5. If that turns out to be true as we continue to enroll the study, the probability of interim analysis, as Zach has pointed out, you know, leading to a statistical significance is very significant. We'll just have to wait and see. Your second question about, you know, you know, would we consider amending the protocol? You know, I think that probably is not something that would be, you know, that's needed or that would be good to do at this point. I mean, I think the best course is just sticking with the original study plan.

Speaker #11: If that turns out to be true, as we continue to enroll the study, the probability of interim analysis, as Zach has pointed out, leading to a statistical significance, is very significant.

Speaker #11: So we'll just have to wait and see. And your second question about whether we would consider amending the protocol—I think that probably is not something that's needed or that would be good to do at this point.

Speaker #11: I mean, I think the best course is just sticking with the original study plan.

Speaker #4: And then the question around where does this fit in the evolving landscape. We actually feel really good about that. And right now, that landscape in the frontline has really been focused for a long time on increasing intensity of those regimens.

Zachary Roberts: The question around where does this fit in the evolving landscape? We actually feel really good about that. Right now, that landscape in the front line is really been focused for a long time on increasing intensity of those regimens and looking directly at the bispecific-based regimens that are being studied, that really do add a lot of complexity and toxicity to those newly diagnosed regimen, the patient regimens.

Speaker #4: And looking directly at the bispecific-based regimens that are being studied, that really do add a lot of complexity and toxicity to those newly diagnosed regimens, the patient regimens.

Speaker #4: So we actually feel really good that no matter what happens up front, an MRD-positive result at the end of frontline treatment could trigger a semicell infusion, and to be able to administer that even in centers that we believe actually may not ever engage fully in frontline bispecific regimens because of the complexity and toxicity.

Zachary Roberts: We actually feel really good that, you know, no matter what happens up front, an MRD positive result at the end of frontline treatment could trigger a cema-cel infusion and to be able to administer that even in centers that we believe actually may not ever engage fully in frontline bispecific regimens because of the complexity and toxicity that those centers could administer cema-cel in a consolidation setting. We actually feel like we have threaded the needle very well with ALPHA3 and are somewhat insulated from all of that competition in the early lines.

Speaker #4: That those centers could administer Semicell in a consolidation setting. So we actually feel like we have threaded the needle very well with Alpha 3.

Speaker #4: And are somewhat insulated from all of that competition in the early lines.

Speaker #11: So, Ryan, does that answer your question, or was the question on 329?

David Chang: Ren, does that answer your question, or was the question on ALLO-329?

David Chang: Reni, does that answer your question, or was the question on ALLO-329?

Reni Benjamin: That last one that Zach answered was on ALLO-329, in particular.

Speaker #12: That last one that Zach answered was on 329. In particular, just trying to understand.

Reni Benjamin: That last one that Zach answered was on ALLO-329, in particular.

David Chang: That's what I thought.

Speaker #11: That's what I thought.

Reni Benjamin: Yeah. Sorry about that.

Speaker #12: Yeah. Sorry about that.

David Chang: Let me, yeah, let me just answer, you know, the question on the ALLO-329. The profile that we are looking for is something that can be administered as an outpatient and patient managed as an outpatient. Also, you know, plus that on top of that, the nature of the cell CAR T is that, you know, this will be a one-time treatment with a possibility of redosing several years down the line if the symptoms were to come back. You know, that is the profile that we believe will remain very competitive when you think about other emerging modalities that's coming, you know, in the T-cell approach towards the autoimmune indications.

Speaker #11: So let me just answer the question on the 329. The profile that we are looking for is something that can be administered as an outpatient and patient managed as an outpatient.

Speaker #11: And also, and plus that on top of that, the nature of the CAR T is that this will be a one-time treatment with a possibility of re-dosing several years down the line if the symptoms were to come back.

Speaker #11: So that is the profile that we believe will remain very competitive. When you think about other emerging modalities, that's coming in the T-cell approach towards the autoimmune indications.

Speaker #2: Thank you. And our next question comes from Brian Chang of J.P. Morgan. Your line is open.

Operator 2: Thank you. Our next question comes from Brian Cheng of JPMorgan. Your line is open.

Operator: Thank you. Our next question comes from Brian Cheng of JPMorgan. Your line is open.

Speaker #13: Hi, guys. Thanks for taking our question this afternoon. Just a quick one from us. Can you talk about the rationale of updating the autoimmune resolution data updates from June to Q4?

Brian Cheng: Hi, guys. Thanks for taking our question this afternoon. Just a quick one from us. Can you talk about the rationale of updating the autoimmune RESOLUTION data updates from June to Q4? Is that decision data-driven, or are there other considerations? Thanks for taking our question.

