Q4 2022 Mink Therapeutics Inc Earnings Call

Speaker 2: Good morning and welcome to Mink Therapeutics fourth quarter and full year 2022 conference call and webcast.

Speaker 2: All participants will be in a listen-only mode until the question-and-answer session. Please note, this event is being recorded. If anyone has any objections, you may disconnect at this time. I will now turn the call over to Zach Armond, Head of Investor Relations at Mink.

Speaker 3: Thank you, and thank you all for joining us today. Today's call is being webcast and will be available on our website for replay.

Speaker 3: I'd like to remind you that this call will contain forward-looking statements, including statements regarding our clinical development, regulatory, and commercial plans, as well as timelines for data release and partnership opportunities.

Speaker 3: These statements are subject to risks and uncertainties and we refer you to our SEC filings for more details on these risks.

Speaker 3: Joining me today on the call are Dr. Jennifer Buell, President and Chief Executive Officer, and Christine Klaskin, Principal Financial and Accounting Officer.

Speaker 3: Now, I'd like to turn the call over to Dr. Buell to highlight our progress in 2022 and plans for the year ahead.

Speaker 4: Thank you so much, Zach. Good morning, everyone. Thanks for joining our fourth quarter and full year 2022 earnings call. It's a great pleasure to be with you today and to share an update on the progress of our company. And I'm really excited and proud to share that our dedication to advance the field of cell therapy has yielded a great deal of value to our company.

Speaker 4: quite exciting and differentiated results in 2022 and set us up for a very active 2023.

Speaker 4: We've made important strides in advancing INKT cells, our platform, and generating critical data in research as well as in the clinic, some of which we've already presented publicly and more of which will be coming your way this year.

Speaker 4: Recall that Agent 797, our lead pro product advancing in the clinic, is an allogeneic, unmodified, or naked INKT cell.

Speaker 4: These cells have shown promise as a monotherapy as well as in combination with approved anti-PD-1s, Keytruda or Opdivo in clinical trials. And these are trials in patients that are heavily pretreated with solid tumor cancers.

Speaker 4: We're excited to present an update on this progress at the upcoming AACR meetings next month, and we'll also be announcing our plans for developing INKPs in solid tumor cancers such as non-small cell lung cancer and relapse refractory gastric cancer in collaboration with world leaders in these diseases.

Speaker 4: These data build upon our earlier presentation at the Society of Immune Therapy for Cancer, or CITSE conference in Boston last November .

Speaker 4: We also detailed our findings in our inaugural R&D day last November , where we reported on our lead program, and we showed that it can be demonstrated tolerably alone and in combination with commercially approved anti-PD-1s. We demonstrated that we could dose patients tolerably up to a billion cells per dose without lymphodepletion.

Speaker 4: and with no observations of cytokine release syndrome, CRS, or neurotoxicity.

Speaker 4: These data enable the development flexibility to deliver the benefit of these cells without toxicity observed with first generation cell therapies.

Speaker 4: Furthermore, we concluded our Phase 1 study of 797, our ALLO-INKT, in patients with viral ARDS. We reported 70% survival, which compares favorably in hospital control and CDC data of survival rates of 10 to 22%.

Speaker 4: Even more compelling were the observations of a reduction in secondary infections that are oftentimes fatal in patients in the ICU.

Speaker 4: We've submitted these data to a top-tier journal and expect a publication this year.

Speaker 4: Now these results in patients with viral ARDS have generated great interest from government and public financing and private financing opportunities. We're currently in discussions to externally finance the development of INKT cells in acute infections and associated fatal consequences like respiratory distress.

Speaker 4: an indication for which there are no approved therapies. We'll be providing more updates on the advancement of these discussions this year.

Speaker 4: The development of Aloe INKT is an indication outside of oncology is only made possible through the manufacturing productivity that our team has made. Minketh addressed the limitations of the use of cell therapy products beyond oncology and in infections in many ways. For more information, visit www.aclu.org

Speaker 4: We focused on the development of INKT cells, which have shown Thomas in treating viral infections and respiratory illnesses. By using INKT cells, we can avoid some of the limitations associated with traditional cell therapies, such as the need for a

Speaker 4: matching donors and recipients, the use of lymphodepletion, and the limitations of cost and scalability. We've addressed this.

Speaker 4: We've invested in high-throughput manufacturing technology, which allows for the rapid production of large quantities of INKT cells.

Speaker 4: generating billions of cells from a single donor and thousands of doses per donor.

Speaker 4: Our process is now FDA-cleared for implementation into our clinical trials without external dependency.

