Good morning, and thank you to everyone for joining us on today's call and webcast to review the exciting interim clinical data from AUGMENT-101, our Phase I/II trial of SNDX-5613 in relapse and refractory acute leukemia. We especially appreciate our colleagues on the West Coast who may have dialed in at this early hour. Let me start on slide two with our forward-looking statement. We ask that you please reference our SEC documents to see all the various risk factors that come with investing in Syndax. Slide three is our presenter for today. We are very pleased that Dr. Eytan Stein from Memorial Sloan Kettering Cancer Center, the principal investigator for the AUGMENT-101 trial, will present our current Phase I data. I will make a few introductory comments, then Eytan will present the data. I will close with a few comments outlining the next steps for 5613, as well as some commentary on the significant market opportunity for the drug. We should have about 15 to 20 minutes for questions. Turning to slide four, let me first begin this data presentation by thanking all the patients and their families who have participated in the trial, and the nurses, physicians, study coordinators, and other healthcare workers at our phase I sites, and the Syndax employees who have faithfully and brilliantly conducted this trial during a very challenging and difficult time. We began the AUGMENT-101 trial in November of 2019. The trial has progressed remarkably despite the COVID-19 pandemic. Before I turn things over to Eytan, let me turn to slide five and provide a perspective on the data that we have accumulated to date. Our intention at the start of the trial was to only present data once we have completed the phase I portion of the trial. You will see today that we are very close to completing the primary objective of the phase I trial, which is to define a recommended phase II dose. We have a dose that meets all of our pre-specified criteria for what we are looking for in a recommended phase II dose, but our investigators are completing their exploration of one additional dose cohort. The results of that cohort are unlikely to materially change our approach going forward, and thus we are eager to present this near-final data. I'll also note that AUGMENT-101 is a well-designed and conducted phase I trial. We are collecting an impressive amount of data as part of the trial, which will, of course, find its way into numerous scientific presentations and publications over time. Today's presentation will focus on the core objectives of the phase I trial, safety, PK, and defining a recommended phase II dose. Let me also emphasize that the data being presented today is from an ongoing phase I trial. The data is current as of the cutoff date and yet will continue to be updated over time. I've had the good fortune to oversee the clinical development of a number of important cancer medicines in my career, including most recently, osimertinib, olaparib, and durvalumab. Our Chief Medical Officer, Michael Metzger, most recently oversaw the development of bortezomib and avelumab. It's clear to both of us that the data we are seeing in this phase I trial of 5613 is highly reminiscent of the early data we saw for those important cancer medicines. 5613 appears to be very well-tolerated. No patient has discontinued therapy for a drug-related adverse experience. 5613 monotherapy is showing exciting early signs of clinical responses, both in patients with MLL-r leukemias and in patients with NPM1c leukemias, with a remarkable overall response rate of 48% in patients with either of these two mutations and 2/3 of those CRs we observe are CRs without measurable residual disease or so-called MRD negative. Eytan will explain the significance of CR without measurable residual disease. It's really quite important. With the data we are presenting today, it should be obvious that we are the leading company in the exciting field of menin inhibition, and we have the most clinical data. We're continuing to learn new things about the mechanism as the trial progresses. I will outline the steps we'll be taking to further our advantage over others entering this exciting field. Let me now turn the presentation over to Dr. Eytan Stein. Thanks, Briggs, for the introduction. For those of you I haven't interacted with previously, I've been an attending physician and clinical investigator on the leukemia service at Memorial Sloan Kettering for eight years, and I focus my research efforts on developing novel targeted therapies for patients with acute leukemias. I'm also fortunate to be the director of the Program for Drug Development in Leukemia, a dedicated phase I program for leukemia and related diseases where we investigate a wide variety of the most novel compounds being brought into clinical trials. You're all aware that acute myeloid leukemia is a terrible disease, on the next slide, with extremely poor outcomes, despite new drug approvals over the past five years. One of the bright spots, though, has been approval of targeted therapies like FLT3 and IDH inhibitors against specific genetic alterations that are found in AML. We lack targeted therapies for the large number of other genetic alterations that exist as part of this disease. One reason I'm so excited about menin inhibition is that it now allows us to target two other subgroups. Patients with