Good day and thank you for standing by. Welcome to the Biomea Fusions conference call. At this time, all participants are in a listen-only mode. After the speaker's presentation, there will be a question and answer session. To ask a question during this session, you will need to press star 11 on your telephone. You will then hear an automated message advising your hand is raised. To withdraw your question, please press star 11 again. Please be advised that today's conference is being recorded. I would now like to hand the conference over to your speaker today, Ramseys Erdman. Please go ahead, sir.
Thank you, Operator, and welcome to this conference call. Today, we will be discussing top-line results from the COVID-112 clinical trial to assess the safety and tolerability profile of ICOVA MINUTE, 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 Biomia. 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 Biomia'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 Biomia's filings with the SEC, including its most recent 10K and subsequent filings. All forward-looking statements made during this presentation are based on the beliefs of Biomia 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, Ramtys, and thank you, everyone, for joining us today. This morning, we are pleased to share top-line results from a covalent 112 study evaluating Icovaminib in people with type 1 diabetes. These data represent an important milestone for Biomere 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 Icovaminib 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 half a 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 and 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. Ovamentib is designed to pharmacologically replicate this biology. In reducing menin levels, our goal is to support and potentially restore beta cell function rather than simply slow its decline. Turning to slide seven, we see the first preclinical validation in a partial beta cell ablation streptozotin RAP model of insulin-deficient diabetes. In this model, Icovamendib 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 involve 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 two 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 by creating beta cells. Prominent examples include teplizumab, an anti-CD3 antibody that modulates autoreactive T cells and promotes immune tolerance. Other approaches include rabbit antithymocyte globulin, ATG, which induces broad T cell depletion. Cytokine pathway inhibitors, such as baricitinib, a JAK1 and 2 inhibitor, annuates inflammatory signaling in agents like akinumab, which targets the interleukin-12 and 23 pathway. Emerging approaches, including polyclonal human antibody therapies, such as SAB142, are also being explored to modulate immune pathways implicated in disease progression. Betasol-focused approaches, by contrast, aim to preserve remaining betasol function rather than directly targeting the immune system. Examples include varapamil, which reduces betasol stress and apoptosis, tuximab, which indirectly impacts betasol preservation through B-cell depletion, and GLP-1 receptor agonists, which provide betasol rest 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 from 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. In that context, I'll briefly touch on the study design on slide 13. Prevalent 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 Icovamentib plus standard of care insulin. The study included patients across a range of disease durations, those that were diagnosed within the last three years and also those that were diagnosed up to 15 years ago to better understand Icovamentib'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, so the data we're presented 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 one, patients diagnosed within three years, treatment with Icovaminib in the 200-milligram group resulted in a mean 52% increase from baseline in stimulated C-peptide mean area under the curb, 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 one 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 I diabetes centers. The study is currently designed to enroll adults within three years of diagnosis who retain measurable C-peptides. The design includes extended Icovament of treatment duration, SIBO 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 how 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, AMIA CEO, who will provide final remarks.
Thank you, Juan Pablo, and thanks to the entire BioMIA 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 ICOVA method 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. 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. One moment will we compile our Q&A roster. Our first question is going to come from the line of Edward Tenthoff with Piper
Sandler. Your line is open. Please go ahead. Great. Thank you very much, and 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?
Hi there. Hey there. What percent 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. Yeah, it would be extremely small and it would be as far as it would be in investigational use only at this point, but as I mentioned previously, I mean, they're really complementary mechanisms by which we feel that Icova Menin, 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 these two as complementary rather than synergistic. And are there other mechanisms that make sense too on public? Thank you. Yeah, I think, you know, 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
year. Great. Excellent. Thank you so much. Thank you. And one moment for our next question. Our next question is going to come from the line of Roger Song with Jeffries. Your line is open.
Please go ahead. Hi, this is Chacha 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 two, 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.
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 Icovamentib only for the initial six months, and then some of those patients would continue with Icovamentib only. Some would come off of therapy, and then others would either have the immunosuppression with continued Icovamentib or after Icovamendib is discontinued, have the immunosuppressive therapy. So we'll really test what Icovamendib alone would do for six months and what Icovamendib alone would do for the entire 12 months or 52 weeks, and then also what the combination of Icovamendib with immune modulator would do in combination through the 52 weeks or stopping the ICOVA meta but six months and then going on to the immunosuppressive therapy. So what will be answered there?
Maybe one more point for you to make, if you could. All these studies that we're 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. Right. That's a standard. And could you describe the mixed meal tolerance test that we do with the four hours so that people understand that it's a standardized format that people use to measure a C-peptide?
Yeah, absolutely. So to measure the C-peptide as we did in the 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 four 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 studies so when you look at all these study results it's a two hour four 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 right Chacha does that answer the question yeah thanks so much 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 who doesn't have type 1 diabetes, and then also, do you foresee Ecovamana potentially reaching that for patients? Yeah, I think potentially it could,
but the levels that we're looking at here, I mean, are certainly very low. In this study, it would have to be over 0.2 nanomolar, and that's already, you know, even over that is extremely low at that point as you're getting below 1, for example. So, you know, these would be patients that absolutely would require insulin and, you know, more than likely be symptomatic and have stage 3 type 1 diabetes. Okay. Great. Thank you.
Thank you. And one moment for our next question. Our next question will come from the line of Michael King with Rodman and Rinshaw LLC. Your line is open. Please go ahead.
Thank you for taking the question. Good morning, guys. Just a couple questions again on the phase two study design. Can you just walk us through the dose titration schedule? I see you start 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 one, too, please.
So that has not been fully worked out yet. But what we've generally done has been, you know, it would be probably, you know, likely four 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. 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? Are they being counseled to not adjust their insulin regimen, or will they adjust it dynamically depending on their blood glucose? And are all of them on continuous glucose monitoring?
