Biomea Fusion, Inc. ($BMEA)

Good day, and thank you for standing by. Welcome to the Biomea Fusion conference call. [Operator Instructions] Please be advised that today's conference is being recorded. I would now like to hand the conference over to your speaker today, Ramses Erdtmann. Please go ahead, sir.

Thank you, operator, and welcome to this conference call. Today, we will be discussing top line results from the COVALENT-112 clinical trial to assess the safety and tolerability profile of icovamenib, along with exploratory efficacy endpoints in people with type 1 diabetes. Before we begin, let me remind you that today's presentation contains forward-looking statements about the business prospects of Biomea. These statements are subject to a number of risks and uncertainty that could cause our actual results to differ materially from those expressed or implied in this presentation, depending on the progress of Biomea's preclinical and clinical development activities, actions of regulatory authorities, availability of capital, future actions in the pharmaceutical market and developments by competitors and those factors detailed in Biomea's filings with the SEC, including its most recent 10-K and subsequent filings. All forward-looking statements made during this presentation are based on the beliefs of Biomea as of this date only, and future events or simply, the passage of time may cause these beliefs to change. Please be aware that you should not place undue reliance on the forward-looking statements made today. With that, I'll turn the call over to Mick Hitchcock, our CEO, who will kick off the call with some opening remarks.

Thank you, Ramses, and thank you, everyone, for joining us today. This morning, we are pleased to share top line results from our COVALENT-112 study evaluating icovamenib in people with type 1 diabetes. These data represent an important milestone for Biomea as we continue to expand our menin inhibitor platform into metabolic diseases. Type 1 diabetes remains an area of profound unmet need. While advances in insulin delivery and glucose monitoring have improved daily disease management, there are still no approved therapies in clinical Stage 3 disease that address the progressive loss of endogenous insulin production. Our goal with icovamenib is to explore a fundamentally different approach, one that targets beta cell biology itself. Today's presentation will walk through the biological rationale underlying menin inhibition in diabetes, the clinical design of COVALENT-112 and the top line results we are reporting. Importantly, these findings are early and exploratory, but we believe they provide encouraging biological signals that warrant continued and more rigorous evaluation. With that context, I'll now turn the call over to Dr. Juan Pablo Frias, Chair of our Scientific Advisory Board, who will place these results in the broader disease and clinical landscape and review the data in detail.

