Welcome everyone. We are here in New York City for day two of Citi's Biopharma Back to School Summit. Sharpen your pencils, take out your notebooks. I am Yigal Nochomovitz, Senior Biotech Analyst here at Citi, and it is my great pleasure to have with me senior management from Syndax Pharmaceuticals. Of course, Michael Metzger, CEO, Nick Botwood, CMO and Head of R&D, and Keith Goldan, Chief Financial Officer. Welcome all of you. Thank you so much for doing this. Michael, obviously a lot is happening in the space. You have two FDA approvals, obviously. One of the questions we are getting recently is just how things are going with Revuforj, given now you have the expanded label. Maybe we could start there, talk about NPM1, what are the forces driving your view that you are taking a leading share of that market? Then we will go from there.
Well, thanks, Yigal. Good to be with you. Good to be back at school. Look, I think it is a very exciting time for the company and a lot going on. Really two important launches. I think what we have done, we have really reset the category in AML in terms of what a launch could look like, which is really exciting. I think people maybe missed that through the trees a little bit. But we are annualizing at about well north of $200 million for its second year of launch, which is fantastic. As you pointed out, we have two indications, KMT2A and NPM1, very broad label, best-in-class efficacy. I think the efficacy story is really resonating with physicians. Using the drug in monotherapy, in combination, and really building the Menin story and the leadership that we have exhibited is really coming through.
We are very excited about the forward, excited about what we are building with that franchise. I think NPM1 has become an increasingly important part of our story, both new patient starts and time on therapy. So duration of therapy is an important driving force behind the whole franchise. Recent Medicare data, as well as script data, indicates that we are firmly in the lead in terms of new patient starts for NPM1 as well as KMT2A. So we are really moving well, dominating, we are at 85% market share plus in the category. Thinking about relapse refractory, I do not think you can get more dominant than that, really building the business, and it is growing, right? We have shown six quarters, quarter after quarter of growth, substantial double-digit growth, and we expect that to continue.
So that is where we are today, and we are certainly going to continue to build as we get to frontline, which is hopefully right around the corner. We are really moving quickly, enrolling trials, and we will talk about how we are doing. Certainly the data that we have and the upcoming milestones, catalysts we will talk about, but really quite exciting year for us.
Okay. Just you mentioned some specifics there in terms of some of the share numbers. The 85% share—
Yeah
—that is across both categories—
It is.
—KMT2A?
It is. Yep.
Okay. All right. Getting a lot of questions about the competitive positioning with regard to NPM1. Anything there you want to share more specifically regarding the confidence you have that you are taking the lead in the market there?
Well, I think the numbers speak for themselves. We posted $55 million in the last quarter, competitor did about 9. You can see that. I do also see or are encouraged by what physicians tell us about the profile and how they are using the drug, using it as monotherapy, using it in combination with standard of care, being supported by the real-world data that we're putting out, as well as what we're producing in trials and so forth. There's a lot of support, and when we speak to physicians, they tell us we're the go-to Menin inhibitor, and we expect that to continue to build as we produce the data that we have set out to bring forward. That's really the sentiment is quite positive.
One of the other drivers, obviously, of the revenue picture is the post-transplant restarting and the maintenance there. Can you talk about that aspect of it in terms of getting to a goal? I think you've referenced something in the 70%-80% range in terms of getting people restarted on Revuforj.
Right. It's a very important dynamic, as you all know if you've been following our story. Revuforj is an opportunity to bring people to transplant in numbers that we've never seen before in AML with patients who have KMT2A and NPM1. We're seeing transplants across both indications. More transplants, of course, on the KMT2A population, and right now we're at about 50% as of last quarter, 50% of the patients going to transplant, which is remarkable. It's remarkable because it drives the ability to get into a response first, then you get to transplant, then you have the opportunity to go back on maintenance, and maintenance can extend the life of a patient and keep them in remission. That's what we're setting out to do. The target is, we tend to call it the target for maintenance.