chromosomal rearrangements involving the mixed lineage leukemia or MLL gene, those are the most common mutations seen in AML and NPM1. You can see here that the annual global incidence for MLL-rearranged leukemias is approximately 5,000-7,000 cases per year. Though these rearrangements occur in both AML and ALL, there is special kind of ALL in infants where 80% of those kids will have MLL rearrangements. The five-year overall survival for adult MLL-rearranged leukemias is less than 25%. NPM1 mutant Acute Myeloid Leukemia is more common. It has an annual global incidence of approximately 20,000 cases per year. The five-year overall survival for adult NPM1 mutant AML is approximately 50%, the co-occurring mutations with NPM1 really dictate the outcome. If you have a FLT3 with an NPM1 mutation, those patients have a very poor prognosis. An IDH mutation with an NPM1 mutation, those patients have a slightly better prognosis. There are known NPM1 co-mutations, which I just mentioned, that offer rational combination approaches. Finally, whenever I'm working with a targeted therapy, I ask myself whether doctors outside of major academic medical centers like Memorial Sloan Kettering will have the ability to identify the target of interest at the time of diagnosis or relapse. Luckily, assessment of MLL rearrangements and NPM1 mutations are part of the standard diagnostic workup for AML, not only in the U.S. but throughout the world. We generally know whether a patient is MLL rearranged or NPM1 positive within two to seven days after the diagnostic bone marrow biopsy. Next slide. What's the connection between menin, MLL rearrangements, NPM1, and leukemia? In the schematic on this slide, you see that the binding of menin to either the wild-type MLL complex for NPM1 mutant AML in the top panel, or to the MLL rearranged fusion transcript in the bottom panel, activates a leukemogenic transcriptional program that leads to the development of acute leukemia. The N-terminus of the MLL complex binds to menin, and what's nice about this, if you move on to the next slide, is that the binding pocket where menin binds to the MLL complex is druggable, with menin inhibitors blocking this interaction. If we go to the next slide and we put this all together, you see that the binding of menin to the MLL complex, whether wild-type like an NPM1 or the rearranged complex as in MLL-rearranged leukemias, leads to the transcriptional activation of leukemogenic genes such as HOX and MEIS1. When 5613, the menin inhibitor we are talking about today, is introduced, it blocks the menin MLL interaction, which turns off these leukemogenic genes, and that leads to apoptosis and more likely a differentiation program and clinical complete remissions. I'm going to show you some pharmacodynamic data in a few slides that highlights that this seems to be exactly what 5613 is doing in the study subjects. Next slide. AUGMENT-101, which is the trial we're talking about today, was designed based on regulatory input and then modified based on emerging data. At initiation, the trial enrolled all comers, regardless of mutational profile, with relapsed and refractory acute leukemia. SNDX-5613 is an oral drug given twice a day in continuous daily dosing, and there was an accelerated titration design that moved into a 3-by-3 dose escalation. As the trial progressed, it became clear that patients on strong CYP3A4 inhibitors, and in leukemia or acute leukemia we're talking really about azole antifungals, had a different pharmacokinetic profile than patients not on strong CYP3A4 inhibitors. Because of this, we felt that we had to split the dose escalation into two arms. Arm A for those not on strong CYP3A4 inhibitors and Arm B for those who were on strong CYP3A4 inhibitors. We amended the study to enroll not only adult patients but also kids from the age of 30 days and above. We restricted the enrollment to patients with MLL rearrangements or NPM1 mutations because this is the population of interest where we think menin inhibition is really working. Finally, we added the ability to backfill cohorts if a dose level cleared and responses were observed. The key endpoints of this study, as in all phase I studies, are safety, the pharmacokinetic profile of the drug, and establishing a recommended phase II dose. We pre-specified recommended phase II dose criteria at the outset of the trial. They are listed here. Number one, no more than one of six of the evaluable patients can experience a DLT. At least two-thirds of the patients have to receive greater than or equal to 80% of their dose in cycle one and cycle two. This gives us confidence that the drug is safe not only in the DLT period but beyond. Finally, the 24-hour AUC has to exceed 15,000 in at least 2/3 of patients. Next slide. Here's what actually has happened so far. If you look on the left-hand side, this is Arm A. These are the patients not on a strong CYP3A4 inhibitor. You can see Cohort One started at 113 milligrams twice a day, Cohort Two at 226 milligrams twice a day, and Cohort Three at 339 milligrams twice a day. There was one DLT in Cohort Two and two DLTs in Cohort Three. All of those DLTs were Grade Three QTc prolongation. We are now enrolling a Cohort four, which is 276 milligrams twice a day, which is an intermediate dose between Cohort Two and Cohort Three. On the right-hand side of the slide, you can