Thank you, Mick. Let me start with the disease context shown in Slide 4. Type 1 diabetes represents a large and growing global health burden, with approximately 9.5 million people living with the disease worldwide and more than 0.5 million new diagnoses each year. In the United States alone, approximately 1.8 million people live with type 1 diabetes, with around 64,000 new diagnoses annually. Biologically, type 1 diabetes is driven by autoimmune destruction of insulin-producing pancreatic beta cells. Once patients reach symptomatic Stage 3 disease, beta cell function declines rapidly. In fact, natural history data suggests that C-peptide declines by almost 50% per year in the early years following diagnosis. Importantly, beyond exogenous insulin replacement, there are currently no approved therapies in Stage 3 type 1 diabetes that address the progressive loss of endogenous insulin production or restore beta cell function. Turning to Slide 6. I'll briefly review the biology underlying our approach. There are well-described physiologic states such as pregnancy and lactation in which menin levels are naturally reduced, enabling beta cell expansion and increased insulin production and secretion. Across multiple preclinical models and human islet studies, reduced menin signaling has been associated with increased beta cell mass and improved function. Icovamenib is designed to pharmacologically replicate this biology. By reducing menin levels, our goal is to support and potentially restore beta cell function rather than simply slow its decline. Turning to Slide 7. We see the first preclinical validation in a partial beta cell ablation streptozotocin rat model of insulin-deficient diabetes. In this model, icovamenib significantly reduced blood glucose levels during oral glucose tolerance testing. This is notable because meaningful glucose lowering in this model is typically achieved only with exogenous insulin administration. Slide 8 provides an important translational bridge to humans. In ex vivo human islet studies, icovamenib reduced menin protein levels and promoted beta cell proliferation. Importantly, this proliferative effect was conditional. It occurred under hyperglycemic conditions, but not under normal glycemic conditions, supporting a disease-relevant and conditional mechanism of action. Turning to the treatment landscape on Slide 10. Most investigational approaches in Stage 3 type 1 diabetes focus on immune suppression, immune modulation or preservation of remaining beta cell function. As a result, clinical success has largely been measured by slowing the decline in C-peptide, which is why most studies enroll patients as early as possible following diagnosis. To date, however, no investigational therapy has demonstrated a durable increase in beta cell mass or function in Stage 3 disease outside of cell transplantation approaches. This is the gap we are trying to address. Slide 11 summarizes representative results with other investigational T1D therapies. There are essentially 2 dominant investigational treatment paradigms, immune-directed approaches and beta cell-focused approaches. Broadly speaking, immune-directed therapies aim to stop or slow the underlying autoimmune attack in pancreatic beta cells. Prominent examples include teplizumab, an anti-CD3 antibody that modulates autoreactive T cells and promotes immune tolerance. Other approaches include: [ rapid ] antithymocyte globulin, ATG, which induces broad T cell depletion; cytokine pathway inhibitors such as baricitinib, a JAK1 and 2 inhibitor; [ anyuates ] inflammatory signaling; and agents like [ ustekinumab ], which targets the interleukin 12 and 23 pathway. Emerging approaches, including polyclonal human antibody therapies such as SAB-142, are also being explored to modulate immune pathways implicated in disease progression. Beta cell-focused approaches, by contrast, aim to preserve remaining beta cell function rather than directly targeting the immune system. Examples include: verapamil, which reduces beta cell stress and apoptosis; rituximab, which indirectly impacts beta cell preservation through B-cell depletion; and GLP-1 receptor agonist, which provide beta cell [ rest ] and may offer protective effects over time. While many of these programs show relative preservation versus placebo, the long-term trajectory across studies remains continued C-peptide decline, as you can see in the small images showing the individual study results. Durable restoration of endogenous insulin production has not been achieved. Importantly, most approaches aim to preserve what remains rather than restore what has already been lost. What's notably absent for most of these approaches is regeneration. The ability to restore beta cell mass has already been lost, where we believe icovamenib could occupy a generally differentiated position. Icovamenib, Biomea's menin inhibitor, is designed to target the regenerative capacity of beta cells through epigenetic reprogramming, driving proliferation of residual beta cells rather than simply protecting the remaining beta cells or dampening the immune attack. With that context, I'll briefly touch on the study design on Slide 13. COVALENT-112 was designed to be a proof-of-concept study to assess beta cell function as measured by changes in stimulated C-peptide and metabolic parameters in patients treated with icovamenib plus standard of care insulin. The study included patients across a range of disease durations, those who were diagnosed within the last 3 years and also those who were diagnosed up to 15 years ago to better understand icovamenib's effect across different stages of the disease. Patients were treated for 12 weeks and followed through 52 weeks to assess both on-treatment effects and durability. Two dose levels, 100 milligrams and 200 milligrams once daily, were evaluated to explore dose response. Study enrollment was interrupted in May of 2024 due to the clinical hold, but the data we're presenting today reflect approximately half of the number of patients we originally intended. Now turning to the data. Slide 14 shows what we believe is a strong on-treatment signal. In Cohort 1, patients diagnosed within 3 years, treatment with icovamenib in the 200-milligram group resulted in a mean 52% increase from baseline in stimulated C-peptide mean area under the curve, AUC, at 12 weeks during the dosing period. This magnitude of increase has not previously been observed in type 1 diabetes studies and stands in contrast to the natural history expectations of progressive decline. Slide 15 focuses on durability. Week 52 C-peptide mean AUC remained largely preserved in the 200-milligram group with only a 7.1% decline from baseline. This compares very favorably with the approximately 50% annual decline reported in third-party literature for untreated patients. Summarizing these findings on Slide 16, we observed a statistically significant increase in C-peptide from baseline during dosing in the 200-milligram group, encouraging durability out to 1 year dose response favoring the 200-milligram group and a generally favorable safety and tolerability profile with no new safety signals observed through 52 weeks. We look forward to presenting additional data at an upcoming scientific conference. Looking ahead to Slide 18, we now have greater clarity about both what we understand to date and what remains to be addressed. We have observed stronger activity at higher doses and greater benefit in patients treated earlier after diagnosis. We also see signals suggesting that longer treatment duration may further enhance beta cell function. At the same time, important questions remain, including the impact of continuous dosing, the interaction between beta cell expansion with immune modulation and whether combination strategies may further improve durability. Finally, turning to Slide 19. This leads directly to our proposed next study. The next trial will be an investigator-led Phase II study, which we plan to conduct in collaboration with leading U.S. type 1 diabetes centers. The study is currently designed to enroll adults within 3 years of diagnosis who retain measurable C-peptide. The design includes extended icovamenib treatment duration, placebo control and comprehensive immune and metabolic assessments with the potential incorporation of a JAK inhibitor to explore combination strategies. This study is designed to more rigorously evaluate both the magnitude and durability of the effect while also beginning to assess beta cell targeted approaches may be combined with immune modulation to potentially impact disease progression. Stepping back, our goal is to build on the biological and clinical signals observed to date and more definitively understand the potential role of this approach in type 1 diabetes. I will now turn the call over to Mick, Biomea's CEO, who will provide final remarks.