It's really what do we think we could achieve? How many patients will go back on maintenance after transplant? We expect the transplant numbers to move up, probably not meaningfully beyond 50% of the patients, but could be higher than 50%. But really the opportunity to bring patients back 70%-80% is roughly the target. We say that because unfortunately, some patients don't make it through transplant, having nothing to do with Revuforj, but just the transplant procedure themselves. Then you have patients who have choice in the matter, and obviously there's some things that intervene and so forth. A high percentage of patients going to maintenance will continue to drive that franchise in terms of TRx, and we see that steadily increasing each quarter, and that's a very positive forward indicator for the growth.
With that dynamic, where do you see the steady state duration shaking out long term?
Yeah.
We've all loved this for the models.
Yeah, it's great for the models. Look, I think we've spoken broadly about 6 -1 2 months of duration of therapy in the relapse refractory setting, and I think we're going to be there this year for sure. What's also very encouraging, if you look at the data from the last quarter, we were seeing patients who had come back from transplant beyond. I think they were on an average of nine- plus months. Again, tracking very well to even exceed our expectations, which we were very encouraged by last quarter. We would hope that would continue to move up. No reason to say that it wouldn't. This is, again, it's an ongoing and an unfolding story, but it's very positive indicator of what could come in long-term duration.
Of course, there's a ton of interest in the earlier line you mentioned already, the frontline opportunities.
Yes.
Love to get Nick's thoughts on the structure and strategy there. You've referenced Revuforj potentially being a $2 billion product.
Yes.
I gather that includes contributions from the earlier settings.
Yes.
Maybe we could just walk through what the thinking is there in terms of getting into those earlier lines and then the strategy with the two important frontline studies you are running.
Certainly.
Yeah.
The data that we have in combination with rev in frontline standard of care for newly diagnosed patients is building. We have data sets you are familiar with, SAVE, BEAT AML, our 7+3 trials. Those phase I, II trials have grown in size and really shown us fantastic category-leading data to date. We will have updates, important data at the end of this year that will further elucidate that profile. But we think we have really de-risked the frontline opportunity quite a bit with these data. With a category-leading agent like Revuforj and the ability to move quickly to frontline and be there first with a best-in-class profile, with a lot of supporting data, it helps to just drive the story in the intermediating time between now and we get to frontline.
But as you mentioned, we believe it is a $2+ billions peak revenue opportunity in the U.S. for Revuforj and driven by a first-mover advantage and best profile. Again, that is across both fit and unfit and, of course, assumes some participation, again, in relapse refractory, a leading category in relapse refractory, but the market will probably change as we get to frontline, and we think we will have a dominant share as well. It is a long-term view, which we feel is very well supported by data to date, but maybe Nick Botwood can take us through the trial.
Yeah, that would be great because I get the question around the reason you are doing two frontline studies. That would be great to get into the details there.
Great. Well, firstly, thank you, Yigal, and a pleasure to be here. Thank you for the invitation. Very exciting time at Syndax and happy to talk about the progress we are making in newly diagnosed AML. We really feel this is the next step in terms of the life cycle of Revuforj. It is an exciting time to be on the program because we are gaining great momentum with both of those two pivotal registrational first-line studies. Very satisfying now to see sites being set up worldwide, activated, patients being enrolled, great momentum behind the study, a series of large, extensive investigative meetings around the world supporting those studies. We are making good progress, and it is exciting to see that, and we are just looking forward to those studies completing and reading out. Now let me just break them down a little bit.
I think most people are familiar, but just to remind everybody how we are approaching this, we have two pivotal studies, and then there are some additional studies that support innovation and clinical practice, which we think are important as well and could be quite differentiating. Let me start with the two pivotal phase III's. We have the EVOLVE-2 study. This is done in collaboration with the HOVON group, so an internationally renowned, well-recognized leadership group in the space of hematology, who we have been working closely with now for two years. This was the first pivotal phase III registration study to get started enrolling for a menin inhibitor, and we started in May 2025. This has been set up for quite a long time and is enrolling very well, and we are happy with the progress.