see Arm B, again, those patients on a strong CYP3A4 inhibitor. Not surprisingly, the two DLTs occur at a lower dose level because the amount of drug in your system is higher when you're on a strong CYP3A4 inhibitor. Those two DLTs were at the 226 milligram twice a day dosing level. Similar to Arm A, we're now exploring an intermediate dosing level between Cohort One and Cohort Two. We're calling that Cohort Three, which is 163 milligrams twice a day. Next slide. We've defined populations both for safety and for the efficacy analysis. The safety population includes all 43 patients who received at least one dose of study drug. For the efficacy population, we removed the eight patients with an MLL rearrangement or an NPM1 mutation. That's not the target population of interest. We also removed the patients who are currently on treatment but have been on treatment for less than 28 days and have not had a response assessment. It's important to note that within the efficacy population, so within those 31 patients, we are including patients who received at least one dose of study drug but may have passed away before getting their response assessment. If a patient got study drug and passed away on day two, they are counted as a non-responder. Next slide. These are the demographics of the patients treated on the study so far. You can see the overall population is 43 patients, and again, this is the safety population. The median age is 54 years old, a little bit younger than you might be used to seeing in a trial of this sort. That's because, number one, we're enrolling pediatric patients, so there was a 16-year-old that was enrolled. Number two, MLL rearrangements and NPM1 mutations tend to occur in the younger patient population. They're less common in a patient who's 70 or 80 years old. 58% of the patients were women. The baseline performance status is what you normally see in a clinical trial of this sort. The genetics of the enrolled patients are below. 61% of the patients had MLL rearrangements, 21% of the patients had NPM1 mutations, and as I mentioned earlier, eight patients had neither an MLL rearrangement nor an NPM1 mutation. 34 of the 43 patients had acute myeloid leukemia. Eight of the 43 patients, 19%, had acute lymphoblastic leukemia, and one patient had something that is intermediate between AML and ALL called mixed-phenotype acute leukemia. The median number of prior therapies for the patients on the study were three. I want to highlight here just how poor risk this patient population is, and one of the things you see that shows this is that nearly 40% of the patients had relapsed after a prior allogeneic stem cell transplant. This is a patient population which has an extremely poor prognosis with currently available therapies. 58% of the patients had received prior venetoclax, and nine patients had received some kind of targeted therapy, either a FLT3 inhibitor or an IDH inhibitor. Next slide. What you will see here is the disposition of the patients on study as of the data cutoff. There are nine patients who are currently ongoing on study. 34 patients have discontinued treatment, 15 for progressive disease, eight for an adverse event, and four discontinued for a good reason, which is they went on to receive an allogeneic stem cell transplant. I'd like to highlight that the eight patients who discontinued for an adverse event had adverse events that were not related to 5613. Next slide. On this slide, you see the adverse events thought by the study investigator to be related to 5613. These are related adverse events. The grade one, two events are on the left, and the grade three and higher events are on the right. When I looked at this for the first time, and then I studied it a little bit, my overall take on the data is that 5613 is extremely well-tolerated. I do, however, want to draw your attention to two particular items. The first is the QTc prolongation, of which there were eight grade-one events, eight grade-two events, and six grade-three events. Of course, these grade-three events were the DLTs I showed you on the previous slide. There were no grade-four or higher QT prolongation events and no ventricular arrhythmias. To put this into context, many of our targeted therapies, including gilteritinib and ivosidenib, can cause QT prolongation. As leukemia physicians, we've all become adept at monitoring EKGs and managing this with dose adjustments if necessary. I also want to point out the five patients who had differentiation syndrome, which is a cytokine-mediated capillary leak syndrome. Differentiation syndrome occurs when the myeloid blasts are differentiating or maturing into neutrophils. Of course, that's what we want to see in any effective leukemia therapy. Next slide. What are the treatment goals for patients with relapsed and refractory acute leukemia? As you might imagine, the first treatment goal is to get rid of the leukemia, to eliminate the leukemia. How do we define whether the leukemia is eliminated? We define it based on morphologic CR. What does that mean? That means that the therapy has reduced the number of blasts to less than 5% of the marrow cellularity. That includes categories that include complete remission, complete remission with partial hematologic recovery, complete remission with incomplete platelet count recovery, complete remission with incomplete neutrophil