Curis - Q1 2024
May 7, 2024
Transcript
Operator (participant)
This call is being recorded on Tuesday, 7th May, 2024. I would now like to turn the conference over to Diantha Duvall. Please go ahead.
Diantha Duvall (CFO)
Thank you, and welcome to Curis's first quarter 2024 business update call. Before we begin, I would like to encourage everyone to go to the investor section of our website at www.curis.com to find our first quarter 2024 business update press release and related financial tables. I would also like to remind everyone that during the call, we will be making forward-looking statements, which are based on our current expectations and beliefs. These statements are subject to certain risks and uncertainties, and actual results may differ materially. For additional details, please see our SEC filings. Joining me today on today's call are Jim Dentzer, President and Chief Executive Officer, Bob Martell, Chief Scientific Officer, and Jonathan Zung, Chief Development Officer. We will also be available for a question and answer period at the end of the call. I'd now like to turn the call over to Jim.
Jim Dentzer (President and CEO)
Thanks, Diantha. Good morning, everyone, and welcome to Curis's Q1 business update call. This quarter, we made significant progress in advancing emavusertib in our three key areas of focus. First, as a monotherapy in patients with relapsed refractory AML with a FLT3 or splicing factor mutation in our TakeAim Leukemia study. Second, as a doublet therapy for patients with relapsed refractory primary CNS lymphoma, combining emavusertib with ibrutinib in our TakeAim Lymphoma study. And third, as a triplet therapy in frontline AML for all comers, regardless of mutation status, that combines emavusertib with azacitidine and venetoclax. Next Tuesday, in connection with the EHA conference's publication of accepted abstracts, we expect to provide a top-line update of clinical data from our TakeAim Leukemia study.
Previously, we had disclosed data for five patients, three patients with a FLT3 mutation and three patients with a splicing factor mutation, including one patient with both a FLT3 and a splicing factor mutation, who was included in both populations. Our update next week will report data for 25 new patients, bringing the total to 30 relapsed refractory AML patients treated with emavusertib as a monotherapy. The mutation status for these patients is 12 patients with a FLT3 mutation and 20 patients with a splicing factor mutation, including two patients with both a FLT3 and a splicing factor mutation, who are included in both populations.
We look forward to discussing the top-line data for these patients on an investor call when the data are released, followed by more detailed presentations at the ASCO and EHA medical conferences that more fully explore emavusertib's potential to outperform, as a single agent, the benchmarks for existing therapies in genetically targeted AML populations. In the relapsed refractory FLT3 population, the benchmark for FLT3 inhibition is gilteritinib, which its FDA label demonstrates can achieve a 21% CR/CRh rate in patients who have failed frontline therapy. With emavusertib, our goal is to beat that benchmark. We think this is possible, even though the majority of patients in our study have failed prior treatment with a FLT3 inhibitor. Because unlike existing treatments, emavusertib targets both FLT3 and IRAK4, the escape path for FLT3. This is the central hypothesis of the molecule's design and is demonstrated in the preclinical data.
With the 12 patients we'll be showing at ASCO and EHA, we hope to further support that hypothesis, namely, that emavusertib has the potential to establish a new and best-in-class benchmark for the FLT3 AML population. As we move to the relapsed refractory splicing factor population, we find that the benchmark is, unfortunately for these patients, far lower. There are no drugs approved, expected survival is only a few months, and existing treatments are ineffective. The only study published for relapsed refractory AML patients with a splicing factor mutation was for patients treated with the Azaven doublet. It was a very small study with only five patients, and the response rate was zero. This is especially notable as Azaven is standard of care in frontline AML for patients ineligible for intensive induction. We hope emavusertib's novel mechanism can show clear single-agent activity in this very challenging population.
