Let's get started. Welcome, everyone, to the Wednesday morning of the 41st Annual JP Morgan Healthcare Conference. My name is Anupam Rama. I'm one of the senior biotech analysts here at JP Morgan. I'm joined by my colleagues, Malcolm Kuno and Priyanka Grover. Our next presenting company is Syndax, and presenting on this behalf of the company, we have CEO, Michael Metzger. Michael. Well, thank you, Anupam. I wanna first start off by saying this is our first time presenting as a company at JP Morgan, we're thrilled to be here. Appreciate the opportunity to do so. Also appreciate the initiation report from Anupam to start 2023. It was a great way to begin the year. With that, this is our forward-looking statements. Of course, I'll be making forward-looking statements today. This is posted on our website. I encourage you to take a look at it. It's also in our presentation. 2023 is shaping up to be what I would call a very special and exciting year for the company. As many of you know, we have two late-stage programs, both in pivotal trials, addressing high unmet medical need. We expect to have data for both programs this year, pivotal data this year for both programs. Importantly, we expect to have two filings for one for each of the molecules. They address, as I mentioned, high unmet medical need, multibillion-dollar markets. We expect to be first and best-in-class for both. They afford us opportunities to expand into multiple markets beyond the early initiation of the registration indications. Importantly, we added to the balance sheet in the fourth quarter. We now are sitting with roughly $500 million in balance sheet cash, which enables us to get through all of our clinical and regulatory milestones over the next year or more, and also potentially to launch these programs into the markets, which I'll outline for you. In addition to that, we also selectively look at business development opportunities to build the pipeline, which of course, these are targeted therapies within the, in the hematological oncology space. We'll look to potentially add to the pipeline in that capacity as well. Let me just first start off by talking about revumenib, which is our first-in-class, potentially best-in-class menin inhibitor, addressing two distinct segments of the population in acute leukemia. First is KMT2A acute leukemia. Rough incidence of 5,000-7,000 patients globally, addresses perhaps 10% of all AML and ALL. It's a very poor prognosis for patients who have KMT2A leukemia, less than three months of survival in the later lines of therapy. This is a very high unmet medical need for the field. We recently received breakthrough therapy designation based on the phase I data that we presented at ASH, which I'll get into in a minute. This is a very important segment of disease and a separate segment of disease. NPM1 mutant AML addresses approximately 30% of all AML. It's the most frequent genetic alteration in AML. Together, they comprise about 40% of AML and ALL, so this is perhaps the largest segment to be targeted by a therapy of its kind. It is potentially first of its kind to do that. There are no approved therapies for either KMT2A or NPM1 acute leukemia. Important to mention that both of these types of mutations are addressable, or at least I should say, identifiable at the time of diagnosis by physicians through cytogenetic testing. Just a simple cartoon on the mechanism of action for revumenib. KMT2A and NPM1 are addressed through the same mechanism of action. Menin is a scaffold protein, interacts with another protein called KMT2A, which turns on transcription through upregulation of HOX and MEIS genes, which leads to leukemia. When you introduce a small molecule, a very specific inhibitor, it fits right in the binding pocket of menin. It displaces KMT2A, turns off HOX and MEIS genes, which leads to differentiation and apoptosis. This is our depiction of our phase I trial, which we recently had data on, and I'll talk about that in a moment. The phase I is the phase I component of AUGMENT-101 and a phase II component, which is the pivotal trials. The phase I component was a dose escalation. We've arrived at a, at a recommended phase II dose. In fact, we had a few doses in both arm A and arm B of the, of the trial that they've recommended phase II dose. These are adult and pediatric patients, relapsed, refractory, KMT2A or NPM1 acute leukemia patients. We'll present this data in a moment. Phase II segment of the trial is an ongoing trial, AUGMENT-101, 2A, 2B, and 2C, separated and individually enrolling patients. KMT2A ALL, KMT2A AML, and then, of course, NPM1 AML. Primary endpoint of all three trials, which again enroll separately, is the same. It's CRCRH rate and 64 patients per arm, up to 10 pediatric patients in addition to the 64 adult patients. This is the baseline characteristics of the AUGMENT-101 trial. The patients were heavily pretreated and have a poor prognosis, as you know. Again, KMT2A and NPM1 patients. Median age is 42 and a half years, comprised in this trial AML, ALL, and MPAL patients. Important to point out, these are patients who have large part failed prior stem cell transplant and venetoclax, which are two important modalities of treatment. They're very late line patients, average of four lines of. Essentially, this is their fifth line of treatment. Many of these patients are co-mutated, which also complicates their prognosis as