We also are working in collaboration with the BEAT AML consortium in the U.S. We have great support and it is a catalyst to enrollment, having that group now enrolling in the U.S., working in collaboration with HOVON. Just as a reminder, this study has dual primary endpoints, so they are independently powered statistically. Either one of them could lead to a positive study. One of the dual primary endpoints is complete response, and the other is overall survival. These are very clean endpoints. Overall survival is obviously the gold standard in hem-onc studies, and we hope to be able to demonstrate a survival benefit, and complete response rate is a surrogate endpoint that we believe could support accelerated approval and indeed has been used before for accelerated approvals in this setting. So that is for patients who are unfit for intensive chemotherapy.
We have a separate international phase III study called REVEAL. This is done under Syndax sponsorship. We are working with a leading CRO, Parexel, to execute that study internationally. It is a true international study, sites across the U.S., throughout Europe, and also important, Asia. So we have China, Japan, Korea, all enrolling in that study. So great momentum behind it. We are going to be at several hundred sites worldwide, and we are doing very well. This is in combination with 7+3 intensive chemotherapy. It again has dual primary endpoints. We are looking at CR, but in this instance, because the CR rate is quite high for patients that get intensive chemotherapy, it is MRD-negative CR. That endpoint has not been used for accelerated approvals in the past.
We feel we have time and sufficient data to support it as a potential for accelerated approval, and that could be quite groundbreaking and innovative, and we are working closely with health authorities to support that endpoint. The other dual primary endpoint is event-free survival. Both of those studies are going well. We have not guided on the timelines. This is a very competitive space. We want speed, we want quality, we also want a good result, so we have not guided specifically. You can probably estimate roughly where we are given the start rates and roughly the size of the studies. I would note that these studies are somewhat smaller than the competitors in the menin space, and there are specific reasons for that. Michael alluded to the strength of the data, and we can maybe talk a little bit about that.
We have generated really compelling data for both a ven/aza combination, working with BEAT-AML and MD Anderson, the so-called SAVE, but also with 7+3 intensive chemotherapy. Those are very supportive. That has allowed us to power the studies appropriately. Also our fit, newly diagnosed study is only two arms, whereas the competitor studies include three, and we made a very deliberate and conscious decision to do that, and we could maybe explain why in due course. That was the decision. So we are feeling very confident about those. I would just mention one last thing, Yigal, which is in addition to those two pivotal registration studies, we want to be differentiated and also to innovate as the leaders in the menin class. There are a couple of things that we are doing separate to that. One is called the RAVEN study.
This is a study we are doing in collaboration with University of North Carolina, Josh Zeidner. This is for patients who have KMT2A disease, where we have consistently demonstrated the best data. This is for patients that would otherwise be fit to receive intensive chemotherapy. They are actually going to get ven/aza plus revumenib with the idea of getting them to stem cell transplant without all of the comorbidities usually associated with intensive chemotherapy. So that is differentiating and we think could offer a viable alternative for those patients.
That is number one. Number two is another study I am very excited about, the MenTain study. This is a study we are doing with Corey Cutler, Shweta Gupta at the Dana-Farber Cancer Institute. This is the first prospectively randomized study specifically addressing the question of maintenance. Michael talked about the importance of maintenance, and to be clear, we do not promote maintenance.
We still have to establish the burden of proof. We know physicians want to treat their patients in a maintenance after transplant because they know that they have a high likelihood of progression. This will actually attempt to address who should get maintenance and what the benefits of maintenance are, and how you optimally manage patients. That's a kind of overview of our newly diagnosed program, and I know I was a little long, but hopefully that was helpful.
No, that's excellent. I'm gathering that the fact that you've split, as you pointed out, the fit and unfit into two separate studies, does that increase efficiency? Does that increase speed? Is there a specific reason for that?