Anything that shows emavusertib can beat the 0% benchmark set by Azaven would be positive. In our expanded data set, we'll be looking for blast count reductions, neutrophil increases, platelet increases, objective responses, and ultimately, of course, extended survival. As we turn to our TakeAim Lymphoma study, we see significant progress there as well. At the most recent ASH conference, we presented data for five patients with relapsed refractory primary CNS lymphoma, who had failed prior treatment with a BTK inhibitor. We expect to provide an update with additional data later this year, most likely at the ASH conference in December. Previously, we have said we expected to report data on 10-15 patients.
Today, we are pleased to refine that estimate to the high end of the range, as we now expect to report data for approximately 15 relapsed refractory primary CNS lymphoma patients, who have failed prior treatment with a BTK inhibitor. We are also pleased to announce the advancement of our triplet study in all comers in frontline AML. We have begun enrollment and expect to have preliminary safety data later this year. Again, most likely at the ASH conference in December. The excitement around this frontline study stems from the novel targeting of IRAK4 and builds upon the clear anticancer activity we are seeing in our monotherapy studies. We know IRAK4 is an important target in AML and that neither azacitidine nor venetoclax addresses it.
So the logical next step is to explore the ema-aza-ven triplet and its potential to establish a new benchmark for frontline therapy in all comers in AML. In summary, we're encouraged by our progress across the board in leukemia and lymphoma, and we look forward to reporting our updated leukemia data next week. With that, I'll turn the call back over to Diantha to review our financial results for the quarter. Diantha?
Diantha Duvall (CFO)
Thank you, Jim. For the first quarter of 2024, Curis reported a net loss of $11.9 million, or $2.05 per share, as compared to a net loss of $11.6 million, or $2.39 per share for the same period in 2023. Research and development expenses were $9.6 million for the first quarter of 2024, as compared to $9.1 million for the same period in 2023. The increase in research and development expenses were primarily attributable to higher employee-related costs. General administrative expenses were $4.9 million for the first quarter of 2024, as compared to $4.8 million for the same period in 2023.
As of 31st March, 2024, Curis's cash, cash equivalents, and investments totaled $40.7 million, and there are approximately 5.9 million shares of common stock outstanding. We continue to be in a solid cash position and expect that our existing cash, cash equivalents, and investments should enable us to maintain our planned operations into 2025. With that, I'd like to open the call for questions. Operator?
Operator (participant)
Thank you, ladies and gentlemen. We will now begin the question and answer session. Should you have a question, please press the star followed by one on your touchtone phone. You will hear a prompt that your hand has been raised. Should you wish to decline from the polling process, please press the star followed by two. If you are using a speakerphone, please lift the handset before pressing any keys. One moment, please, for your first question. Your first question comes from Soumit Roy with Jones Research. Please go ahead.
Soumit Roy (Managing Director and Head of Healthcare Research)
Everyone, and congratulations on progress on multiple fronts. Really, really clearly presented. A couple questions on the data, expected data next week. I don't know if I missed it, are you going to present data for both the FLT3 mutant and splicing mutants in the relapsed refractory setting? And what kind of details could we expect? Are you gonna give us fair details around baseline blast count levels, how much % reduction and, response rate, neutrophil recovery, et cetera?
Jim Dentzer (President and CEO)
Hi, Soumit. Thanks for joining. So yes, we are absolutely going to be presenting data for both the FLT3 and the splicing factor mutation populations. It is gonna be a top line review of data. Obviously, we need to be a little sensitive to the conference. We can talk to the abstract, but of course, we're gonna need to wait for the poster to come up to have the more detailed discussion. So, we think there's some exciting news next week. We're looking forward to talking about it, and we look forward to having the conversations at both ASCO and EHA at a more detailed and granular level.
Soumit Roy (Managing Director and Head of Healthcare Research)
Totally understandable. My last question is around path forward for the splicing mutant patient population in the relapsed refractory setting. So the FLT3 population, I think the registration path is much clearer. On the splicing mutation, how are you planning to go forward? Are you going to develop any companion diagnostic, or is it included and fairly routinely screened for that mutation? If you can give us any color.
