Syndax Pharmaceuticals, Inc. (SNDX) Earnings Call Transcript & Summary

Hey, everyone. So thanks for joining us this afternoon. We're so excited to have the team from Syndax Pharmaceuticals here today to tell us kind of an update on where things are, where things are headed. So I'll let Mike Metzger give us some introductory remarks, then we'll just dive right in.

Great. Well, thanks, Madhu. Thanks to the Goldman team for inviting us to the conference. It's a great venue. Great to see people in person. So I appreciate that. So most of you are familiar with Syndax, but just a reminder, we're a targeted oncology company, developing 2 agents in our pipeline, both are in registration trials for relapsed/refractory disease. Importantly, we have the opportunity to bring data -- pivotal data in 2023, the first half of 2023. So that's in the next 12 months as well as have regulatory filings, 2 regulatory filings in 2023. Both assets are poised to be first to market and best in class and address multibillion-dollar markets. So big opportunities. We did present positive data most of you know last year at ASH on both of these programs, so highly supportive of what the thesis is here. The first drug is known as Revumenib. We'll discuss that today, SNDX-5613. It's a small molecule inhibitor of the menin-MLL1 interaction targets specific patients who have either an MLLr or MPMC mutation. And these 2 distinct lesions actually account for about 40% of AML, so a big opportunity. And it will be the first drug to actually specifically target these mutations. The life cycle opportunities for both of these drugs are vast. Specifically on the menin side, the opportunity to get into frontline setting is something we're exploring. We also recently announced that we're going to start a colorectal cancer or solid tumors at the end of this year. And then the second molecule is axatilimab. It's a CSF-1R antibody. We're developing that in chronic graft versus host disease. We'll also be starting an IPF trial as a life cycle extension of that program at the end of this year. We recently announced -- at the end of last year, we recently announced a partnership with Incyte to develop this molecule globally, so it's a co-development co-commercialization opportunity. We're excited about that opportunity, obviously, because they are a leader in this space, in chronic graft versus host disease the first indication, and we see the opportunity to really expand it with their expertise as well as resources. I'll mention our balance sheet, $400 million on the balance sheet, funds us into the second half of 2024, allows us to get through all of our regulatory and development milestones, expand the pipeline selectively with business development, which we have been known to do and really sets us up for success as we expand the organization for commercialization. So it's an exciting time to be at Syndax. We're obviously happy to be here to tell you about the story, which I think we'll get into some more detail. So thank you.

Okay. Great. So let's start with the discussion of the acute leukemia program, the menin-MLL drug revumenib for all rearranged AML, ALL and NPM1 AML. So kind of at a high level, let me start by walking through the rationale for targeting the menin-MLL interaction in these [indiscernible]

Right. So the MLL1 gene interact with a scaffold protein called menin. That interaction has been shown to be quite important for the formation of leukemia in specific types of patients, MLLR and NPM1 patients. So the opportunity that we see is to take a small molecule inhibitor, a highly selective one in revumenib and block the interaction between menin and MLL1. That basically turns off the leukemic process. And so that's been the foundation of that program mechanistically.

Okay. So based on that rationale, can you kind of walk through, as you mentioned the earlier, the existing clinical results for revumenib in these genetically defined AML populations from the Phase I part of AUGMENT-101?

Right. So that -- this is the study that I mentioned earlier. We presented data at ASH in December of '21. hallmark study for us, 51 patients with either of the 2 mutations, NPM1c or MLLr. Again, I'll mention this is relapsed/refractory disease, so highly, highly pretreated patients or heavily pretreated patients had seen multiple lines of therapy. And so of the 51 patients that were treated, the overall response rate was 55%. So more than half of the patients had received a complete response with varying levels of hematological recovery. So that includes patients who had a CR CRh or CRP or CRI or MLFS. These are all different designations of CR, complete response. So this is an absolutely phenomenal result. And further that, the primary endpoint that we're looking at in the Phase II study is CR CRh of the patients of the 51, 24% received a CR or CRh. And out of those patients, 92% of the patients had what we call an MRD-negative response. So minimum residual disease, all the cancer had disappeared from -- based on any detectable -- the most specific detectable method of detection. So that was the endpoint that people were following in the trial. Again, this is -- these 2 lesions cover about 40% of AML. So it's a very large patient population. Importantly, we talked about median durability, meeting duration of response, which hadn't been reached in the trial as of that point of the data cutoff. Half of the patients had been on trial for 6 months or greater. So the opportunity here is to keep these patients on in the relapsed/refractory setting for quite a long period of time. So that's something we'll follow up on. You'll see an update on the durability in the Phase II trial as well. So what I think this data set really established is the activity that we see in NPM1 and MLLr being 23% for NPM1 and 24% for MLLr shows that they're compatible. They're both highly relevant and accessible based on what we're seeing in this trial for potential approval down the line.