Yeah, very briefly. That was a conscious decision, and I'm very happy with that design. It allows us flexibility. One's under our sponsorship, one we leverage the benefit of working with HOVON, which is great, and it allows us to be flexible should we need to change or amend either of those studies. I'm very happy with the model in which we're executing those.
I know you're not ready to provide timelines yet, but I guess in next year, would we get a sense as to when we may see the top line, or is it still a bit too early to know that?
Well, we may guide in due course, but for now, we're just focused on execution, and we'll see. We're feeling good about the momentum behind those studies.
Okay. There's another mutation which is less common, this NUP98. Can you just comment briefly on how you're going to get that one into the regimen?
Yeah, let me try and be brief because I get excited about all of this science and the opportunity. I don't want to go off too long because I could talk a lot about NUP98. This is a very important subtype of AML, and the reason it's exciting is because these patients are highly chemo-refractory and previously didn't have really viable treatment options available to them. We always like focusing on these areas of high unmet need. Because of the breadth and the profile of revumenib across NPM1, KMT2A, NUP98 is a little like KMT2A. It's a relatively small subset of AML, although I think actually more prevalent than we think because physicians are now increasingly looking for it. So it could be as high as 3%-5% of AML.
We presented some data at EHA in a series of about 28 patients, which is quite a lot, showing just over a quarter of those patients actually showing some sort of response, which is really encouraging for a subset of patients who are refractory to chemo who really don't have a treatment option available to them. So those data working with MD Anderson are being prepared for manuscript, and we think that that could be very important data for the NCCN guidelines committee to consider at least as to whether they meet the criteria for guidelines. Given the paucity of options for those patients, that's something we would be keen to submit to them in due course when we have the manuscript.
Okay. Well, look forward to that. Let's move on to Niktimvo for a bit. There's obviously a lot of excitement there as well, not just because of the strong launch with your partner, Incyte, but you have a very important readout coming up, which is highly anticipated in a lung disease called IPF. We'd love to understand that study a little bit. There's a lot of interest in what you need to show there to have a good target profile to take it forward. Can you introduce that to us and sort of explain how you're thinking about what you want to achieve there?
Well, again, I'm extremely excited about axatilimab and IPF, so I will try and be succinct, but it's very exciting. We could talk about it a lot, and this is an extremely promising and important study, the MAXPIRe study. To be candid, this could be a novel and groundbreaking outcome for a completely new modality in idiopathic pulmonary fibrosis, and that's important. Nobody's looked at CSF1R and its activity against monocyte- derived macrophages, which we truly believe are the underpinning pathology in idiopathic pulmonary fibrosis. This is a proof of concept trial. It's not a phase III, and this is why we do the experiments.
But when you look at the totality of the data from mouse models through the data we've already generated in patients with graft-versus-host disease and specifically the lung manifestations of graft-versus-host disease. We're going into that study, and the outcome of that study with, I would say, a high degree of confidence. The MAXBio study itself is the most robustly designed proof of concept study in the field of idiopathic pulmonary fibrosis. It's 135 patient randomized study. We actually over-enrolled by about 10 patients because of the momentum and enthusiasm in the study. It's randomized 2 : 1. It's placebo control, double blind, so we have no indication what the readout is yet. It has the most statistically rigorous approach to the derivation of the primary endpoint, which is forced vital capacity, which of course is the FDA and worldwide regulatory standard.
This is a very rigorously designed study to give the best possible indication of whether axatilimab would be a study we'd want to take into a confirmatory phase III. We talk quite a lot about what you would expect to see. In idiopathic pulmonary fibrosis, obviously we've spoken to thought leaders worldwide. We have a very eminent steering committee supporting this study. They're very excited about the potential of CSF1R inhibition in idiopathic pulmonary fibrosis. We will be focused on forced vital capacity. It's a 26-week endpoint annualized to 52. We've guided towards about 30, 40 mils. Maybe a 40% relative retention of FVC would be encouraging. I think a couple of things I would highlight. Number one is that axatilimab is particularly well-suited conceptually to treating in combination because of its unique mechanism of action.