Thank you, Juan Pablo, and thanks to the entire Biomea team for the work behind these data. To step back for a moment, we are very encouraged by the results from COVALENT-112. Although this was a small exploratory study, the magnitude of the on-treatment C-peptide response, along with the observed persistence after treatment cessation, stands in clear contrast to the natural history of type 1 diabetes. We believe these findings provide important clinical validation of menin inhibition as a therapeutic target in diabetes. Seeing evidence of improved beta cell function even in a limited number of patients reinforces the biological hypothesis that underpins this program and supports further investment in this approach. At the same time, we are appropriately cautious. These data come from small cohorts, and important questions remain around optimal dosing, treatment duration, durability and the interaction between beta cell regeneration and the underlying autoimmune process. That is precisely why we are enthusiastic about moving forward with the next investigator-led study, which is designed to more rigorously evaluate these factors and to further define the role icovamenib may play in type 1 diabetes. We are grateful to the investigators and clinical sites for their interest, collaboration and commitment to advancing this work, and we are excited to get the next study up and running in the near term. Finally, I want to thank everybody on the call today for your continued interest in Biomea. We look forward to updating you as this program advances and to sharing additional data in future scientific forums. Operator, we are now happy to take questions.

[Operator Instructions] Our first question is going to come from the line of Edward Tenthoff with Piper Sandler.

Congratulations on encouraging results. This is really exciting in an area that needs new therapeutic development. Question, based on the mechanism and -- what percentage of T1D patients are on a JAK inhibitor? And can you kind of get into a little bit more detail about the potential synergy or additive mechanism of action between the two things?

Thank you, Edward. I'm going to turn that question over to Juan Pablo.

Yes, it would be extremely small, and it would be -- as far as [indiscernible], it would be investigational use only at this point. But as I mentioned previously, I mean, they're really complementary mechanisms by which we feel that icovamenib through inhibiting menin is going to be replicating beta cells and any other adjunctive therapy such as a JAK1 inhibitor would be providing -- or helping not have these cells, if it is an issue, have an immune attack, if you will. So really, it's using the two as complementary rather than synergistic.

And are there other mechanisms that make sense too, Juan Pablo?

Yes. I think theoretically, it would be any of the mechanisms that we discussed that are more focused on the inflammatory response that may -- again, we don't know. That's why the study will be conducted. That may certainly help the cause here.

Our next question is going to come from the line of Roger Song with Jefferies.