Okay. Great. So with all those results on hand, can you walk us through the design of the Phase II portion of AUGMENT-101? I guess, more practically, so there's 3 independent cohorts in the study, talk to us about the kind of cadence of data updates from those.

Right. So the -- these are 3, as Madhu mentioned, there are 3 independent cohorts of patients, we call them trials, 2 for acute leukemia, or AML, MLLr and NPM1 and a third independent trial being in ALL MLLr. They enroll independently, 64 patients per trial up to 10 pediatric patients as well. While the powering is identical between the 3 trials, the endpoints are the same. So we'll be looking at CR CRh as the primary endpoint; secondary endpoints, median duration of response, overall survival and transfusion independence. The dose is 163 milligrams BID given twice a day on top of a strong CYP3A4 inhibitor so it's evenly distributed between the trials. The data cadence, as we've indicated, is -- because they enroll independently, it's hard to predict whether one trial will enroll faster than the other. But we've said AML is likely to enroll more quickly than the ALL cohorts based on the number of patients in the -- that are available to us. And we have guided that we'll have top line data or full enrollment, I should say, in at least one of the cohorts by the end of this year, add 6 months to follow-up patients, so we should have data -- the first data available in the first half of next year.

Okay. Great. So thinking about the CR/CRh primary endpoint, what should we think about in terms of the magnitude of benefit needed on both the primary and also secondary efficacy measures in these cohorts from AUGMENT 101?

Right. So I think what we can say is, I don't think there's a regulatory -- real regulatory precedent around certainly, drugs in the MLLr and NPM1 space because none have been approved, but I would say that we look at targeted therapies, other targeted therapies and what has been approved in the past. FDA has not given us a specific bar but we know that other drugs -- targeted drugs have been approved at roughly 20% CR/CRh rate and durability, [ meeting ] duration of response of 4.6 months or greater. So we think somewhere in the 20% to 30% range on CR/CRh is a reasonable place to target. We were in the Phase I, as I mentioned before, 24% CR/CRh rate, which is, we think, an approvable number, if you will, and quite competitive.

So drilling in on that a little bit, I want to follow up on kind of an observation being the Phase I study about patients going to transplant. How is that treated in the Phase II portion of the study? And how should we think about kind of how that influences the drug's profile when assessing that data in the Phase II [indiscernible].

Right. So patients are -- so they just kind of walk through the paradigm a little bit. So patients -- a lot of the patients on our trial and key endpoint or key opportunities to get a curative bone marrow transplant. And so physicians are treating with our drug in order to potentially get them to a transplant or keep them on drug, suppress their -- and get them to complete response if they're not eligible for a transplant. In our trial, once they reach the transplant, the drug is stopped, they're transplanted. And then they're continuing to be followed through the transplant and potentially put back on drug. Not every patient will be put back on drug, but some will have the opportunity to go back on drug. So they'll be followed and the regulatory endpoint of duration of response is calculated all the way through transplant until relapse. So that whole period of time is covered. If the patient stays on, is able to be put back on drug post transplant, they'll be followed until -- all the way until the time that they relapse. So that could be an extended period of time.

Okay. Great. So one of the questions we get from investors a lot about this menin and MLL space is the notion of differentiation syndrome. And how should we think about the risk benefit of differentiation versus unmet need? And how much [ differentiation ] syndrome is almost like a de facto PD biomarker for these menin MLL class?

Yes, I'll let Anjali handle this question.

Sure. Yes. Thanks, Madhu. Yes, we anticipated seeing differentiation syndrome. As you said, it's kind of a mechanism of action of the drug and getting the leukemic cells to differentiate and transform. And we've seen so far, as Michael mentioned, the data set we presented at ASH, we've seen about a 14% rate of Grade 1 or Grade 2 differentiation syndrome. We have been -- because we knew it was something we anticipated, we have been actively asking our physicians to monitor for and if suspected, treat differentiation syndrome. So that could be a reason why we've been able to manage and maintain low rates of events. But we've also heard from thought leaders that it could be a pharmacological -- specific pharmacological aspect of these different menin inhibitors that have caused a differential in the severity of differentiation syndrome amongst the menin inhibitors. But for us, it doesn't seem like it's a major risk-benefit trade-off. We're getting good results and minor events.