Most of the currently approved and in development agents target more the fibroblasts that drive pathology. CSF1R is completely different. It targets monocyte-derived macrophages, both inflammatory and fibrotic. It is particularly well-suited to combination, so it could be an important addition in the armamentarium, number one. Number two is I think people underestimate the importance of tolerability. We know axatilimab is extremely well-tolerated. It is approved at 0.3 mg per kg and has a very favorable profile.
Many of the current approved standards of care are associated quite significant GI toxicities, which we know are problematic for patients, nausea, vomiting. I think you have to look at the totality of the data, the science supports it, of course, the FVC, the endpoints, the absolute difference in mils, the relative difference, but also the tolerability and importantly, the symptoms and some of the other correlatives we will look at in that study.
When we read that study out, we will report on all of that, and I think it will give us a very good sense of whether we should be transitioning into phase III. What I can say, if the study is positive and we are happy about it would be very predictive for success in phase III because of the way we have designed it. We are using the most rigorous statistical methodology to interpret the study, very similar to how the FDA design and ask for phase IIIs to be designed and interpreted. We are feeling very good about that study. We will have the data in Q4, so very soon now. We are tracking well. We are tracking to time in terms of data quality, and we are feeling in very good shape.
The patients that are enrolling, you mentioned some background therapies. You are allowing patients to enter that are on background therapies like pirfenidone, for example, as well as ones that are not. Is that-
Yes, we allow standard antifibrotics. Most of the patients, as you would expect, by far the majority are on a background antifibrotic, which I think is good because again, I think the mechanisms are very complementary. They do not overlap. We will see. We will of course, look at it by background antifibrotic and that small proportion of patients that are not on any background antifibrotic, Yigal. I think, we would like to see consistency of effect. You probably would expect a slightly bigger delta for those patients that are not on any antifibrotic. We know that from historical studies. Our expectation is we should see pretty if the study is positive, we should see pretty consistent effects across those groups, and we are feeling quite good about that. Again, when you think mechanistically about how axatilimab works.
Presuming success there, and you go into phase III, you start to think about the commercial setup. There is a sub-Q version that I believe you're working on for axatilimab. How important is that in terms of driving uptake in IPF relative to the current approved indication in GVHD?
Yeah, maybe just to comment. I think the sub-Q is going to be very helpful to the franchise. It's not the be all, end all, right?
Yeah.
I think having the drug, the activity of the drug, the profile of the drug, it well established as an IV already, and being able to deploy into this population, would be sufficient. But we have I would say plans to bring sub-Q forward, and I think it could be additive to the franchise for sure. That's a longer-term plan that we-
Okay
integrated into the development.
Speaking of moving into earlier lines of therapy, if we could go back to chronic GVHD for a second, there's another important study, which I also believe is reading out by the end of the year in combination with Jakafi. Could you just speak to that, and what the benchmarks are there in order to advance the combo?
Yeah, briefly. This is a study we're doing in collaboration with our partners, Incyte. It's an important study because steroids, dexamethasone, is the current standard of care for frontline GVHD, but it comes with significant morbidity, and this is a potential steroid-sparing approach. We have another study, again, working with Incyte, in combination with dexamethasone, which is a pivotal phase III with an event-free survival endpoint. So that's also an important study, but this is a different approach. It's a proof of concept phase II. It's three arms, dexamethasone, Jakafi, and then the combination of Jakafi and axatilimab. Our hope and expectation is both of the experimental arms will be better than dexamethasone. The question is, does axatilimab add over and above what you might expect with Jakafi alone?
Now, the response rate at six months might be quite high for both of those arms, and it may be important, the addition of axatilimab may actually contribute to the durability of that response. I think that's going to be important. six months may be too soon to show a benefit. We'll see. But I think that both of those will potentially be better than dexamethasone. We're hopeful that the combination will add something over and above Jakafi alone, and that may be manifest by, number one, the response rate, but importantly also the duration of the response, the time that patients are able to stay off steroids, and also potentially, in due course, event-free survival. We'll have those data again in Q4. Important proof of concept, and that will inform clinicians about how best to manage their patients.