This is Cha Cha Yang on for Roger. Congrats on the data update, and also agree with the last speaker that this is definitely an area of great unmet need. So I have two questions, one is just to confirm. For your Phase II, will patients need to be on immunosuppressants during the follow-up period or just the treatment period? And without the immunosuppressants after the treatment period, how are you going to work to overcome the immune-mediated attacks on the new beta cells? And then my second question is, can you just confirm, Were patients on exogenous insulin for this trial? And were they able to stop using it at any point?

Juan Pablo, I'll let you take that one.

So let me start with the second. These patients were all on exogenous insulin throughout the trial period, so in the COVALENT-112. With respect to the proposed trial design -- and this hasn't been finalized yet. I mean, the participants would receive icovamenib only for the initial 6 months, and then some of those patients would continue with icovamenib only. Some would come off of therapy, and then others would either have the immunosuppression with continued icovamenib or after icovamenib is discontinued, have the immunosuppressive therapy. So we'll really test what icovamenib alone would do for 6 months and what icovamenib alone would do for the entire 12 months or 52 weeks and then also what the combination of icovamenib with immune modulator would do in combination through the 52 weeks or stopping the icovamenib at 6 months and then going on to the immunosuppressive therapy. That will be answered there.

Maybe one more point for you to make, if you could. All these studies that we are presenting here are -- every patient is on background insulin because that's the standard of care. And if you wouldn't have them on insulin, they would have severe side effects. I mean, that's a standard. And when -- could you describe the mixed meal tolerance test that we do with the 4 hours so that people understand that is a standardized format that people use to measure C-peptide?

Yes, absolutely. So to measure the C-peptide as we did in the 112 [ and ] other studies is having a mixed meal, which stimulates the pancreas to secrete insulin, and C-peptide is what's measured to look at insulin secretion and beta cell function. So during the 4 hours subsequent to ingesting the meal, C-peptide is measured at specific intervals, and that's how we measure beta cell function and the change in beta cell function over time.

And the others do the same in their study. So when you look at all these study results, it's a 2-hour or 4-hour test. You can cross reference at least to a degree that they are all treated or they're all tested in a similar mechanism to understand what does the pancreas do for any of these patients.

Correct.

Cha Cha, does that answer the question?

Yes. And then one more question, if I may. Can you just tell us what are the baseline C-peptide levels required for insulin dependence, so somebody not on -- somebody who [ doesn't ] have type 1 diabetes? And then also, do you foresee icovamenib potentially reaching up for patients?

Yes. I think potentially, it could. But the levels that we're looking at here, I mean, are certainly very low in this study would be -- it would have to be over 0.2 nanomolar. And that's already -- even over that is extremely low at that point as you're getting below 1, for example. So these will be patients that absolutely would require insulin and more than likely be symptomatic and have Stage 3 type 1 diabetes.

Our next question will come from the line of Michael King with Rodman & Renshaw LLC.

Just a couple of questions again on the Phase II study design. Can you just walk us through the dose titration schedule? I see you started at 100 and gradually move up to 200. How will that be gated? Is it time gated? Is it tolerability gated or otherwise?

I'll pass that one to Juan too, please.

Yes. So that has not been fully worked out yet. But what we've generally done has been -- it will be probably -- likely 4 weeks at 100 milligrams and then escalating. But the idea will be to start at the lower dose and then escalate to 200. So exactly how that will be done and the timing is not yet fully decided.

Okay. I'll follow up on that in a second. But just as far as the patient's insulin regimen, are they allowed to be on any insulin regimen? And are they being counseled to not adjust their insulin regimen? Or will they adjust it dynamically depending on their blood glucose? I mean, are all of them on continuous glucose monitoring?

Yes. Again, I'll say a lot of those details are still being worked out, but they absolutely will be able to, and hopefully, they will need to make insulin dose adjustments to maintain euglycemia or not have hypoglycemia, certainly. So there will be adjustments. I imagine most of these or all of these patients will be on continuous glucose monitoring. And again, the final eligibility criteria is still being worked out. But I would say, yes, most of these patients will be on CGM, and they absolutely will be allowed to make insulin dose adjustments.