Yeah, 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 eucalycemia 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, you know, 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, I guess, a bit of a compound question about the 200-milligram dose and the combination with immunosuppressants. You know, we did see, you know, a clinical hold in the phase one 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, you know, just the possibility of confounding or complicating the safety attributes of COVID-19 because of the combination with immunosuppressants? Thank you.
Yeah, all I would say to that is that, you know, we'll be monitoring this obviously extremely closely, you know, during the six 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 that COVID-19. 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 aminotransplace elevations or any issues with liver during the six-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. But clearly, this will be monitored very closely through the trial.
Steve, do you have that?
Okay, thank you for taking – oh, sorry, go ahead.
Steve, do you have anything further to add? You've looked at significantly higher doses.
Yes, thank you, Mick. First of all, we do not, as one Pablo mentioned, anticipate any drug-drug interactions between Icovaminib 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.
Great. Thanks for the added explanation. And congrats. This is a great group, a great cooperative group you guys are working with.
Thank you, Mike.
Thank you. And one moment for our next question. Our next question comes from the line of Joe Pan Guinness with H.C. Wainwright. Your line is open. Please go ahead.
Thanks for taking the questions. So first on the phase two, so can you define the enrollment criteria a little better? Is it just the 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 it's from an ISP standpoint. What is the potential that you've been discussing internally to have higher numbers in the cohort?
So, Juan Pablo, I'll let you take that one, too, please.
Yeah, I mean, what we're disclosing now is with respect to the entry criteria, diagnosed stage 3, type 1 diabetes, diagnosed within three years of 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 immunosuppressor 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, or 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 when we approached the investigators with this study design, they said, this is unbelievable that you're targeting a patient population between zero and three 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 weed out. This is 40 patients. We can do 40 patients with four 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 actually valid for a phase three design, theoretically.
no that's helpful and then if i could just switch back to today's data um which are very encouraging signals i guess i want to focus on the c-peptide concept so first you know what do you potentially attribute the initial drops in c-peptide is this a potential for uh you know patients on their current trajectory continuing before evocomenev can uh you know engage its mechanism of action first, and then second, how would you define, you know, 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?
Back to you, Wong.
Yeah, so, I mean, it's a very small, I would say that during, going to the decrease you mentioned it really doesn't with the 200 milligram dose there's really no change um and and then a week eight you start seeing it go up so i i think any very small decrease maybe a week four there it just all has to do with the end i mean these are these are three participants in that group in the 200 milligram group in the cohort one 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 left 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've 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 thank you. 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 I've never seen anything, any drug that would increase the C-pepsides 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.
Great. Thanks, guys.
Thank you.
Thank you. And one moment for our next question. Our next question will come from the line of Yigel Notramovitz with Citigroup. Your line is open. Please go ahead.
Hi, guys. Thank you for the questions. I just had a question on the Phase 2 strategy. You know, 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, you know, 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.
Yeah. This is Nick. I think that 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 six months. If we saw any concerns about six months, we could go back to three. But I think what we're looking for now is that 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, this glucose tolerance test assay, and how much of that variability is being reflected in this data set or whether it's, you know, well beyond that inherent variability of the assay.
Juan Pablo, can I get you to take that one?
Yeah, you know what, I think obviously the higher ends 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 three patients, which is consistent in each of the patients, you know, I think that's why, you know, we absolutely need the bigger
numbers to confirm this. Okay. And then, Juan Pablo, just kind of getting your thoughts on the slope, you know, yes, you get to the negative 7% after 52 weeks versus the 50% for a year, but just getting your thoughts in terms of, you know, whether you're pushing out the the decline because you're getting a you're getting a bump at 12 at 12 weeks and then you kind of resume the original decline because the slopes are very similar um can you know you know what i mean so like does that how do you think about that in terms of possible redosing to to kind of keep keep that slope from you know returning to that natural
history decline right well i think it goes to your first question and the need to to potentially go out further. So I think we'll see that with the six months. And I think what the trial provides as well, the upcoming trial provides six months of therapy and see what happens. And then also then coming off of therapy at six months versus continuing the therapy. So I do see your point and the slope looks the same. You're in a sense, you're at least buying time, if you will. But I think that really has a 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 two, that data is coming later at the
meeting? Yeah. Okay. Okay. Thank you. Thank you. And one moment for our next question. Our next question comes from the line of Anupam Rama with J.P. Morgan. Your line is open. Please go ahead.
Hey, guys. This is Joyce on for Anupam. Thanks for taking our question. Maybe just as a follow-up to the previous set of questions, regarding your next phase two, looking at extended dosing out to six 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. Thanks. I think at this stage, it's all, you know, 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, you know, 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. And now that we can continuously dose patients, we can actually get an answer to your question well. And with 12 months of dosing of ECOVAMENID, we will see how far reaching this increase can be and how endurable 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 this study.
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 one 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. The reason why we put this here, this is the top line. And 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 two, three 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.
Got it. Thank you. Thank you. And one moment for our next question. We have a follow-up question from the line of Michael King with Rodman and Renshaw LLC. Your line is open. Please go ahead.
Mike, we can't hear you.
Sorry, I was waiting. 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 three years as well as three to 15 years? Will they be analyzed in a stratified manner, or will they all be pooled? Do you know the answer to that?
Yeah, it's only zero to three years.
Only zero to three, okay.
And just not to get into, obviously, there is a chance that we have an effect in these other more burdened patients or 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 ICOA has in the bag potentially for zero to three years. They go after zero 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 three to 15 years. We can look at all these other patient subsets because then we understand the signal better. But we want to get out and fast and show that we are actually, we could have a dominant role in type 1. Thanks for taking the follow-up.
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 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