Speaker #13: Is that decision data-driven, or are there other considerations? Thanks for taking our question.

Speaker #11: Yeah, Brian, let me take the question. I think our intent is to provide data updates in a very meaningful way. In terms of the maturity of the data and what we have now, I think what we can say is enrollment is very robust and also there are very sort of interesting signs of clinical activity.

David Chang: Yeah, Brian, let me take the question. I think, you know, our intent is provide, you know, data update in a very meaningful way. You know, in terms of the maturity of the data and what we have now, I think what we can say is enrollment is very robust. Also there is, you know, very, you know, sort of interesting signs of clinical activity. I don't think, you know, definitely I think, you know, this is for, you know, now. As we dose escalate, I mean, keep in mind, we intentionally started the study with very conservative dose to ensure the patient safety. You know, 20 million, I think there was an earlier question about whether that may be low. In my view, it probably was lower than what was necessary.

David Chang: Yeah, Brian, let me take the question. I think, you know, our intent is provide, you know, data update in a very meaningful way. You know, in terms of the maturity of the data and what we have now, I think what we can say is enrollment is very robust. Also there is, you know, very, you know, sort of interesting signs of clinical activity. I don't think, you know, definitely I think this is for now. As we dose escalate, I mean, keep in mind, we intentionally started the study with very conservative dose to ensure the patient safety. You know, 20 million, I think there was an earlier question about whether that may be low. In my view, it probably was lower than what was necessary.

Speaker #11: I don't think definitely—I think this is for now. And as we do escalate, I mean, keep in mind, we intentionally started the study with a very conservative dose to ensure the patient's safety.

Speaker #11: So, $20 million—I think there was an earlier question about whether that may have been low. In my view, it probably was lower than what was necessary.

David Chang: As we dose escalate, and certainly we are going to the dose levels that in other programs that we have done, you know, 80 million or 120 million is sort of the range that we have seen activities in programs like ALLO-316 or cema-cel. We're getting to that dose range and as we update the data in Q4, we will have patients treated at the dose that may be more in the right range. You know, definitely, we are enrolling this study rather briskly, and we'll have a lot to talk about in Q4.

Speaker #11: And as we do escalate, and certainly we are going through the dose levels that, in other programs that we have done, 80 million or 120 million is sort of the range that we have seen activities in programs like ALLO-316 or Semicel.

Speaker #11: So we're getting to that dose range, and as we update the data in the fourth quarter, we will have patients treated at the dose that may be more in the right range. But definitely, we are enrolling this study rather briskly, and we'll have a lot to talk about in the fourth quarter.

Brian Cheng: Great. Thank you.

Speaker #13: Great. Thank you.

Speaker #2: Thank you. That concludes our question-and-answer session. I would like to turn the conference back over to management for any additional comments.

Operator 2: Thank you. That concludes our Q&A session. I would like to turn the conference back over to management for any additional comments.

Operator: Thank you. That concludes our Q&A session. I would like to turn the conference back over to management for any additional comments.

Speaker #12: All right. Thank you. We said at the onset that this would be a year of defining proof, and the Alpha 3 instrument analysis represents an important first step.

David Chang: All right. Thank you. We said at the onset that this would be in a year of defining proof, and the ALPHA3 interim analysis represents an important first step. The signal we see today must be validated through EFS, but it provides early support for a fundamentally different approach to CAR T, one that is earlier, more accessible, and potentially scalable. Our focus now is execution, completing ALPHA3 enrollment, advancing ALLO-329 through dose escalation, and continuing to generate the data needed to define the role of allogeneic CAR T across oncology and autoimmune disease. We believe we are well-positioned to do that. Thank you for your continued support. Operator, you may now disconnect.

Speaker #12: The signal we see today must be validated through EFS, but it provides early support for a fundamentally different approach to CAR T—one that is earlier, more accessible, and potentially scalable.

Speaker #12: Our focus now is execution, completing ALPHA-3 enrollment, advancing ALLO-329 through dose escalation, and continuing to generate the data needed to define the role of allogeneic CAR T across oncology and autoimmune disease.

Speaker #12: We believe we are well positioned to do that. Thank you for your continued support. Operator, you may now disconnect.

Speaker #2: Thank you, ladies and gentlemen. Thank you for your participation in today's conference. This does conclude the program, and you may log off and disconnect.

Operator 2: Thank you. Ladies and gentlemen, thank you for your participation in today's conference. This does conclude the program, and you may log off and disconnect.

Operator: Thank you. Ladies and gentlemen, thank you for your participation in today's conference. This does conclude the program, and you may log off and disconnect.