Okay. Great. And then -- so I guess a bit of a compound question about the 200-milligram dose and the combination with immunosuppressants. We did see a clinical hold in the first -- in the Phase I at 200. So is there any concern about combination with immunosuppressants? Are any excluded from the second half of the study because of potential interactions? And just from a high-level standpoint, is the company concerned about -- just the possibility of confounding or complicating the safety attributes of icovamenib because of the combination with immunosuppressants?

Yes. All I'll say to that is that we'll be monitoring this, obviously, extremely closely during the 6 months when the patients are up or dose escalating from 100 to 200 and beyond that. I don't think theoretically, there's no concern above and beyond what we've seen with icovamenib. So all I would say is we're going to monitor it extremely closely. And certainly, patients who have issues, if they have them with aminotransferase elevations or any issues with liver during the 6-month period would not continue therapy. But again, we're very confident from what we saw with 100 and then escalating to the higher doses that we shouldn't have a problem that clearly, this will be monitored very closely through the trial.

Steve...

Sorry, go ahead.

Steve, do you have anything further to add? We've looked at significantly higher doses.

Yes. Thank you, Mick. First of all, we do not, as Juan Pablo mentioned, anticipate any drug-drug interactions between icovamenib and immunosuppressant agents. These agents are metabolized and have an impact on various metabolic pathways that are not overlapping. So again, we don't anticipate any issues with DDI. With regard to the liver safety profile, based on our type 2 study, COVALENT-111, we did in one cohort in that study, do this ramping up from 100 milligrams daily to 200 milligrams daily. And with that ramp up, we did not observe any clinically significant LFT elevation. So we don't anticipate that being a limiting issue with the planned type 1 study.

Congrats. It's a great group, a great cooperative group you guys are working with.

Our next question comes from the line of Joe Pantginis with H.C. Wainwright.

So first on the Phase II. So can you define the enrollment criteria a little better? Is it just a focus of [ time ] for diagnosis, similar to now? And then also, as you said and as we believe this is a very rigorous design that you're looking at, but from an IST standpoint, what is the potential that you've been discussing internally to have higher numbers in the cohorts?

So Juan Pablo, I'll let you take that one, too, please.

Yes. I mean, what we're disclosing now is with respect to the entry criteria, diagnosed Stage 3 type 1 diabetes diagnosed within 3 years at the time of entry and then with some residual C-peptide, so C-peptide greater than 0.2 nanomoles per liter. That really is what we have at this point. I don't know what the discussions have been with respect to increasing the numbers, but I think this is quite robust and will give us an idea of where we would move forward, particularly with respect to the need for adjunctive immunosuppressive therapy. And I'll add that it has a placebo arm as well. So I think these numbers are quite reasonable.

Can I make a point, Joe. Every study that you see, if you do a little bit of digging, over 90% of them try to find the patient very early on, 0 to 90 days, 0 to 100 days from diagnosis. And that is where most of these therapies need to be because of this progressive decline, just to have an impact and to move that curve a little bit over. And you can see in all the charts, they're all trending down, or most of them, if not all of them. And so we -- when we approach the investigators with the study design, they said, this is unbelievable that you're targeting a patient population between 0 and 3 years. It's unheard of, actually. And so we see not really a problem in finding those patients because they're very much available because they're not picked up by the other studies. And then two, to have a pathway or a drug that potentially works in patients that have been so far into their disease is a very welcoming fact for these investigators. So we found great response with them. It's a great group of professionals there. And if we were to enlarge the numbers of patients, it's an IST. If they want to go higher, for us, time is of the essence. The more patients we enroll, the longer it takes to read out. This is 40 patients. We can do 40 patients with 4 centers fairly fast. But if we increase the numbers, maybe we do it in a secondary study. But the intent is go in, understand the signal, really confirm all these points we made in the script. And once we have that data, come out with results very quickly so that we know this pathway is fully -- is actually valid for a Phase III design theoretically.