Well, let me ask a question that exposes my ignorance to follow up. What is the treatment protocol for differentiation syndrome?

Yes. So mainly, you can treat with steroids or hydroxyurea. So very manageable treatment to avoid pretty severe and potential death in a couple of cases of what they've seen.

Okay. So the other, I would say, kind of tolerability question obviously has come up with the Phase I merchant of AUGMENT 101 is questions around QT prolongation. So can you give us for some context when I think about QT prolongation from revumenib and how we should think about it on the forward both in terms of risk benefit and management of those QT events in the Phase II portion of this trial?

Anjali?

Yes. So QT prolongation in and of itself is really just a marker of increased risk of cardiovascular events. So patients don't actually notice their prolongation of their QT interval, and physicians have become fairly adept at managing patients because it's something that they've seen with multiple drugs they use today in treating leukemias and tumors or cancers in general. What we've seen so far in the trial is a very manageable events. If, in the off-chance, we see a Grade 3 event, we can simply reduce the dose given at the next dosing interval to eliminate the chance for a Grade 3 risk. We were -- we've been actively monitoring, as we said, it was -- as with the differentiation syndrome, it's something that we anticipated seeing. And we wanted to make sure we understood and could contextualize the clinical manifestation. And what we've learned is that it's a Cmax effect of our drug. So within a few hours, it's cleared as a drug gets cleared from the system. So a simple dose reduction has been sufficient. And many of these patients have gone on to a complete response even with -- even at a reduced dose. So patients are not walking around for days or even weeks with a prolonged QT interval. It's managed right away because of our aggressive monitoring and [ resolve ]. And so what we've seen is physicians being really excited to use our drug and patients, as I said, don't notice this aspect. And so again, I feel like we're in a very good therapeutic window here. We've been able to further manage this risk by making sure patients that are treated are in the upper level of the normal range of electrolytes and that has reduced the risk as well as the rate of QT prolongation that we've seen in the trial.

So I guess kind of following from that, is there any kind of obvious precedents that exist in the HemOnc space for managing QTc prolongation and kind of be able to manage that in the kind of practical course of therapy in very -- these types of leukemias?

I mean, I think they know how to monitor. There are other -- I think, [indiscernible] has a 10% risk of QT prolongation. And so physicians that we've talked to have indicated that they can do Holter monitors in their clinic. And we've noticed that within -- it usually shows up within the first week of treatment. And so if they see it, it's, like I said, a simple dose reduction of our drug.

Okay. Great. So kind of moving beyond AUGMENT-101. So as you mentioned at the beginning, Michael, could you guys provide some context about the rationale for the 102 study where you combine revumenib with chemotherapy in the relapsed/refractory setting?

Yes. So this is a trial that we're looking at combining our drug with salvage chemotherapy. It's the first foray for us to do such a combination trial with chemo. It has implications in this particular population. Specifically, this is a regimen for ALL and AML, but also has been known to be used in this particular salvage chemotherapy for pediatric patients. And so we will be dosing adults and pediatric patients in this trial. It's about 27 patients per arm, and it will give us a good sense on what we can do with chemo, at least this regimen of chemo, and perhaps will give us some indication of what we are likely to see in the frontline setting when we go there and combine with 7+3 and some of the other agents.

So kind of following from that, are there any combination toxicities one might kind of [indiscernible] predict for combining revumenib with chemotherapy based on what you know from the agent?

No. Yes, it's pretty -- I mean that's one of the advantages, I think. We don't see overlapping toxicities.

Okay. So then kind of moving beyond the relapsed/refractory setting, can you tell us about how we should think with the opportunity for revumenib to expand both in BEAT AML and Intercept?

Anjali, can you take that?

Yes. No, we're really excited about the opportunity beyond relapsed/refractory and the BEAT AML trial represents our ability to move in the front line. And we're working with the Leukemia and Lymphoma Society in their master protocol to study revumenib in combination with ven/aza. And the trial started enrolling this quarter. We should have data in 2023, and it will give us a good sense of the safety of the combination as well as some initial efficacy. And then the goal is to follow that with a Phase II/III trial that could support filing in the frontline patients unfit for chemo.