well. These are the tables that list our adverse events. On the right, I'll just highlight for you the dose limiting tox for this drug is QTc prolongation. We've known this since early on in development where we test for QTc prolongation. It's a simple EKG that's administered at the beginning of treatment and throughout treatment. Important to point out, we identified 10% of patients had grade three QTc prolongation, which again, is easily identifiable. What we do when a patient has a prolonged QT is we drop the dose. They continue on, they don't even stop dosing, they continue on treatment, and many of these patients have gone on to have complete responses, go to transplant and do very well on the drug. QTC prolongation has not led to arrhythmias or Torsades or anything other than a lab abnormality, so patients have done really, really well. It's important to point out is physicians are very familiar with QTC prolongation. They've seen it with other targeted therapies. With our particular drug, it has a reasonably short half-life and does not accumulate, so as we drop the dose, the Cmax comes down from the drug. Patients continue on, they don't see additional QT. It's controlled. Easily identifiable, controllable, we administer some other potential calcium and potassium and other oral supplementation to help control and blunt the effects of QT which is pretty much standard of care. This again, is a very easy to manage phenomenon, is the only thing that physicians see and it's a lab abnormality. We do see some differentiation syndrome. I know this has been the subject of some of our competitors, all grade two, and not of significance with this drug. This is the data from the phase I that we updated at this year's ASH. It continues, we believe, to support the best-in-class thesis around this molecule. 60 patients in the efficacy population. Of the 60 patients, 32 had responses, complete responses, or otherwise known as CR, CRH, CRP, or MLFS. That's 53% of the population had a clearance of the leukemia, which is a, we think a very strong result. MRD negativity was especially high in the patients who had received CR or CRH. 78% of the patients had achieved a MRD negative response. As we look at breakdown between KMT2A and NPM1, both at the RP2D had 27% CR CRH, which again is a, we think a very positive result. I'll point out the median duration of response which we updated in this data set was at 9.1 months, as well as the fact that patients are receiving a response very quickly, 1.9 months, median time to response. Overall survival, this data set allows us to look at for the first time overall survival. As you may know, that patients who are at this late line generally have three months or fewer overall survival. And in this particular study, we saw seven months overall survival. Again, what we think is a pretty impressive result. The second presentation that was done at ASH is shown here. These are 12 patients. These are the 12 patients that went on to transplant from the phase I. As you'll notice, many of them have MRD negative status, which is not a surprise. That's a marker, an important indicator for physicians that their patients are eligible to go to transplant and do potentially well in transplant. Ninety-two percent of the patients achieved an MRD negative response. Many of these patients remained in remission as of the data cutoff, and many in excess of one year. I'd say that the important. One of the important aspects of this trial was the follow-up that we did relative to compassionate use, where we were able to put patients back on therapy following engraftment, which is, we think an emerging thesis for this drug. Patients staying on drug for longer than a year in addition to having their transplant. Again, patients are able to do very well on this drug, get to a complete response, go to transplant, potentially go back on drug and stay in remission for quite a few months, maybe an unspecified number of months at this point, but very, very encouraging. The question is, hopefully get this drug approved in the relapsed refractory setting, which is AUGMENT-101. Where do we go from here? It's an important question, and I think we have aspirations for this drug to take it, not only combine it with other standard of care therapies such as chemotherapy, which is the subject of AUGMENT-102. That's a company-sponsored trial which we've started and will have, hopefully have some data for before the end of this year. We have a frontline trial that's ongoing with The Leukemia & Lymphoma Society, Beat AML, which is a combination of our drug with venetoclax and azacitidine. In the frontline setting, this is in the unfit patient population. Then an important question about maintenance. We're exploring that at first, of course, with AUGMENT-101 in the phase II, where you can put patients back on drug after engraftment, which I just described. We think that's an important indicator of what patients may be able to do in the frontline setting when you get to them earlier in treatment. That is in part what we're looking at with the INTERCEPT trial, which is a cooperative group trial, looking at converting naive patients from MRD positive to MRD negative disease. All in all, this is a group of trials that we're hoping to get, some of them are up and running, and we're starting other ones. We'll be designing additional trials both to get at the chemotherapy