Jim Dentzer (President and CEO)
Sure. So we need, of course, to have a discussion with FDA. So I want to be careful here that we're giving you our thoughts, but it's gonna really depend on how the conversation with FDA goes. The complicating factor here, I would say, at the highest level, when we think about the design of the study, is we need to put into context nothing is approved.... Because nothing works. This is the first drug that's shown single agent activity in this population.
So whether or not the FDA looks for something like an objective response rate, whether they look for survival, whether they want a single arm study or whether it would be comparing to something else, all of these questions are great questions, and we've got some thoughts on those, but it's really gonna depend upon a conversation with FDA. So I, I'm gonna have to hold off on that one a little bit. If we go forward, and we think about any new genetically driven population, I think it's fair to assume that we're gonna need a companion diagnostic. Again, that will depend on the conversation with FDA of what the timing is for that and how that gets incorporated into a pivotal study. But I'd say stay tuned.
Soumit Roy (Managing Director and Head of Healthcare Research)
Got it. And if I may sneak in one last question, is around the bar to beat for the relapsed refractory FLT3, you mentioned gilteritinib with CR rate of 21-ish%, but those weren't FLT3-experienced patients. So in our mind, the bar to beat was more like 11, 12% response rate. Is that fair, or are you setting up a high bar for yourself?
Jim Dentzer (President and CEO)
Yeah, actually, Bob's maybe the best person to talk to that. Bob, would you mind jumping in?
Robert Martell (Chief Scientific Officer)
Yeah, thanks, Jim. I agree, Sumit. You know, the bar in terms of, you know, what we might expect from a new drug in targeting FLT3 in this area would be much lower than 21% because obviously, these patients have demonstrated resistance to FLT3 inhibition. And that's exactly where emavusertib is so critical because targeting IRAK4 is key. The TLR pathway, as you know, is strongly upregulated following FLT3 inhibition. In fact, TLR signaling through IRAK4 is a resistance mechanism, and that's why we think even though a patient has had resistance to FLT3 inhibition, we can rescue that with this combination. The 21%, you know, we don't know what the FDA will require as the hurdle for this.
We presented that as a prior precedent for approval of gilteritinib in the earlier line of therapy. It may be that they would accept lower than that. And so that really, as Jim mentioned, will require some discussions with them.
Soumit Roy (Managing Director and Head of Healthcare Research)
Thank you for taking all the questions. I'm looking forward to the data next week.
Jim Dentzer (President and CEO)
Thank you.
Operator (participant)
Your next question comes from the line of Li Watsek with Cantor Fitzgerald. Your line is open.
Li Watsek (Biotech Analyst)
Hey, good morning. Congrats on the progress. Just a couple questions here. Should we expect additional set of data at EHA conference relative to the abstract data cuts? And then maybe comment on whether we're gonna see some MRD data and what will be the median follow-up?
Jim Dentzer (President and CEO)
Thank you, Lee, and I appreciate the question. So yes, there, there certainly will be additional detail at, at both conferences compared to what's in the abstract. So, similar to my answer to Sumit's question, we're gonna have a discussion about top-line detail, next week, and we're really looking forward to that, but it's gonna be limited to data that are in the abstract. There is by, by definition, as you can, as you can imagine, there's gonna be much more detail that comes, at the posters and in the presentations at ASCO and EHA.
Li Watsek (Biotech Analyst)
Okay. And the median follow-up?
Jim Dentzer (President and CEO)
Let's wait and have a discussion about the data when the data are released, if that's all right.
Li Watsek (Biotech Analyst)
Okay, that's fair.
Jim Dentzer (President and CEO)
Great.
Li Watsek (Biotech Analyst)
And then, if I recall correctly, these patients have less than two prior lines of therapy. Maybe just expand a little bit on what these treatments are for both FL, FLT3 and splicing patients enrolled in the study, and how should we think about the impact of prior lines on the response to this?
Jim Dentzer (President and CEO)
Yeah. Yeah, thank you. So it's actually less than three prior lines coming into the study.
Li Watsek (Biotech Analyst)
Okay.