recovery, and what we call a morphologic leukemia-free state. The important point here is that the morphologic CR is important. That means that you've gotten rid of the leukemia to less than 5% blasts in the bone marrow, and how the CR/CRh/CRp defines varying levels of blood count recovery. An MRD-negative CR means that by the most sensitive methods we have available to look for any evidence of leukemia cells in the bone marrow, the investigator or whoever's doing the assay is unable to find any evidence of residual leukemia, and that can be done either by multiparametric flow cytometry or by very sensitive molecular testing. After you eliminate the leukemia, let's look at what's next. We ask ourselves, if you have less than 5% blasts, and in this case, it can be MRD positive or MRD negative, we ask ourselves, Is the patient eligible for an allogeneic stem cell transplant? If yes, we get them to an allogeneic stem cell transplant, and if no, we want to maintain remission. Because if you maintain remission, you avoid infections, you minimize the need for transfusion, and you maximize the quality of life. Of course, doing an allogeneic stem cell transplant, you're also trying to maintain that remission. Next slide. These are the responses that we've seen so far to the 31 patients and the efficacy evaluable population. The overall response rate is really an impressive 48%, with 15 of 31 patients achieving a response. Five of those patients had a CR or a CR with partial hematologic recovery, five of those patients had a CR with incomplete platelet count recovery, and five of those patients had a CRi or an MLFS. I want to point out that the MRD negative overall response rate, so the levels of measurable residual disease, so no evidence of measurable residual disease, is 67%. Two-thirds of the patients were MRD negative. The overall response rate in the MLL-rearranged population was 13 out of 24 patients, the NPM1 mutant population was two out of seven patients. Obviously, the numbers for the NPM1 mutant population are small, I think we're going to need to wait for larger numbers of NPM1 mutant patients to get a better idea of what the true response rate is. There were four MRD negative patients who went on to receive an allogeneic stem cell transplant. Next slide. Okay, a few more things about the activity of the drug. There are responses observed both in AML and ALL. There are responses observed whether a patient is in arm A on without the strong CYP3A4 inhibitor or in arm B with a strong CYP3A4 inhibitor. There are responses observed in half, 50% of the patients who had previously undergone an allogeneic stem cell transplant and relapsed. I again want to highlight, this is a patient population that generally and unfortunately we have no good therapy for. Finally, responses were observed in nine out of 25 patients who received prior venetoclax. Next slide. I'm going to take you through three patient vignettes which highlight some important parts of this drug that were not caught on the response slides that I showed you a second ago. The first is a patient who's 69 years old with an MLL-rearranged leukemia. She received intensive induction chemotherapy with HiDAC and MVD and then received the targeted FLT3 inhibitor, gilteritinib, and achieved a complete remission. She subsequently relapsed and went on 5613, 226 milligrams twice a day with the strong CYP3A4 inhibitor, posaconazole. The patient was dose-reduced at day 17 because of a Grade two prolonged QTc, and again, she was reduced to 113 milligrams twice a day. If you look at the top here, you can see, obviously, she's got leukemia at Cycle one, day one. By Cycle two, day one, despite the dose reduction, she achieved a CR with partial hematologic recovery that is MRD negative, and then that evolves into a CR with full hematologic recovery that is MRD negative by Cycle four, day one. What this highlights is that the responses to this compound seem, at least in this patient, to evolve over time. You get blast clearance and an MRD negative state by Cycle two, day one, and complete count recovery by Cycle four, day one. I do want to highlight that at Cycle nine, day one, the patient had progressive disease, not systemically, but in her central nervous system. This highlights also, I think, that 5613 is not found primarily in the central nervous system and because it doesn't really cross the blood-brain barrier. Because of that, one might need to think in patients who are high risk for CNS disease, that those patients should receive prophylactic intrathecal chemotherapy. Next slide. This next patient is a 66-year-old woman with an MLL-rearranged leukemia. She got intensive induction chemotherapy with 7+3, achieved a complete remission, went on to receive an allogeneic stem cell transplant, remained in a complete remission, she's one of these patients that relapsed after her allogeneic stem cell transplant. She received entospletinib at the time of relapse. She was refractory to that, went on SNDX-5613 at a dose of 339 milligrams twice a day without a CYP3A4 inhibitor. She had a prolonged QTc at Cycle one, Day four, was dose-reduced to 226 milligrams twice a day. If you look at the top, you can see that despite the dose reduction, she achieves a CR with incomplete platelet count recovery by Cycle two, Day one, and that evolves into a CR that is MRD negative by