Speaker 4: Our manufacturing approach is designed to make INKT cell therapy more accessible to patients and to approve the scalability of cell therapies overall.

Speaker 4: As we continue to make progress in our clinical programs, we're also making important advancements in deepening our understanding of the novel mechanisms of action of INKP cells and their unique advantages over available cell therapies.

Speaker 4: At the end of last year, we presented data elucidating the long hypothesized mechanism of INKT cells and underscore their potential as a highly effective living medicine for patients with cancer.

Speaker 4: Specifically, our scientists demonstrated that INKPs have the killing power of NK cells and the memory of T cells. They activate dendritic cells. These are signalers that help the immune system recognize tumors.

Speaker 4: We've shown that INKT's also kill M2 macrophages.

Speaker 4: M2 macrophages are immunosuppressive cells that constrain the body's ability to fight tumors.

Speaker 4: And we also reported that INKT can restore the tumor killing capacity of exhausted T cells.

Speaker 4: This is a very important mechanism in which CD8 T cells become exhausted and lose their tumor fighting capability. And as we reported at CITSE last year, INKTs can overcome this mechanism and reinvigorate exhausted CD8 T cells, restoring their killing capacity.

Speaker 4: These mechanisms help to explain some of the early signals of benefit that we've observed in solid tumor cancers.

Speaker 4: Additionally, our research team has made important progress on our pipeline, including the development and advancement of MINK-215.

Speaker 4: MINK215 is an armored IL-15 FAPCAR-INKT designed to target the tumor stroma and modulate the tumor microenvironment to increase tumor killing capability.

Speaker 4: Targeting SAP, which is fibroblast activation protein, with CAR-INKT's, these are chimeric antigen receptor invariant natural killer T cells, can benefit patients in several ways.

Speaker 4: SAP is a protein that's found in high levels in the stroma of many evasive solid tumor cancers, but it's absent in most normal tissues.

Speaker 4: By targeting fat car INKT, we could specifically seek out and destroy cancer cells that express fat while leaving healthy cells intact.

Speaker 4: Moreover, SAP is known to play a key role in promoting tumor growth and metastatic disease.

Speaker 4: and stop inhibit the body's immune response against cancer.

Speaker 4: So by targeting FAP with CARiNKT, it's possible to overcome these barriers of resistance and activate a potent immune response against cancer.

Speaker 4: So in summary, targeting FAP with CARA-NKTs can provide a highly specific and effective approach to fighting cancer while minimizing damage to any healthy tissues and boosting the body's natural immune defense. The molecule is an IND-enabling study for an IND submission planned in 2024.

Speaker 4: Now, we are in dynamic markets and a unique time where fiscal responsibility and prudence will be critical to delivering the value of our science and the potential of our technology for patients with cancer.

Speaker 4: Partnering remains core to our strategy to fully leverage the potential of our platforms and products quickly.

Speaker 4: and these include public and private collaboration.

Speaker 4: At MAINC, we'll focus our internal efforts on deepening our datasets and select solid tumor cancer indications where INKT's can complement the

Speaker 4: At MINK, we'll focus our internal efforts on deepening our datasets and select solid tumor cancer indications, where INKT's can complement available and approved standard of care.

Speaker 4: and we believe expands the benefit of available therapies to patients with specific tumor types.

Speaker 4: and will further elucidate our development plans with the data release at the upcoming AACR conference.

Speaker 4: We will continue to leverage our research productivity and exciting findings outside of oncology through strategic collaborations.

Speaker 4: I will now turn the call over to Christine to go over our financials.

Speaker 5: Thank you, Jen.

Speaker 5: We ended the fourth quarter 2022 with a cash balance of $19.6 million as compared to $38.9 million at December 31, 2021.

Cash used in operations for the year and fourth quarter ended December 31, 2022 with $18.9 million and $4.4 million respectively.

This compares to $12.8 million and $1.7 million for the same periods in 2021.

This increased funding was related to the internalization of our CGMP manufacturing of agents 797 for clinical trial supply, which has increased our production and results in decreased supply cost prospectively.

Net loss for the quarter ended December 31, 2022 with $7.8 million, or 23 cents per share, compared to a net loss for the same period of 2021 of $5.8 million, or 18 cents per share.

Net loss for the year was $28.0 million for 83 cents per share, compared to $30.2 million in 2016 for the year ended December 31, 2021.

Thank you. We'll now turn the call over for questions. Operator? The floor is now open for your questions. To ask a question this time, please press star 1 on your telephone keypad. At any point you'd like to withdraw from the queue, please press star 1 again.