So to that end is -- again, is there any kind of [ apriori ] safety combination concern for ven/aza with revumenib relative to ven/aza on its own?

No, I mean, there's no -- as Michael suggested, there's no overlapping toxicities with ven. Ven can have a hard to tolerate profile in and of itself. And so trying to make sure that isn't something that prevents us from giving revumenib. I think that's what we're looking for. But we've seen a really nice tolerability profile with revumenib, and we don't think there should be anything additive in the combination.

And then in this MRD population study, can you kind of walk us through the design of that?

Yes. So that's another esteemed group of thought leaders are running a trial where they're looking at the ability to prevent or -- yes, basically prevent relapse in high-risk patients who have achieved a response. And so we're working with the Australasian Leukemia and lymphoma group who have a master protocol there. And we would give revumenib as monotherapy to patients who have achieved MRD-positive CR that are thought to be at high risk for relapse and seeing if you could delay the relapse or enhance the response in that patient population and get more patients to an MRD-negative state.

And in that case, that's kind of an open study. So it's not like a clear evidence of when you would get to a readout from INTERCEPT from that MRD study?

Right. Yes, it could be a prolonged -- it's an initial look into the maintenance setting if you will. So it could be a prolonged treatment benefit there.

Okay. So I went to your earnings, you all announced exploring the use of revumenib in microsatellite stable colon cancer, as Michael mentioned at the beginning. So I mean the obvious question we got from investors is, can you provide some context for why you think a drug like revumenib, why menin MLL would provide therapeutic benefit in colon cancer? And I guess when we can get more details on the trials starting in fourth quarter?

Yes. So maybe I'll take that first. So I think we'll come back on the next call, and we'll talk a little bit about what that start date look like and give a little bit more color and detail around the trial. But I think the concept here, the rationale for doing colorectal cancer is related to beta-catenin and that pathway. And recent evidence has shown that there's -- the MLL1 gene is implicated in that pathway. And by blocking MLL1 with menin you actually displace MLL1 from that cascade in the beta continuum cascade, and that leads to the halting of colorectal cancer, specifically metastatic cancer. And so that's been shown in a couple of publications, one in nature, one in science as of late last year. And so this was sort of an important finding for us, and we tend to follow that science carefully. So we're going to test this, as we said, in a small signal-seeking trial starting in the fourth quarter, and we're excited to see where it takes us. Obviously a huge opportunity, about 50,000 patients, 50,000, 60,000 patients in the U.S. in this setting. They tend to take other therapies [ fail those ] therapies, 2 drugs, in particular, standard of care, about 5% response rate and disease control rate of about 15%. So a very low bar, if you will, for what we could potentially add to this treatment regimen. So we're excited to at least explore it. We think there's good scientific rationale for doing it, and so we'll take a measured shot at doing so.

So following from that, are the kind of blue skies that you see signal in microsatellite stable colon cancer, given the kind of beta-catenin kind of MLL co-factor hypothesis I mean there are other tumor types that we know are kind of [indiscernible] beta-catenin. Is there a notion that that's context dependent? Or is it the kind of thing where colon cancer is kind of the test case for testing other beta-catenin dependent cancers?

I think it's the latter. I think that -- we're thinking about this as a test case. We recognize that beta-catenin is implicated in a lot of different cancers. And that caught our attention too. So we'll first test the hypothesis in metastatic colorectal cancer, and then we'll see where it takes us from there.

Okay. Great. So moving on to axatilimab, I guess kind of the most practical question is, how should we think about the cadence for data reading out from the AGAVE-201 study?

Yes, it's actually quite similar to what we're seeing on the menin program. We had guided that we'll have full enrollment this year. And so in the second half of this year, we'll have to wait for about 6 months to follow the patients. And so that puts us into the first half of next year for data disclosure, potentially top line data disclosure.

Okay. I guess then kind of with that in mind, kind of getting -- stepping back a little bit, remind us what the existing efficacy profile is for [indiscernible] disease? And what the kind of landscape is in this kind of like later line refractory chronic GVHD setting.

Do you want to take that question?