Jim Dentzer (President and CEO)
So yeah, typically in AML... Well, actually, you know what? Bob, maybe you're the better person to talk about the lines of therapy that typically happen in these patients in AML.
Robert Martell (Chief Scientific Officer)
Yeah, so, right. So oftentimes, patients with a FLT3 mutation may get some cytotoxic intensive chemotherapy upfront or a lesser intensive, but generally, they will have had prior FLT3 inhibitor, like we were just discussing, a bit ago. Patients who are very fit and eligible for intensive induction oftentimes will get that therapy, but those patients, once they fail, would go on to Azacitidine therapy. And then all of the patients who really are not eligible for intensive induction will get Azacitidine. So as you may know, patients who fail or progress on Azacitidine or are resistant to that have extremely poor outcomes. There's been a couple of studies that have looked at outcomes following failure of Azacitidine, and the survival in both of those studies is about two to three months.
across the board on those patients. So really a difficult population to treat. And, you know, our data should be viewed in that perspective as well, which we're really excited about.
Li Watsek (Biotech Analyst)
Thank you.
Operator (participant)
Your next question comes from the line of Yale Jen with Laidlaw. Your line is now open.
Yale Jen (Senior Managing Director and Senior Biotech Analyst)
Good morning, and thanks for taking the questions. I just want to tap on the last question, just ask, which is, you mentioned that the Azaven is the, I guess, third line for FLT3 inhibitor patients. So you mentioned about the survival. What, what about the ORR? Because I think that probably would be a benchmark actually you might have to compare it to as well.
Jim Dentzer (President and CEO)
Yeah. Actually, again, Bob, you're probably better to take that one.
Robert Martell (Chief Scientific Officer)
So the response rate. So there's not a lot of data on splicing factor mutation post post-Azaven. There is one really interesting study looking at first-line treatments with AML that demonstrates splicing factor mutations have an extremely low response rate. So patients who don't have a splicing factor mutation have approximately 80% response rates, and only maybe 20% who can achieve that, whereas almost 80% of the patients with a splicing factor mutation are unable to achieve a CR in the first line. It's dramatically, dramatically reduced. In terms of a FLT3 subset of population, that is roughly similar, although there aren't as detailed data on that. Does that answer your question?
Jim Dentzer (President and CEO)
Yeah, and that was frontline, by the way, Yale.
Yale Jen (Senior Managing Director and Senior Biotech Analyst)
Mm-hmm.
Jim Dentzer (President and CEO)
Um, so-
Yale Jen (Senior Managing Director and Senior Biotech Analyst)
Yeah.
Jim Dentzer (President and CEO)
Of course, in relapsed refractory, it gets far worse across the board, right? So it's one of the reasons why we're excited about the populations that we're going after, is that they're so underserved. The hurdle to show something is lower, and we're excited to talk about the age and activity that we're seeing in that population. Again, it's relapsed refractory in our case, not frontline, even though in both settings there's a dramatic drop-off in performance for existing therapies.
Yale Jen (Senior Managing Director and Senior Biotech Analyst)
Right. And, it's just a hypothesis to think whether these patients will be... I mean, in these patient population, would you anticipate potentially accelerated approval pathway if the data was robust?
Jim Dentzer (President and CEO)
So it's interesting that you say that. We look at the precedence in AML, specifically for gilteritinib, for IDH1 and for IDH2. In all three cases, the FDA approved those drugs on, for trials that were single-arm studies based on a CR/CRh endpoint, and that led to full approval, not even accelerated approval. So, you know, we can't, of course, put words in the FDA's mouth. We need to have the discussion with the FDA, but we believe that those precedents reflect an understanding at FDA that these diseases are really underserved by existing therapies, and these patients are in need of new therapies.
So our hope would be that if we can bring a data set to FDA that can show that we can see single-agent activity and pair it with, you know, early but still indications of survival, that the FDA will hopefully be in a position to agree to a registration path that can get these drugs in the hands of physicians and patients as quickly as possible.