combination in the frontline setting, as well as looking at maintenance and other frontline combinations, really to address all aspects and all segments. That's what's shown here. I think the exciting aspect of this drug is that we can address 40 up to 40% of all AML and ALL through these two mutations. Relapsed refractory is about 5,000 patients worth of that. We're looking to push this into various lines of therapy all the way to, you know, potentially up to 12,000 patients worldwide. It's a, it's a value proposition that has really not been seen with other targeted therapies, and we think we can explore based on the profile of this drug, also the segments that we target with this agent. That was revumenib. Let me turn our attention to axatilimab, which is our second drug, but equally important in the sense that this is a first-in-class, we believe, best-in-class agent, a CSF1R antibody, specific antibody addressing first indication being chronic graft-versus-host disease. For those of you who are not familiar with chronic graft-versus-host disease, it develops at approximately 40% of patients who have gotten a stem cell transplant. That equates to about 14,000 patients in the U.S. It is an immune-mediated, systemic disease that affects multiple organs, through an inflammatory response and then a follow-on, fibrotic response as well. As I mentioned, it affects multiple organs. The mechanism of the disease, CSF1R, depletes macrophage, the macrophage lineage, which ultimately intercepts the formation of fibrosis, which of course is the hallmark of disease for chronic graft-versus-host disease. This is the trial that we ran. It's a phase I/II trial highlighting the therapeutic benefit of axatilimab in these relapsed refractory patients. First, the phase I was 17 patients where we did a simple dose escalation. It sometimes happens with targeted therapy. You tend to have quick responses. We actually saw responses throughout the dosing continuum, so this is very exciting from the very beginning when we started to see responses. The phase II was an expansion at the 1 milligram per kilogram. We're administering once every two weeks. This is what we believe to be one of the doses that we hope to get into the label. We'll see how the phase II works out. This is 23 patients, and the overall response rate is the based on NIH criteria. That is the endpoint for the trial. These data were presented at 2021 at ASH, recently published in JCO. This is the baseline characteristics. I'll just point out that, you know, this is a little bit older population than what I presented with revumenib. Median prior lines, 3.5, this is a very sick population. Many of the patients who came on our trial had failed ibrutinib, ruxolitinib, and belumosudil, the most recent agent that Sanofi launched. These are patients who have seen prior therapies. I'll point out that this mechanism of action, affecting the macrophage, this is the only drug that, of the approved agents, this is the only drug that affects the macrophage. All the others are more targeted towards the B cell. Potentially, what does that mean? That means that we could have a profound effect not only on fibrosis, but we could affect through combinations other aspects of the modality as well. This is the AE table. I point out that, you know, it's a very well-tolerated drug, safe and well tolerated. I think what. We have seen some serum elevations, serum enzyme elevations related to the on-target effect of the drug on Kupffer cells, which are macrophages. These are transient effects, things that physicians watch out for. There's no end-end organ damage that we've seen, no cytosis or pancreatitis associated with the enzyme elevation. Overall, the drug has been extremely well tolerated and, as you can see based on the data on this page, 82% of the patients received an overall got an overall response by criteria based on cycle seven, day one, measurement. 77% of the patients had failure-free survival at 12 months, also an impressive result. Again, not unlike revumenib, the drug works quickly. In four weeks, we're getting time to response. In the middle panel here, the responses were long-lived for many of these patients. They're on drug for six months or more. We have patients out two years, so they're doing quite well on the treatment. As you look at what this drug does, you wanna see that it actually has an effect across organ systems. As I mentioned before, it's a multi-organ system failure and problem. We're having both complete responses and partial responses across all the organ systems, including those that are hard to treat, like lungs and skin. It's a, we think, very impressive data set going into the phase II. Before we get there, I'll talk about the Lee Symptom Scale for a second. This is the assessment of symptoms and symptom burden on patients. 