Cycle three, Day one, again, showing you the evolution of responses with this compound. Next slide. The last patient here is a 30-year-old woman, unfortunate 30-year-old woman, with a therapy-related acute myeloid leukemia with an NPM1 mutation. She received intensive induction chemotherapy with daunorubicin and cytarabine, the liposomal formulation, and was refractory to that. She received SNDX-5613 at a dose of 113 milligrams twice a day with posaconazole. She was not dose-reduced, did not need to be dose-reduced. Again, you see that at Cycle two, Day one on the top, she had a CRi that was MRD negative, and at Cycle three, Day one, that evolved into a CR that was MRD negative. Next slide. The pharmacokinetic profile of the drug is shown below. Dose proportional exposure is achieved across both arms, with steady-state levels achievable in approximately two days and no evidence of drug accumulation. Next slide. Here's that interesting pharmacodynamic activity I was telling you about before. You'll remember that when menin inhibitors block the interaction of menin and the MLL complex, what was predicted preclinically was that you would get a turning off of the transcriptional activation of leukemogenic genes. If you look on the left-hand side here, you see in 16 patients how MEIS1, PBX3, and HOXA9, all leukemogenic genes, all really go down by Cycle 2, Day 1 in the bone marrow samples of patients taken at screening and, as I said, at Cycle two, Day one. In addition, on the right-hand side, and this is going to be a discussion for a future academic conference, you get the upregulation of differentiation markers because I firmly believe that one of the ways this drug is working is as a differentiation therapy, as I mentioned earlier, allowing the malignant myeloblast to mature to healthy adult neutrophils. You can see here the upregulation of these differentiation arms. These gene expression changes are seen across arms, dose ranges, and in both MLL-rearranged and NPM1 mutant patients. Next slide. I talked about the pre-specified selection criteria for advancing to phase II. We feel that we've met all three of these criteria and that those doses would be 226 milligrams twice a day for those patients not on a strong CYP3A4 inhibitor and 113 milligrams twice a day for those patients who are on a strong CYP3A4 inhibitor. That is because, just to remind you what the criteria were, no more than one of six of the evaluable patients experienced a DLT. At least 2/3 of the patients received greater than or equal to 80% of their dose in Cycle one and Cycle two, and the 24-hour AUC exceeds 15,000 in at least 2/3 of the patients. The adverse events and response results in the patients who received the candidate recommended phase II dose are consistent with the overall population, and perhaps importantly as well, the Grade 3 QTc prolongation at the candidate recommended phase II dose is 9%. That is consistent with other approved drugs for relapsed and refractory and newly diagnosed acute myeloid leukemia. Next slide. In conclusion, targeted therapy for MLL-rearranged and NPM1 mutant leukemias are desperately needed. That's sort of the understatement, I guess, of the week, at least. These patients do horribly, and they need something to get their leukemia into remission. 5613 is a well-tolerated oral therapy with a very favorable adverse event profile. We think we've met the criteria to establish a recommended phase II dose. The pharmacodynamic data is really cool and really interesting because I think it shows target engagement and downregulation of leukemia-causing gene expression. There is evidence of single-agent anti-leukemia activity, again, with an oral therapy that is well-tolerated with an overall response rate of 48%, 67% of those responders achieving an MRD negative status. This certainly compares favorably with other agents that are available for relapse and refractory AML. If you think about the chemotherapy that we give these patients for relapse and refractory AML, that chemotherapy rarely works, and it has all sorts of really, really difficult side effects for the patient that causes significant toxicity. Finally, the phase I results in this relapsed and refractory population strongly supports moving SNDX-5613 into phase II and earlier lines of treatment. I always want to see active agents that are being used in relapse and refractory acute leukemia, certainly SNDX-5613, moved earlier up into treatment because you want to give the drugs to patients before they've had a chance to relapse. With that, I thank you very, very much for your attention, and I'm going to turn it back over to Briggs. Thanks so much, Eytan. We're very grateful for your leadership of the study, for your very clear explanation of the data, and of course, your perspective on this data, given your extensive personal experience in developing molecularly targeted agents for AML. On slide 31, I outline our next steps. As we've noted, we have a dose that meets all of our criteria for recommended phase II dose, but our investigators are completing their investigation of the one additional dose cohort. We anticipate completing these additional cohorts and starting our phase II expansion cohorts later this quarter. I'll remind you that we have planned three phase II expansion cohorts in the relapsed refractory setting, MLL-r AML, MLL-r ALL, and