Sure. Yes. So right now, there's 3 drugs that have been approved to treat graft versus host disease, 2 in sort of the earlier lines, ibrutinib and Jakafi and then REZUROCK, which is approved for the same patient population that we're studying with axatilimab. We know that with REZUROCK and Jakafi, there's been a really positive launch trajectory. The -- REZUROCK specifically called out that they had $40 million in sales in the first quarter, which I think is really outstanding and a testament to the need in this setting. And I think there's a strong opportunity to build a treatment algorithm and establish how these patients will flow through the various agents. And it's great to be working with Incyte because they're out there right now establishing the treatment algorithm, and they know that axatilimab is coming behind it, so it can start to the stage. They were letting us know they were at TCT in April and axatilimab was a big buzz. So we're pretty excited, and it's great to have a partner that's equally excited and really out there making the market, if you will.

That's good. So with that in mind, what is the bar you think you need in terms of the primary endpoint from AGAVE-201 in this kind of later line relapsed/refractory GVHD population?

I think there's no bar per se, right? I think it's based on precedent, just as we talked about for menin. And I think we've had some recent approvals to sort of justify that bar. I think with Jakafi, I think they showed the endpoint being a response at 6 months. I think they showed a little less than 50% response rate. And so I think the bar for us would be somewhere in the range of 50%. And you think about duration of response in this, call it, 6 months time frame, anything better than 6 months. And I think that's all reasonable. This is again, all based on precedent. And on the -- based on the Lee Symptom Scale, the majority of patients having a better than 7-point improvement on the Lee Symptom Scale. So I think those are the 3 measures that we look at. And based on the precedent and based on the fact that our Phase I/II data was certainly well within that range, I think we're well set up for a potential filing.

Okay. Great. So following from that and following from what Anjali said earlier, can you walk us through the opportunity to expand axatilimab into earlier line chronic graft versus host in combination with JAK inhibitors with Incyte?

Yes, sure. I mean I think the big promise of axatilimab is its effect on the fibrotic pathway. And so the earlier you can treat patients, hopefully, the better off they will be with their disease and maybe you can prevent the formation of fibrosis, which is what causes their ultimate demise. So we're excited to move it up. And the hope with a combination with a JAK inhibitor is that you could displace the use of steroids, which -- though it does help control disease, it also contributes to downstream effects that lead to death. And so if by targeting both the monocyte macrophage pathway as well as the TMB cells, could you control the disease at such a level that you know longer need steroids and you can give patients a steroid-free regimen and hopefully prolong their survival.

Okay. So with that in mind, can you -- when can we expect to hear more about the design of that study combined with JAK inhibitors, obviously, end points, size of the trial and the natural question we'll have is like what JAK inhibitor would be used?

Yes. We're still working through all of that with Incyte, and we have to kind of do this and lock step with our partner. But we're working on it, and we hope to be able to share our decisions in the next few months.

Okay, great. So kind of moving beyond chronic graft versus host disease. Could you walk us through the mechanistic rationale for using axatilimab and other fibrotic indications? And I think to what Michael mentioned earlier, the one that's on top of mind for most people is idiopathic pulmonary fibrosis or IPF.

Right. So interestingly, we started with this molecule. Actually, when we in-licensed it from UCB, they were working on IPF as their preclinical thesis. But we actually came back to that later on. So it was just an interesting way that the molecule got developed. But it's a CSF1R antibody, so it targets the CSF1 receptor. And there are -- in turn, there's downstream effects on macrophages. So the downregulation of macrophages has a profound effect on fibrosis. We know that to be true. We've seen this effect in chronic graft versus host disease. There's a manifestation across different organ systems, which is profound. The data that we presented at ASH really laid out the impact that we've had across organ systems such as lung and skin, which are intractable and difficult and highly fibrotic. There are other indications such as IPF, where we've seen indications where the lung is implicated that we've seen profound effects things like FVC, which is potentially an endpoint for us in the IPF trial. So we've seen the effects on different organ systems that was available to us through the GVHD trial that kind of confirm the pathophysiology of the disease and also our impact of our drug on that disease. So that's the idea.

Okay. So with that context in mind, I mean, a lot of hearts been broken in IPF, you trying different modalities of all different sorts. And so kind of what both gives you confidence in seeing signal -- and kind of more importantly, how far along in development do you think you need to get to have a signal that is really [ meetable ]? Does it have to get all the way to FVC and a randomized controlled trial to be a believer? Or is there some things along the way they can kind of build confidence on that IPF [ trial ]?