Yale Jen (Senior Managing Director and Senior Biotech Analyst)
Maybe last question here, again, a little bit forward-looking type of thoughts, which is that in terms of the FLT, FLT3 patients, would you—I mean, if the data is robust, would you consider a combination? And, or in other words, to move up to the first line instead of in the refractory patients at this stage of development? And thanks.
Jim Dentzer (President and CEO)
Yeah. So in fact, the answer is we've already started that, right? And it's not just for FLT3, it's for all comers, whether you have a FLT3 mutation or not. And the reason for that, of course, is that, you know, our, our drug, emavusertib, does target FLT3, but it also targets IRAK4. It targets the CLKs, CLK1, 2, and 4, targets DYRK. I mean, this is a multi-targeted drug that hits a number of targets of interest in the context of AML. So, and that is precisely why we've, we've already started the frontline study, the triplet study of EMA in combination with Azaven.
So our hope would be with this initial study, that we can show safety, and with those safety data in hand, by the time we get to year-end, we'll be in a position to have the drug be what I would call partner-ready. We'll have a mature data set in splicing factor patients and FLT3 patients as a monotherapy, and we will have shown, hopefully by the time we get to ASH, and even though it's just in a handful of patients, that adding ema to the azaven doublet in frontline is safe. And if we can do that, I think we can make the case with the regulatory authorities that we are prepared to go simultaneously in the relapsed refractory setting as a monotherapy and a frontline setting in combination.
I think we'll be in a position to have a conversation with partners to get access to, obviously, non-dilutive financing, but access to a broader clinical infrastructure so that we can accelerate the pace of clinical development and increase our ability to maximize commercial launch. All of those things are part of our thinking at this point in time.
Yale Jen (Senior Managing Director and Senior Biotech Analyst)
Okay, great. That's very helpful, and we look forward to see the data next week. Congrats.
Jim Dentzer (President and CEO)
Thank you very much. Appreciate it.
Operator (participant)
Your next question comes from the line of Billal Jahangiri with Curis. Your line is open.
Billal Jahangiri (Senior Equity Research Analyst)
Hi, congratulations on all the progress. I have a couple questions here. Your split for FLT3 and spliceosome patients inside the study, is that representative of the real world? And then also, I'm gonna move on over to the triplet study. Is there a way to, I don't know, maybe pick a subgroup of patients to de-risk on the safeties, since this is the first time we'll be seeing this triplet? And I guess that's-
Jim Dentzer (President and CEO)
Yeah.
Billal Jahangiri (Senior Equity Research Analyst)
My question. And then for PCNSL, are you guys still enrolling by BTK, BTK naive patients as well, so that we can compare and contrast those two data sets between experience and naive later this year?
Jim Dentzer (President and CEO)
Yeah. Thank you. Appreciate it, Bill, and thanks for joining us. So let me try and knock off those three questions in a row. So first, the split on FLT3 patients versus spliceosome patients. So this one is really, really interesting, and I think it reflects the unmet need in AML. Both of these studies are recruiting quickly. As you may recall, we came off our partial clinical hold mid-year last year, got our sites up and running, and we are seeing really strong enrollment rates across the board at our sites. There's a real pent-up demand in AML for a novel target. In particular, as you note, the pace of spliceosome has been really interesting. So FLT3 constitutes roughly a third of AML. One-third of AML patients have a FLT3 mutation.
Patients with a splicing factor mutation make up a much smaller portion of that community. Maybe 10% of AML patients have a splicing factor mutation, and yet that has outpaced enrollment in FLT3, and I think it's precisely what we said: There are no drugs available. Not only is nothing approved, nothing works for these patients. This is the first time people are seeing activity, and to see that kind of activity with a single agent is really compelling. So we look forward to sharing our results with you next week in those two populations, and we look forward to having the discussions with FDA, as well. We've got to our data set in 20 patients with spliceosome.
We're gonna add another couple in FLT3 and follow these patients and take those data to the FDA and begin the discussions on registrational design, and we're looking forward to that.