58% of our patients were evaluable and had a 7% or 7-point scale improvement, which is an impressive result. Importantly, you wanna be able to take down the dose of steroids that these patients get, which is standard of care. By introducing our drug, we're able to reduce, at least in this trial, we're able to reduce the use of steroids, which is really important to physicians. They often identify that as a key driver to how they prescribe. This is the phase I pivotal trial that I was mentioning. It's a robust trial, looking at patients who have had two prior lines or more. As I mentioned in the phase I/II, we looked at slightly sicker patients, third line plus. Most of them are fourth line. I think if you look at this trial, it's a three-dose randomized trial, 1-1.3 milligrams every two weeks, 1 milligram every two weeks or 3 milligrams every four weeks, which is more of a convenience dose. The top-line data for this trial, which has already been enrolled, in fact, we over enrolled the trial to 240 patients. Top line data is expected in mid-2023, and BLA filing by the end of 2023. I will mention that we have a partner, Incyte, for this program. We did that collaboration, a global collaboration in 2021. We're very excited to be working with Incyte. They're a known commodity in this space. They've have ruxolitinib, and they've launched an acute and now chronic graft-versus-host disease. It's important to note that their drug actually has a different mechanism, as I mentioned earlier, and the ability to potentially combine these agents is one advantage that we think is key to the partnership, as well as the fact that they have commercial infrastructure and really understand how to, how to promote in this space. We'll be combining this drug in a frontline trial, which will be starting in the first quarter. Actually, Incyte will be leading that trial, and it's an exciting way to potentially expand the opportunity. Speaking of expansion, this is just a depiction what we plan to do beyond chronic graft-versus-host disease, which I mentioned we expect to submit the package in 2023, hopefully get the drug approved in 2024 and launched in 2024. We'll also be looking at frontline trials, the combination I just mentioned. Also, Incyte will lead commercialization outside the U.S., so that further expands the pie to those patients. We're gonna be starting an IPF trial this half to look at the drug in that indication as well, which of course, could be a very large upside to this program. There may as be other indications that we pursue in addition to these with Incyte to be determined down the line. Just a bit on our financial guidance. As of September 30th, we had $337 million on the balance sheet. I mentioned our follow-on financing that we did in December, $161.5 million net, adds to about $500 million, which is a healthy balance for us. Shares outstanding 69.2 million. The R&D budget, which we'll update on our quarterly call, $145 million-$155 million has been the guidance. We adjusted that as of last quarter. We're, you know, with the cash on hand, I think it gives us ample opportunity to pursue all the things that we talked about today, and hit all of our clinical and regulatory milestones, as well as selectively add business development opportunities. With that, I will pause. I think it's a exciting year for the company. I hope I came through to you today. I'm happy to answer questions and get into anything in particular. Thanks, Michael. Just as a reminder, many of you heard me say this over the last two days, but there are three ways to ask a question, right? You can send it to the digital conference book, and I'll get it on this iPad. You can email me, or you can go old school and raise your hand, and we'll make sure a microphone gets to you. We do have a question in the portal actually, which is, how do you handle transplant in the DOR calculation? And if these patients get censored at the time of transplant, can you show durability over six months? Yeah, it's a good question. Actually, point of clarification, we do not censor at the time of transplant. That's based on FDA guidance. If you look at the guidelines, the 2021 AML guidelines, they're pretty specific. There's not censoring for patients. The measurement of duration of response is literally time to relapse. You actually are calculating through the time that they get their transplant. The opportunity for us will be, in some ways different in the sense we can put patients back on. In the pivotal trial, we'll be able to put patients back on drug posting graftment, which I explained. That we've shown 9.1 months of median duration in the phase I that we updated at ASH. We expect that could potentially lengthen with the addition of, drug back, you know, at the, at the back end of treatment. Maybe expanding on this question a little bit, but in the ASH 22 update, you had 40% of patients that went to transplant, right? How are you thinking about the revumenib as a maintenance therapy post-transplant? I guess, what evidence is there to date on this setting? Yeah, I mean, I think we'll have some evidence, you know, in the phase II. I think this is an emerging, as I, as I like to talk about, it's an emerging paradigm for revumenib. The application is patients get, will get drug, go back on after engraftment. As you said, it's a high percentage of patients who get to MRD negative response and do very well, and we're hoping that we can hold them in response for, you know, months if not years. These are relapsed refractory patients. These are patients who are fifth line, and they have, you know, limited capacity to potentially respond long term. We think we're doing quite well in that setting. We're gonna have that data as part of the phase II. The opportunity is really to get into what we call maintenance in a frontline setting, where you access patients earlier and you're able to, you know, treat their disease, get them to a complete response, MRD negative response, either