You'll be provided the opportunity to ask one question and one further follow-up question. We'll now take a moment to render a roster.

Our first question comes from the line of Emily Bodnar from HC Wainwright. Please proceed.

Hi, good morning. Maybe for without like specifically talking about data, can you just comment on what made you select gastric cancer for an expansion cohort? And are gastric and lung the only indications you're planning to evaluate or are these just the first and then you kind of will look to see if there's any others after that.

And are these going to be combination cohorts or monotherapy cohorts?

Are these going to be combination cohorts or monotherapy cohorts? Thanks.

Emily, thanks for your question. We are currently focused on expanding data sets and indications where we are quite enthusiastic about the results. Gastric and lung are opportunistic for two reasons. One, when patients are refractory to anti-PD-1 therapy, there are very limited treatment options for them.

PD1s. These indications enable a path forward where we may be able to develop the product quite rapidly.

as a monotherapy on top of available standard of care. So those are the two that we've spoken about and we'll deepen the discussion following our data presentation at AACR on some other areas where we'll be continuing to explore the benefits of INKT in different solid tumor cancers. Okay, that makes sense. And then we'll move on to the next slide.

could be ready for IND enablement in 2024.

Our next question comes from the line of Kalpreet Patel from B. Riley. Please proceed. Yeah. Hey, good morning, and thanks for taking the questions. Maybe starting with expectations for the AACR update, can you give us a sense of how many patients worth of data?

What we have spoken about is we launched the trial in March and had completed a call for the phase one dose escalation and preliminary expansion. So it is a phase one solid tumor study. It does have a mix of patients, predominantly those who are refractory to all prior therapy. So these are late line patients.

They are a standard phase one cohort with some operational enrichment for certain tumor types, which you may see some enhanced representation of specific tumor types in the cohort, most of which is a measure of the limited therapeutic options for patients at this stage.

in development. But our cohort, we completed accrual to it at the beginning of the year, so those will be presenting as much data as possible from that cohort by the time of the data presentation in AHCI. Okay, and then

In the planned expansion cohorts for lung cancer, are the patients going to be primarily checkpoint-naive, or are you going to include both checkpoint-naive and checkpoint-refractory patients in the study? In the planned expansion cohorts for lung cancer, are the patients going to be primarily

Mostly checkpoint refractory for a few reasons. We have been able to demonstrate that we can dose monotherapy, INKT's in patients who have failed prior iotherapy and we have been able to dose in combination. We can do so tolerably to a billion cells.

and we'll be sharing the data from those signals. I think importantly, one thing that is commonly observed in patients who are PD-1 refractory is the exhausted CVAT cells. For those cells that actually cannot enter the stroma of 50 this past November .

We presented data demonstrating that our INKPs can actually reverse the CD8 exhaustion signature and also kill M2 suppressive, immune suppressive macrophages. Both of those, we believe, set us up for bringing benefits in patients who have actually failed anti-PD-1 therapy because of the translational data that we've been able to...

Our next question comes from the line of Jack Allen from Baird. Please proceed.

Thank you so much and congratulations on the progress. I guess my first question was around the decision to move forward with the PD-1 inhibitors. I was wondering if you had any comments about the thoughts that you previously had around a Genesys proprietary CTLA-4 inhibitor, both Bolytizumab and any potential combination used there. Jack, I'm so glad you asked. We will be...

recent data presentation was that AscoGI and Botanilumab and for those who may be less aware the product appears to be bringing extraordinary benefits to a host of solid tumor cancers that have failed prior therapies that includes MSS colorectal cancer as well as PD-1.

refractory non-small cell lung cancer. At their most recent earnings call, they shared the response rates that are really exceeding, I think 50 percent in that cohort of patients with non-small cell lung cancer. What we had previously collaborated on were preclinical.

studies that actually demonstrated the synergy and complementarity of H797 or INKT cells in combination with Botanilumab, the urinized version, and Valcilumab. So in the model, it was a B15-ova model.

with metastatic lung disease and we saw that the combination of CTLA-4-PD-1 eliminated about 30 to 40 percent of the disease. The cells alone did about that same reduction in liver mass. When you put the three or two together, so the cells in combination with the two cells in combination with the two cells in combination with the two cells in

the benefits of what we see with boat and Silamab because of the complementarity of the mechanisms that I mentioned before. We have some additional preclinical data that we will also be releasing and other indications where the combination may be quite productive. One of the areas that we believe the cells can expand the benefit of boat and Silamab is...

but also modulate the disease and eliminate the disease in some settings in those liver mats. So we do believe that there's an enormous opportunity to expand the benefits of boat and fill map by adding the INKT cells, HIN 797 to this combination. And we'll be talking more about that at AHCR.