When the frontline study reads out for axatilimab in combination with dexamethasone, that provides a variety of options to select from, whether patients want steroids, need steroids, maybe they could have Jakafi or a combination of Jakafi and axatilimab. We're really covering all of the bases there.
That would inform, I gather, a longer phase III trial once you get the clarity there?
It do. When we see the results, we'll look at them with Incyte, and we'll make a decision based on the landscape and the other options at that time.
Okay. Important other topic is, you had your R&D day, I guess it was earlier in the summer, and you introduced some new topics. One of which was this interesting drug that targets EGFR, which is a new area, at least from our perspective. Would you love to hear your thoughts on that in terms of the design of that molecule, how it's different. It has this allosteric inhibition feature, which is apparently unique relative to the class. Can you just talk through the design there and the strategy?
No, thank you, Yigal. This is a new topic and incredibly exciting. New to Syndax, maybe not so new to me because I've spent 20 years looking at targeted agents in EGFR mutated lung cancer. I cannot underestimate the excitement and the importance of having a drug that is unique and targets a completely different binding pocket on the EGFR receptor in a disease like lung cancer. This is an incredible opportunity to validate an entirely new hypothesis, which we have seen before in diseases like melanoma with allosteric inhibition and leukemia with allosteric inhibition, but it's never been shown before in lung cancer. Very proud to be working with leading scientists and clinicians at Dana-Farber who have again been pioneering. They were involved in the original discovery of the activating mutation in EGFR. This is novel. They've been working on it for many years.
This is almost their fourth generation. It is a highly potent allosteric inhibitor that we believe could be very good in osimertinib-refractory patients and potentially in combination with osimertinib. We are progressing it now through the IND-informing studies. We have said we should anticipate having it in clinic in 2027. The really exciting thing about this particular development program, because we are taking it in as a monotherapy, we would expect to see activity quite early on in the development program. We will have a dose escalation, as typical in a first-time-in-human study, but we will very quickly from dose one onwards, get to doses that we would consider therapeutic. The first time, should we see responses either in the lung or in the CNS metastases, that will be validation of an entirely new concept and hypothesis in lung cancer, which is incredibly exciting new science.
This is a drug that could be very, from the preclinical models, could be particularly well suited to patients that have resistance mutations to osimertinib. We know that patients with L858R subtype of EGFR do particularly poorly. We know that from the FLAURA study and FLAURA2 with osimertinib, which was an OC chemo combination. This study has shown preclinical activity in patients with, for example, C797S, which is a common resistance mutation for osimertinib. That will be our intent going into the first time in human and then dose expansion. Very exciting new science and opportunity for Syndax. Couldn't be more pleased to get that into the clinic next year.
Would this have applicability in the broader set of what people are calling these atypical EGFR mutations? Is there the potential there or that is still to be-
Yes, we are going to learn a lot, Yigal, about this. What we have shown and what Dana-Farber have shown is that the classical exon 19 and exon 20 don't exhibit the allosteric binding pocket. There is an alpha helix in the receptor that obstructs it. But for L858R, which is the highest unmet need, and some of the other atypical mutations like L861 and other common ones, this drug has very profound activity. Also in preclinical models of, again, C797S, so refractory models to osimertinib, again, very, very good activity because it is binding a completely separate binding pocket. If you think about all of the other drugs that are in development in EGFR-targeted disease, and there are many of them, all of them are targeting, chasing resistance mutations in the catalytic binding pocket. This targets a completely separate binding pocket.
The other beautiful thing about this hypothesis, which we've shown in the preclinical models, is the potential to double drug. So by combining osimertinib, and we'll look at this in our phase I expansion, osimertinib with SNDX-4321 could potentially really block that receptor. Yigal, we'll learn as we go into the phase I and expansion, who are the patients that are most likely to benefit? We know there are some types of resistance that may escape the receptor, like c-MET, and we'll look at that, whether c-MET amplification are not the patients you want to target. But this is such a high area of unmet need, and there are many patients with these types of diseases. We're not talking about small populations. This is unfortunately a very common disease and a high unmet need.