get them transplanted or not, but keep them on therapy to keep their disease at bay for who knows how long. That is a paradigm that we think we can exploit based on the properties of our drug and the data that we've seen sort of, you know, bears that out at this point. We'll see more in the phase II. We have an email question here as well, which is, can you explain the CR versus CRH rate in NPM1? You had two doses. How do you think about efficacy by dose? Right. we had what we had shown in the data at. Maybe I can flip to it here. The data that I showed. Sorry, here. That's shown here. I think the question's referring to the CR/CRH rate for both NPM1 and MLLr. We broke it out for the first time at the RP2D. the that's the analysis that FDA asked us for relative to how we do it. These are pool all the data at the RP2D. That means you would exclude some patients that got dosed above the RP2D or below the RP2D. That analysis is what we've done here for both MLLr or known as KMT2A or NPM1, and both of them, as you see, yield 27%. Our view is longer term, we expect the response rates of both NPM1 and KMT2A patients to be roughly the same. Questions from the audience. Malcolm? Hi. Hi. Maybe it's too early to tell, but in the maintenance portion of Augment, would you expect safety to hold up post-transplant in patients? It's a great question, and an open question. The best indicator we have when patients get MRD negative CRs, that means that they have very deep responses. That means that all their leukemia is gone, and their count recovery is either fully there or close to being fully there. Their bone marrow is recovering as well. After they engraft to go back on drug, it seems to be a very well-tolerated drug with side effects at a minimum. As long as the fitness of the patient remains, we would hope to be able to contain their leukemia as well. That's, that will be borne out in the phase II, but that's the promise. Let me see if there's any questions from the audience. Another question is, have you ever broken down the efficacy by AML and ALL for the, I guess it should say MLLr portion. MLLr? Yeah, MLLr portion. Will this and other indications be part of the submission? Yes. We have not broken out AML versus ALL at this point. In the phase I, I believe 11 patients were ALL, so it's a small segment. I think the best indicator of how these look like so far is based on what the FDA has asked us to do for our breakthrough therapy designation. They asked us to pool the data, cut the data, look at it different ways, adults, pediatrics, AML, ALL. We did based on the RP2Ds, and they gave us a very broad designation covering adults, pediatrics, AML, and ALL. To them, it looks sort of like one disease, which is an exciting and a big advantage for us. Specifically, we haven't broken that out for the reason that these are small patient sets. The phase II, as I kind of went through, is three separate trials, right? It's KMT2A AML, KMT2A ALL, and NPM1 AML. They're separate, they're enrolling separately. We'll see that data specifically in the in the completion of the phase II trials. Questions from the audience. On AUGMENT-101, the, you know, the pivotal portions are supposed to start reading out in the third quarter. Have you ever provided any cadence on the readouts of 2A, 2B, 2C? How do we think about that? Yeah, it's a good question. We haven't yet given guidance which of the three we'll read out first, second or third. I think the new element of this is, of course, the FDA giving us Breakthrough Therapy, and we'll have more discussion with the agency about how we might have an advantage of putting, you know, maybe two of the cohorts together around KMT2A to have one filing. We'll have more to say about the cadence of which will be first and second or third, as we, as we go a little bit longer into the, into the quarter. Excuse me. Yeah, I think the guidance remains first cohort will be delivered for enrollment by the end of the first quarter, and then we'll have data in the third quarter and a filing by the end of the year. I guess based on what you know today, how are you thinking about sort of the minimal threshold for success on CR/CRH, across the indications in AUGMENT-101? Yeah, I mean, I think the what we said, there's the people refer to it as the bar, right? What's the bar for efficacy? We like to rely or think about precedent, what other drugs have achieved in terms of CR/CRH rate. If you look at other targeted therapies, there have been approvals down to 20%, all the way up to pretty much where we are, like around 30%. That seems to be the range that people talk about, the bar, if you will. Then there's the what the physicians wanna see. They wanna see MRD negativity. They wanna see beyond response. They want to see utility for patients going to transplant. There's a, there's a lot more in terms of what physicians wanna see and potentially what the FDA wants to see. This is a risk-benefit analysis that they do. That means that 20% may be, you know, may be the bar for efficacy across one or two or three of the cohorts. Obviously, the higher the better, it's a risk-benefit analysis that the FDA does to look at the profile of the drugs. I'll also say that each of our, you probably notice each of our trials are sized the same. Whether it's AML or ALL, NPM1 or KMT2A, they're all the same size, which goes to the powering calculations. We haven't talked