The second question was about triplet safety. So, the design of this study, as you may remember, I think is really interesting, and it's all about, as I mentioned to Yale, ensuring that our leukemia program is partner-ready. So we will have, by year-end, mature datasets in two distinct genetically driven populations in FLT3 and splicing factor mutation. The study we just started in triplet is a study that enrolls patients who are currently on Azaven in the frontline setting, who have achieved CR, but are still MRD positive. We're gonna then take those patients into the study and add emavusertib to their therapy, turning the doublet into a triplet.
Of course, what we're hoping is that we can see efficacy and get those patients to MRD negativity. But the key is that we will have been able to isolate the safety effect of adding emavusertib to that Azaven doublet, to the current standard of care. So that by the time we get to year-end, obviously, we're always hoping to see signs of efficacy, but what we really want to be able to say is: We've got a drug that's hitting a novel target in IRAK4. That novel target clearly matters because we're seeing single-agent activity. We know that the existing standard of care of Azaven doesn't hit it, and then we hope to add to the discussion by year-end, we can add a drug, emavusertib, to that doublet that allows the current standard of care-...
to address this new novel target of IRAK4, and we would hope, of course, that we would then see in the clinic, in that setting, what we saw in the preclinical data, which is we have the potential to establish a new benchmark and establish a new standard of care in frontline therapy and AML across the board, all comers, FLT3 mutation or not. Then your third question was on BTK-naive patients in the study in lymphoma. So just as a reminder, we have tested the combination of emavusertib with ibrutinib in multiple indications within an NHL, and specifically with primary CNS lymphoma in BTK-naive patients, as well as BTK-experienced patients.
You know, the underlying logic of the drug is that patients who are on ibrutinib or NHL patients who are on ibrutinib, are on it precisely because it allows them to down-regulate NF-kappa B overactivity by blocking the BCR pathway. There are two pathways that are driving NF-kappa B overactivity in these patients. There are a lot of BTK inhibitors today. There's only one drug that blocks TLR pathway, that second pathway, driving NF-kappa B overactivity, and that's emavusertib. Now, our view would be blocking both of those pathways that are driving NF-kappa B, which is driving disease in NHL. Blocking both pathways is always going to be better than blocking either one alone.
So if we can then take that mechanistic logic into the preclinical setting and see the hypothesis is supported, which we've already done, and now go into the clinic and compare and contrast, as you say, BTK-naive and BTK-experienced patients, being able to show both is good, and we already have, but we think it's even more powerful. We. If all we had were BTK-naive patients, someone might wonder whether the efficacy was coming from the BTK inhibitor. But because we know these patients are on a BTK and then fail, either relapsed or refractory, you would, of course, expect that to immediately rechallenge them with ibrutinib yet again, the response rate is probably gonna be zero.
So if we can show that we can get activity in those patients, even though they've just failed BTK, then it's obviously either the performance of emavusertib alone or emavusertib's synergistic combination with BTK and its ability to resensitize patients to BTK that is driving that. And so we think that's a really powerful thing to do. Thank you for asking that question.
Billal Jahangiri (Senior Equity Research Analyst)
I guess-
Jim Dentzer (President and CEO)
That was pretty long. I hope it, I hope it answered your question thoroughly.
Billal Jahangiri (Senior Equity Research Analyst)
It did. It did. I just... One more on the comparison front, but back in the triplet.
Jim Dentzer (President and CEO)
Yeah.
Billal Jahangiri (Senior Equity Research Analyst)
I know, it's meant to be safety, but, I guess just for those of us who this is our job, right? So how would we—It would be unethical of you to not give emavusertib to some of these patients for the sake of comparison, right? So are there any historical benchmarks that you can point to for-
Jim Dentzer (President and CEO)
Oh, sure.
Billal Jahangiri (Senior Equity Research Analyst)
patients who get Azaven and then have MRD positivity and how they fare off, just so that we have something to compare it to when that time comes?