NPM1c mutant AML populations. These are three parallel and independent phase II expansion cohorts. We are opening clinical sites across multiple countries to enable rapid enrollment. We anticipate holding our end of phase I meeting with FDA in the third quarter to discuss whether these expansion cohorts could potentially be registrational and what level of evidence would be needed if they were registrational. If all goes well and our data holds up, we could potentially have top-line data and file our first NDA in 2023. Let me now turn to slide 32 and share our vision for 5613 as I think introduced by Eytan. To introduce this, I want to first touch on a key lesson that Michael Metzger and I have learned over our many years of developing cancer drugs. The earlier you treat patients, the better they do, and the longer the patients stay on drug. To achieve this, you need a drug that works and a drug that is well-tolerated for chronic use. We believe we have that in SNDX-5613, our plan is to aggressively move to treating patients as early as possible in their disease course. Our goal, put simply, is to redefine the leukemia patient journey. If we look at patients today, we think there are three key goals that need to be addressed. First, get more patients into CR with their initial therapy, therefore increase the% of patients who could potentially progress to curative bone marrow transplant. For all patients, use long-term maintenance therapy to extend the time that patients are in remission. We are necessarily starting our development program on the far right side of this figure with patients who have relapsed or refractory disease with extremely poor prognosis. In his presentation, Eytan mentioned four cases where we could get relapsed patients into remission and allow them to progress to potentially curative bone marrow transplant. This is, of course, incredibly exciting, and yet we believe we could have a much greater impact on the disease by rapidly moving into earlier lines of therapy and into the maintenance setting. As shown on slide 33, we're planning to initiate trials potentially later this year in which we ask whether we can increase the CR rate in combination with standard agents used in the first-line setting, and additional trials to ask whether 5613 can be used to maintain CRs, whether that occurs with first-line chemo or after a transplant. Let me now turn to the final slide and summarize why we are so excited about the 5613 program. It's clear to us that, at least today, we feel like we are the leading company in the exciting field of menin inhibition, and that 5613 is well-positioned to be the first approved molecule in this important field. In a little over 16 months, in the midst of a global pandemic, our team, working closely with investigators like Dr. Stein and with the FDA, has generated a significant phase I data set consisting of 41 total patients and 31 patients with MLL-r NPM1c mutations. We've identified a candidate-recommended phase II dose that meets all of our pre-specified criteria. At that dose, SNDX-5613 has shown promising responses and good tolerability. We anticipate initiating our pivotal trial this quarter. I think we have a clear and broad development strategy that will further advantage us over others entering this field, including both in frontline and in maintenance settings. As we speak to more and more physicians, we are more and more convinced that menin inhibition, specifically 5613, could potentially be the most important molecularly targeted therapy in acute leukemia, benefiting up to 40% of patients with AML and the 10%-15% of patients with ALL whose disease is not adequately treated today. With that, let me open the line to questions. At this time we would like to take any questions you might have for us today to ask a question press star one on your telephone keypad, again star one. We ask that you please limit yourself to one question and one follow-up question. From online webcast please mute your computer before asking a question. Your first question comes from the line of Phil Nadeau with Cowen and Company. Morning. Thanks for taking my question. One on side effects and a follow-up on the efficacy. First on the QTc. We've seen the grade three QTc for the recommended phase II dose, but I don't believe you broke out the grade one and two for that dose. I guess out of completeness, what was the grade one and two rates of QTc at the phase II dose, and how does that inform the overall dose response relationship for QTc and the chances of seeing a somewhat different profile as you move into a larger study? What's your second question, Phil? The second is just on duration of response. It seems like 80% of the patients have actually left the study. I'm curious if you have a preliminary early read on the durability of the CRS. Sure. Let me take the first question first. I don't think I have the exact number on the grade ones, twos at the recommended phase II dose. Eytan showed you the numbers for the population overall. Again, those grade 1 and 2s generally are intermittent, so they occur once, so they don't occur later on in the study, and none of the grade one or twos do we have For duration, I think we showed some of the vignettes to give you some sense of how the drug is performing. Obviously, it's relatively early in the trial. There's nine patients still