No, that's helpful. And then if I could just switch back to today's data, which are very encouraging signals. I guess I want to focus on the C-peptide concept. So first, what do you potentially attribute the initial drops in C-peptide? Is this a potential for patients on their current trajectory continuing before icovamenib can engage its mechanism of action, first? And then second, how would you define, for these patients, the clinical relevance in the changing of the slope positively to say, only seeing a 7% C-peptide decreases or even potential increases over time? Can you discuss the clinical relevance around that?

[ Do you want ]?

Yes. So I mean, it's very small. I would say that going to the decrease you mentioned, there really doesn't -- with the 200-milligram dose, there's really no change. And then at week 8, you start seeing it go up. So I think any very small decrease, maybe at week 4, there just all has to do with the end. I mean, these are 3 participants in that group, in the 200-milligram group in Cohort 1. So I really think it's no change until we see out to week 12, where we're seeing this 52% increase. And I think it's highly relevant, even maintaining C-peptide, but certainly the increase in C-peptide. We know that these patients do better overall with less hypoglycemia likely will, and this is something we'll look at further, would have a reduction in insulin dose as well. They're much easier to treat from a clinical perspective if they have remaining C-peptide secretory capacity. So I think they're very clinically relevant. But again, as we mentioned, the numbers are very small here, and that's why we want to explore this further. But I would say that even no progression in the decline of C-peptide is clinically relevant. But certainly, the increase in C-peptide really hasn't been seen before, and that's what we're striving towards.

And a little bit of color because I've talked to all these investigators. And when you show them these graphs, you hear comments such as this is provocative data or never -- I've never seen anything, any drug that would increase the C-peptide that patients are using so fast. And I refer you to the quote from Alexander Fleming in our press release. We put that there because we found it was just so telling of what we're trying to do and the excitement around what we think is potentially there. And just read that quote, and then you can see what professionals think about what we're doing here.

Our next question will come from the line of Yigal Nochomovitz with Citigroup.

I just had a question on the Phase II strategy. Over the years, you've talked about doing a short course of treatment as you did in this study, the 12 weeks to boost the beta cells and then take a pause. And obviously, acknowledge that this is a small study with low end. I'm just wondering if you'd considered basically repeating this type of study with the 12 weeks for a larger set of patients to sort of further anchor these conclusions before moving to change variables and do a longer study and then add the immunosuppression? I just wanted to get your thoughts on that first, please.

Yes. This is Mick. I think all the investigators that we've talked to look at this data and say, "This is great, but we want to do more." And so this is part of why we want to go to a longer term of treatment. In addition, we now have the preclinical data that would support us to go into a longer treatment paradigm. So I think it makes sense for us to go after 6 months. If we saw any concerns about 6 months, we could go back to 3. But I think what we're looking for now is this is a great response, but if we can do better, then we certainly want to see what happens there.

Okay. And then can you just comment on the -- just the inherent variability of the C-peptide, the glucose tolerance test assay and whether -- and how much of that variability is being reflected in this data set or whether it's well beyond that inherent variability of the assay?

Juan Pablo, can I get you to take that one?

Yes. You know what, I think -- obviously, the higher end will help with that. There clearly is some variability, as with any assay. So there is variability there. So although we're seeing this improvement with the 3 patients, which is consistent in each of the patients. I think that's why we absolutely need the bigger numbers to confirm this.

Okay. And then Juan Pablo, just kind of getting your thoughts on the slope. You get to the negative 7% after 52 weeks versus the 50% for a year. But I'm just getting your thoughts in terms of whether you're pushing out the decline because you're getting a bump at 12 weeks, and then you kind of resume the original decline because the slopes are very similar. You know what I mean? So like, does that -- how do you think about that in terms of possible redosing to kind of keep that slope from returning to that natural history decline?

Right. Well, I think it goes to your first question and the need to potentially go out further. So I think we'll see that with the 6 months. And I think what the trial provides as well, the upcoming trial provides 6 months of therapy and see what happens, and then also then coming off of therapy at 6 months versus continuing the therapy. So I do to your point, and the slope was the same. In a sense, you need to buy in time, if you will. But I think that was the rationale behind dosing for a longer period of time, seeing if we can have a more sustained reduction and then also seeing what the immunosuppressive therapy, adjunctive immunosuppressive therapy does, whether that improves that slope or not.