Jim Dentzer (President and CEO)
Yeah. Actually, within the leukemia setting, Bob, maybe you're a better person to talk to that.
Robert Martell (Chief Scientific Officer)
Yeah. I don't have the details right in front of me, but clearly there, it's a major problem for AML and induction because if a patient continues to have molecular evidence of disease, that implies that the disease has not been taken care of. So you know, a significant portion of patients are able to get to MRD negative, but there's also I'd say a significant majority of patients who can't achieve that, who maybe they achieve a CR or a CRh, but when we do a molecular analysis, it is not MRD negative, and that correlates very strongly with relapse. And so that's what we're ultimately would be looking to achieve.
In this early study, like Jim said, we're looking mainly for safety, and so, you know, we don't have that as a goal for this particular study, but ultimately that would be the long-term goal, ultimately in earlier, sort of upfront situation, where we would start out the study in combination with Azaven from the beginning.
Billal Jahangiri (Senior Equity Research Analyst)
Thanks. Appreciate it.
Operator (participant)
Your next question comes from the line of Sean McCutcheon of Raymond James. Your line is open.
Jean McCutcheon (Director of Biotechnology Equity Reseaarch)
Hey, guys. Thanks for taking the question. Definitely look forward to the top line next week. Correct me if I'm wrong, but you've said previously that, you know, the potential pivotal cohort in the relapsed refractory AML setting, you're probably gonna end up having to go after either FLT3 or spliceosome in a single study with the co-mutations maybe going into the same bucket. So first, is this consistent with your current understanding or your current plan? Can you walk us through, you know, the decision between FLT3 and spliceosome in that context? What factors you're considering? Obviously, FLT3 a bit more well-established in terms of the scale and scope of a data set that you'll need. Thanks.
Jim Dentzer (President and CEO)
Yeah. No, thank you, Sean, and thanks for the question. So yes, you're right. In the past, we have certainly said that, and I would say the same thing today, with the very significant caveat that we need guidance from FDA on this issue. Our expectation is that, you know, it's very clear for patients that have a FLT3 mutation only or a splicing factor mutation only, they're gonna go into their respective studies. And as we've talked about, it's roughly 1/3 of the population in AML has a FLT3 mutation, and roughly 10% have a splicing factor mutation. There are a small number of patients, and we've seen it. You know, in our 30 patients, we've got two. So there are gonna be a small number of patients who would qualify for both studies.
And I suspect, again, we haven't had that conversation with FDA, but I suspect what they're gonna ask is that we put patients with dual mutation in one study and not in both studies. But we need to have that conversation with them to make sure that that's what they'd like to see. How you decide which one they go in, you know, that's, again, that's gonna be a subject of discussion with FDA, but those patients would presumably be eligible, for both populations.
Jean McCutcheon (Director of Biotechnology Equity Reseaarch)
Yeah, thanks. Just a quick point of clarification. Sorry if I missed this, but will the EHA and the ASCO data sets be the same data cut?
Jim Dentzer (President and CEO)
Yes, is the short answer to that question. It's the same data cut for both populations. We'll talk about that more, next week when the data come out, but absolutely. The, they're gonna be different presenters at both conferences. You know, sort of the behind-the-scenes story of working at a biotech company and managing a novel target is that you... high-class headache. You get a lot of physicians, on both sides of the pond that wanna present your data. And so we're gonna have different people at different conferences, but the data set, the data cutoff is the same.
Jean McCutcheon (Director of Biotechnology Equity Reseaarch)
Great. Thank you.
Operator (participant)
There are no further question at this time. I'll turn the call over to Jim Dentzer. Please continue.
Jim Dentzer (President and CEO)
Thank you, operator. And as always, thank you to the patients and families participating in our clinical trials, to our team at Curis for their hard work and commitment, and to our partners at Aurigene and the NCI for their ongoing help and support. We look forward to updating you again soon. Operator?
Operator (participant)
Ladies and gentlemen, this concludes today's conference call. Thank you for your participation. You may now disconnect.