Yes. We're going to say more about our IPF trial at our next earnings call. We'll get into some detail. But what I can say is that we took that into consideration. That very question was really important. We spent a lot of time with thought leaders and treating physicians that really understand this disease and some of which who really understand our drug as well. And I think the idea was to design a trial that really was meaningful in terms of patient numbers and duration of endpoint. So looking at it over a 52-week time frame versus a short very much of a signal-seeking trial. We want this to be a meaningful signal to determine whether or not we continue with development. So I think that's the idea. We'll say more about it, but it's a -- it will be a robust trial, which we'll be able to get a real feel for whether this is a drug for IPF.

Yes. Okay. And I'll ask one more question based on the investor conversation we've been having recently, which is kind of the -- after what happened with the Galapagos is -- has axatilimab been tested in combination with some of the approved agents in terms of combination toxicity? Is there any [ apriori ] reason to think that this drug can't combine with kind of the approved IPF drugs?

There's no reason in our hands or that we've seen that there's no reason to think that we can't combine them.

Okay. Great. But when we move on to kind of bigger picture stuff to kind of an obvious question we get in -- both for Syndax and for various names in this space is kind of catalyst [ path ]. So top line data from revumenib and axatilimab in their kind of registrational studies first half '23, is there any more kind of data releases like updates from the Phase I studies anything we should be aware of between now and then to kind of speak to the trajectory of these 2 drugs kind of ahead of 2023?

Yes. I know it's an excellent point. I think we've gotten some questions about whether we would update the Phase I data set. And I think we haven't officially committed to doing so. It's something we think about. And that would be a look at the ongoing durability from the -- I mentioned the 12 patients who had reached CR/CRh, that endpoint, and we had reached the median durability at that point. So could we take another look at that data set to update it? It's a consideration. It's something we think about. Ultimately, the Phase II data set will really be determinative in terms of what we see for responses as well as how long patients can stay on drugs. But that same question will be answered a couple of months later, we hope so. So we're determining whether that makes sense to update that data set. It's possible. We just haven't decided yet.

Okay. And then I guess on axatilimab as well, given the same -- [ which is still ] durability response questions there as well in terms of how long patients are staying on axatilimab.

Yes. We haven't committed to putting out any additional data from the Phase I or Phase II. I think the next thing you'll hear is that the trial has been enrolled and that will kick off the, call it, the clock to data.

Okay. Great. So at a high level, you mentioned at the beginning of the idea of internal R&D versus external business development. How are you thinking about the expansion of the pipeline now? Kind of essentially as we look at -- as much as I try to avoid looking at the XPI these days like wanting to be internal pacifists [ versus ] internal optimist. Internal optimist can be like it's shopping time. So how are you thinking about kind of external business development, both on public and nonpublic kind of assets?

Yes. I mean we've been externally focused for all -- the entire time Syndax has been in business. And I think bringing in new molecules is something we're very serious about. We've been successful with the 2 that we've brought in so far. So I think the environment is -- doesn't lower our bar. We have a very high bar for what we'll do. We're focused on the early stages of development. So lead stage preclinical to early clinical stage assets, and we'll continue to look for targeted therapy opportunities. We're hopeful that we can bring in additional assets to the pipeline. But I think the availability -- potential availability of additional assets doesn't necessarily improve the quality of what we're trying to find. And so we'll continue to plug away till it's something that we're really, really focused on. And time will tell when we bring in additional assets.

Okay. Great. Well, finally, the question we're asking every company at the conference is the classic question, what is the reason to own Syndax stock in the next 12 months?

Yes, I think it's simple. I think you've kind of just stated it for us. I mean, we have 2 molecules that are potentially first to market and best in class in their respective areas. We have just a fantastic team of which to execute on our mission to bring these drugs to patients. We have a balance sheet that's supportive of our life cycle opportunities, which allow us to expand these molecules. We do have a real penchant for business development and expanding the pipeline. So I think it's a great time to own Syndax. It's a great time to be involved with the company. And in the next 12 months, we'll have a lot to say and a lot of data to approach investors about.

Excellent. Great. Well, with that, I'd like to thank everyone for joining us this afternoon, joining us was Syndax Pharmaceuticals, and thank you guys for joining us today as well.

Great. Thank you.

Thanks, everyone.

Thank you.