much about exactly what those powering calculations are, being that they're all the same, you could kinda come to the conclusion that we have pretty much reasonable similar expectations for each of the cohorts. Pending positive updates in AUGMENT-101, what would be the size of the field force here in the U.S., and are you considering partnering OUS? Yeah, that's a good question. What's nice about both of these drugs is actually the focus aspect of the commercialization effort. For revumenib, it's roughly, if you look at some of the other targeted therapies that have launched, it's roughly 40 reps or so in the U.S. That is something that we can accommodate, we believe ourselves, and our plan is to launch this drug ourselves, build a commercial field force, again, a very focused effort, and promote the drug ourselves in the U.S. Ex-U.S. is a slightly different equation. We don't expect to have a field force ex-U.S. promoting the drug, so that would mean that we'd have to rely on the efforts of a partner. The question there is, what's the timing of doing that? We're not in a particular rush to go out and partner the drug ex-U.S. We have significant interest to do so, but we'll have the opportunity to assess partnerships as we get closer to commercialization. Question from the audience. Maybe we'll switch gears a little bit. Sure. Axatilimab. There's an update coming also this year. Yeah. In the middle of the year. On that trial, what's the minimal threshold again for ORR, for clinical meaningfulness and particularly in this relapsed refractory setting? No, it's a great question. I think our setup is actually quite good with this molecule. I'm sorry. The data that we showed earlier and we published shows a response rate of, you know, upwards of 80% at cycle seven, day one, which is very competitive with other agents that have been approved. I think anything probably greater than 50% response rate would be very meaningful to physicians. I think it's, as I mentioned, a multi-organ disease where not only does the drug need to be very well tolerated, but it has to have an effect across multiple organs, and that's a tall order. We've been able to show that. I think that, you know, the data that we've shown in phase I and II, if we could replicate that or anything close to that, I think we'd be, you know, really, really excited that meets the bar. I'd also say that it's a different mechanism of action. It's one that you can combine with the B-cell directed therapies that we talked about are approved today. The combinability of these agents allows you to kind of move it upline, and that safety profile will play in favorably to that. I think that's the general parameters we have. We haven't talked about, again, powering calculations on this trial, but that's how I think you should generally think about it. Questions from the audience. Based on the agreement with Incyte, what would be your contribution from a sales force commercial perspective for axatilimab? Right. This is just to remind people of what the partnership is. This is a global collaboration, 50/50 profit and loss sharing in the U.S. We split the P&L in the U.S. They actually cover 55% of the development costs in the U.S., 45% to us. Ex-U.S., they cover all costs of development specific to that region, and they're gonna be promoting outside the U.S. They do lead commercialization in the U.S. The opportunity for us is to promote 30%, do 30% of the commercial effort in the U.S. It's an election that we have, this is an option. Regardless of whether we promote or not, we're going to be contributing 50% of the P&L. Commercialization effort on our side doesn't actually impact our economics, right? We do have 50% of the economics here, but 30% of the potential opportunity. you could ask yourself, why does it make sense to promote? There may be, you know, considerable overlap between our two programs. They're on the exact same timeline to get launched. you know, calling on the same physicians could have a unique opportunity for a company like ours to have very focused effort with two products versus one product in the bag. That's a uniqueness to our situation with Incyte. Maybe final question from me. You talked about the synergies between the two products and the initial indications. Right. You're also starting a trial in IPF. Right. When you looked at the whiteboard of indications, that could have been a second indication why IPF versus something that could have been more synergistic with your first two lead programs. Right. I mean, mechanistically, the impact on the macrophage could be very important for these patients who have lung fibrosis, and that's the hallmark of the disease. We've seen really significant reversal of fibrosis and improvements in FVC in the GVHD patients. That excited physicians to wanna pursue this. Interestingly, when we in-licensed this drug from UCB early on, when it was preclinical, all of the work was done in IPF. This was intended to go into that indication, and then we took it into other indications. There's a lot of supporting preclinical information that actually leads to the credibility of why IPF makes sense. It was early data plus the fact that we have real good clinical data indicating that this could have an impact in that disease. That was a natural second one. There are other indications that we could pursue as well. Cool. Thanks, everyone. Thanks, Mike. Thank you.