We think this could be an incredibly valuable opportunity if we're able to validate its activity. Based on all of the preclinical data and the very clean profile that we're beginning to now show through all of the R&D informing studies, as we take that into the clinic, I think it bears much promise.
Another topic you introduced, I believe, recently is the SNDX-62122 in myelofibrosis. So if you could speak to the thinking in terms of the therapeutic hypothesis there regarding menin inhibition in MF and what your clinical strategy is.
Yes. Briefly, again, I think nice demonstration of our leadership in the menin class. We were the first working with John Crispino and collaborators to show the potential for menin in myeloproliferative neoplasias. This was based on a hypothesis around thrombocytopenia, and then on trying to understand mechanistically what was driving that. Through the very elegant work that John did that got Best of ASH last year and is now published in "Cancer Cell," he and his collaborators were able to show that actually normal megakaryopoiesis is dependent on the menin scaffold complex, and that there are certain genes that are transcribed, so MEIS and MEF2C, that are very dependent on that menin complex, which if you inhibit, then you can actually reduce normal megakaryopoiesis, which is one of the pathologies in myeloproliferative neoplasias that drives all of the issues like thrombocytopenia, platelet dysfunction, anemia, and splenomegaly.
He's shown this in vitro and in mouse models. We're working with John Mascarenhas, the MPN Research Consortium, to test this hypothesis with revumenib, and at the same time progressing SNDX-62122, which is a new and novel menin inhibitor. It's optimized for many aspects of its profile that we think could be particularly well-suited to patients with diseases like myelofibrosis. We should have that in the clinic next year as well. It's progressing through IND and forming studies. This is a potentially very exciting lifecycle management opportunity for us in a new setting, where we could generate proof of principle with revumenib and then rapidly follow that, taking all of the learnings with SNDX-62122. So another nice opportunity for us to demonstrate our scientific leadership in menin inhibition.
Then just to close out here, Michael, if you could speak to what we should expect at ASH briefly, and then a question we've been asking all the companies, AI, obviously a big topic, but to what extent are you using AI at Syndax, either just to improve efficiencies internally or with regard to filings or other aspects of the company?
Yeah. Nick highlighted the programs and all the excitement on the pipeline. I think ASH for us is always a very big meeting, wraps up the year, and we're doing a lot of work to get ready for that. Certainly, the presentations on the frontline, newly diagnosed patients, both updates to SAVE, updates to BEAT AML, and our 7+3 combination trial, those will all be updated. We're excited about things like overall survival. Looking at that over a longer horizon really should continue to de-risk our frontline trial. So very important real-world data as well that we'll be presenting. So more to come. You'll see the abstracts, I think, on November 4th. But we're excited about how that's looking for us. Certainly, I think as we think about the pipeline, the excitement around beyond ASH, I'll just make a comment that the pipeline's starting to really bear fruit.
It's a first and best-in-class approach, much like what we've done with Revuforj and Niktimvo being approaching really high unmet need areas and bringing the best science forward. So we're excited to not only conduct trials, but get data early that could be quite informative and exciting. So that's to come, so more on the horizon. Then maybe I'll ask Keith if you want to comment on the AI topic. Thanks.
Yeah. Thanks, Michael. I would just say briefly, we're using AI probably like every company is, just to improve individual performance. I think more importantly, using it where we have large data sets, and those large data sets may be in commercial, medical, pharmacovigilance, biostat, or biometrics, where we want to look for signal detection in those large data sets, which would be otherwise very time-consuming or impossible. That signal detection can yield valuable insights. So that's probably where it's most valuable to us.
Okay. Good to hear. Well, we look forward to attending ASH and seeing the next layer of data. So thank you all very much.
Thanks, Yigal. Great to be here.
Thanks, Yigal.