Okay. And then just one other thing. On the Cohort 2, that data is coming later at the meeting?

Yes.

Yes. Our next question comes from the line of Anupam Rama with JPMorgan.

This is Joyce on for Anupam. Maybe just as a follow-up to the previous set of questions, regarding your next Phase II looking at extended dosing out to 6 months and also 12 months, as you mentioned. I was just curious if there's anything in your work so far to help inform what the right duration of treatment might be here? At 12 weeks, it seems like there's no plateau yet. Obviously, small end still, but just wondering if there's anything in your modeling work that might suggest when the max benefit might be reached here?

I think at this stage, it's all hit and hope. We're really trying to sort of figure this out in real time. There's no precedent for this. So I think we need more experimental data to come to the conclusion about what the best dosing period is going to be.

That's exactly the purpose of the study, right? The purpose of the study is to answer all these questions quickly, not overload the study with too many questions. But the question you're asking is our question. We couldn't answer that question before because we didn't have the tox data. Now that we can continuously dose patients, we can actually get an answer to your question well. And with 12 months of dosing of icovamenib, we will see how far reaching this increase can be and how durable it then is. Another theory that we heard from investigators was if you have a buildup pool of beta cells, could they survive better? Meaning, is there a mass that you have to reach or overcome in order to have a sustained effect? Those are all the things we will find out in the study.

Okay. And then if I could just follow up with another question. At ADA, I understand you'll have full data from both cohorts. I was just wondering if you'll have any additional analyses specifically from Cohort 1 relative to today's top line update that you would have us focus on as we look to that upcoming presentation?

That's a good question. I -- the reason why we put this here, this is the top line. This is the big update that we wanted to give everybody and that we took out of the ADA because it's important for you to know and to have. The ADA will provide further details. But as you can imagine, if you go to Cohort 2, 3 to 15 years, the effect is not as impressive as you see here. It's sustaining, yes, but you can debate that, meaning, don't place undue importance on the ADA as if we come out with another set of data. This is the data here that you see that is most important.

[Operator Instructions] We have a follow-up question from the line of Michael King with Rodman & Renshaw LLC.

Mike, we can't hear you.

Sorry. What I was going to ask is on the cooperative group study. Is this only going to be in patients -- it looks like less than 3 years as well as 3 to 15 years. Will they be analyzed in a stratified manner? Or will they all be pooled? Do you know the answer to that?

Yes. It's only 0 to 3 years.

Only 0 to 3. Okay.

And just not to get into -- obviously, there is a chance and that we have an effect in these other more burdened patients where type 1 has just decreased the pool too far. But that would be so much work for us to do now. We're a small company. We want to find -- we really want to solidify what you see here today very quickly and then see how far this can take us. If you look at the teplizumab results that they have with the FDA right now, look at the results and see the lasting effect of their drug and compare that to ours, and then draw your conclusions of the potential of what icovamenib has in the bag potentially for 0 to 3 years. They go after 30 to 90 days. And I think when you compare just what we show here with what's currently at the FDA, you can see that, one, we can potentially -- and that's the goal -- achieve a lot more just with this study design to show that there is a greater effect size potential, one. And two, later on, we can look at 3 to 15 years. We can look at all these other patient subsets because then, we understand the signal. But we want to get out and fast and show that we are actually -- we could have a dominant role in type 1.

Thank you. And I'm showing no further questions at this time. And I would like to hand the conference back over to Mick Hitchcock for further remarks.

Well, thanks very much for being on the call today, guys. We appreciate your interest, and we're really excited about the data. And if anybody has any further questions, please feel free to reach out to us. And thank you for your interest, and that's all we'll do today. Thanks. Bye-bye.

This concludes today's conference call. Thank you for participating, and you may now disconnect. Everyone, have a great day.