Great. Thank you so much. I just have two quick follow-ups. I guess the first one outside of oncology, how are you thinking about the timetable as it relates to development in graft versus host disease and should we expect that that's going to be a partnered indication at this point? And then outside of the broader mink portfolio, so two things that we're in for our discussion today.

I was wondering if you had any comments on a recent clinical hold from one of your competitors on an autologous INKT program and how we're thinking about the safety of allogeneic versus autologous INKT's. Okay, great great questions Jeff. So on the first as I mentioned of course we're in a really dynamic market where we need to be quite thoughtful.

And for GVAC, we see an enormous potential there, and we have some supportive data to indicate a quick path forward to bring benefits to patients, both not only for GVAC, but also for engraftment success. This is an area where we are looking at...

and it is designed in a way that we believe can bring themselves forward to a potential very rapid approval and we'll be making some announcements about that program in the upcoming weeks.

The, the SBI data that you're referring to, that was a patient who had had a fatality on a clinical trial. This is a patient with neuroblastoma. And that patient actually had a metanumovirus, which is commonly seen and it's fatal in pediatric patients who are lymphodepleted.

And as you can see from the trial with Aconex, they actually lymphodepleted their patients, which is not something that we believe we need to do. We have not lymphodepleted. We've demonstrated that we can administer the ALLO-INKT very tolerably, no neurotox, no CRS, no related serious toxicities above grade three. So we're in a position...

to lymphoid depletion and subsequent viral infection secondary to the lymphoid depletion that led to a very unfortunate circumstance for this patient. I don't think that it reads through to the safety or teller ability of I and KP cells.

Thanks so much. Thank you. Our final question comes from the line of Matt Phipps from William Blair. Please proceed. Is the live qualitysten idea possible? Yes.

I was wondering on the FAFSCAR, in the preclinical approach you guys had CITC, some of the efficacy data was actually best combined with an NYISA-1 T-cells. So how does that…

kind of preclinical data influence your thoughts around maybe combination development of this program and then do you plan on trying to look at any

biomarker for enrollment or like an immune excluded phenotype or just how do you pick patient populations for that program.

Well, that's a great set of questions, Beth. Thank you. So for that program, we actually set it up using the NYA's OTCR and that model to exemplify what a chronic antigen stimulated environment would look like. So what happens when immune cells are sort of constantly perturbed and then can these cells actually overcome that perturbation? Well, that's a great set of questions.

of that molecule with that targeting gives us opportunities for potential biomarker selected population. We won't restrict for that at the beginning but we will measure for it up front. So we will look if it will be necessary to enhance clinical benefit by restricting the population to stop expressing tumors or if we may have more broad activity independent of the biomarker selection.

So we'll start broad and then we will assess and then decide if we need to exclude or enrich for the FAB expressing tumors. Thanks. And then on the BCMA program, you know, if you guys have...

evidence yet I can't remember I don't think this is a 50 but of kind of treating a multiple myelin with cell line that relapsed or grew out of previous DCMA therapy.

exposure with something maybe that's kind of commercial or late stage. And I guess why not go actually in different like GPR or C5D or maybe a dual targeting construct just given how entrenched BCMA therapies are becoming.

You know Matt, BTMAs certainly are competitive. I hear that we're seeing some remarkable progress with some of the more modern BTMAs therapies including very high response rates. But there is a continued problem and we have Marcella Mouse on our scientific advisory board and what we see is that patients continuously progress.

on BCMA and two-thirds of them still express the BCMA antigen. So there does appear to be a challenge with respect to durability of response in those patients despite the high response rates. And we also still see challenges in access for those patients, both of which I think that the INKT product can address.

that actually demonstrated superior anti-tumor immunity using our IL-15 BCMA car, INKT, compared to what's commercially available right now. That program, due to its competitive nature, has prioritized that program and we've announced that previously.

in order to be really selective with opportunities that we believe can bring significant value creation even sooner. Now the VCMA program is very exciting for us and a program that we're committed to advancing because of the reasons that I mentioned previously. It is a program that we would contemplate strategic collaborations for as well and we've...

I would now like to turn the call over to Jen Buell, CEO , for closing remarks.

Thank you very much, operator. It was a pleasure to be with you all today. Looking forward to speaking with you at AACR.

Thank you again. Bye-bye. Thank you, ladies and gentlemen. This does conclude today's call. Thank you for your participation. You may now disconnect.

I have you.

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