on trial, We'll update the durability as we present data potentially later this year at ASH. Perfect. Thanks for taking my questions, and congrats on the data. Looks great. Thanks, Phil. Your next question comes from the line of Bert Hazlett with BTIG. Yes. Thank you for all the comments. Could you just give us the rates of minimal residual disease by NPM1 and MLL-r? I think we have, excuse me, we have a response rate of 29% in NPM1 and 54%. Could you give us the MRD statistics in those groups? Yeah, Bert. Again, I don't think I have that number off the top of my head. Remember, as of the data cutoff, there are only two responses to the NPM1, so I don't know the relatively small number, be able to break out the MRD negative by MLL-r. Okay. Just let me slide in a quicker one. With regards to the QTc, handling the patients with QTc, were they mostly dose reduced and is that a concern as you might consider this molecule earlier on? Thank you. Right. The grade three QTcs by protocol, the requirement was to pause the drug until the QTc adverse experience resolved and then dose reduce. As Eytan showed in a couple of the vignettes, two of the vignettes were dose reduced, went on to have very nice MRD negative CR. Eytan, you might want to just give a comment about sort of the clinical utility and having to monitor for QT. Yeah. We monitor for QT prolongation with, as I mentioned in the talk, we monitor for QT prolongation with a lot of our drugs. You think about ivosidenib, you think about gilteritinib. We monitor for QT prolongation with Levaquin and with Cipro and when psychiatrists give Seroquel, they tell you to monitor for QT prolongation. This is something that we do all the time, and honestly, not just leukemia doctors, but all doctors. If you need to, you hold the dose and you wait for the QT to shorten a little bit, or there are dose adjustments that can be made. From a clinical perspective, it's really of no clinical import at all. Thank you. Great data. Thanks. Your next question comes from the line of Peter Lawson with Barclays. Great. Thanks. Congrats on the data. Maybe a question for Dr. Stein, just when we look at the kind of QT prolongation, it seems to be similar to what we see for things like IDHIFA. Do you exclude patients for that kind of level of QT prolongation? No. By the way, IDHIFA doesn't have QT prolongation. It's the IDH1 inhibitor that has the QT prolongation, so that's ivosidenib. The answer is no. We would never withhold a treatment like this for a patient. You would certainly never withhold it for a patient because of a concern for QT prolongation. If they had QT prolongation, you would do everything you possibly could to continue the treatment. The overall survival of these patients is less than 5% probably at one year. Just not speaking about 5613, but speaking about the other drugs that can cause QT prolongation, like gilteritinib and ivosidenib, I have never, ever withheld a drug from a patient because of that. I don't know anyone who has. Thank you. Thanks for putting that into perspective. Just the CYP3A4 and QT prolongation that we're seeing with the drug, do you think that changes in any way the combinations that you'd want to try, whether it's venetoclax or others? Yeah. Thanks for the question, Peter. I think as Eytan pointed out in his presentation, the rational combinations you would think about in the NPM1 population based upon co-mutations, and there are combinations with standard agents that are used in the first-line therapy of these patients, whether it be chemotherapy or Venclexta. I don't think there's anything in the profile of the drug that would prohibit us from studying those rational combinations and upfront. Great. Thanks so much. Congrats on the data. Your next question comes from line of Justin Walsh with B. Riley Securities. Hi. Thanks for taking the question. Are you able to provide any color on additional mutations that the NPM1 patients harbored? I'm just wondering if they had better or worse prognostic factors. Then a sort of follow-up for Dr. Stein. I'm just wondering from your experience treating patients with this drug, what feedback did you receive from the patients with respect to how well, how tolerable they felt the drug was? Let me take the first question on the mutation. As I said at the very beginning, there's a ton of data being analyzed as part of this trial, but we are doing full exome sequencing on the patient samples. That data is just coming together, so we don't have that in final form. Great question about the mutations that Eytan pointed out. Patients with NPM1 and co- mutations tend to have a worse prognosis than those that don't, but I think these patients have already declared themselves as having a bad prognosis because they have relapsed refractory disease despite all their previous therapies. We'll see. As we gather all the exome sequencing data, we'll say more about the mutation. Eytan, you might want to comment on your view about patient tolerating the drug. I want to just build on something you just said, Briggs, because I do think this sometimes gets lost. There are certain NPM1 mutant patients that, at the time of diagnosis, are considered favorable risk. Any patient who has relapsed and refractory acute leukemia is by definition unfavorable because they've proved that whatever you thought their favorable risk was at the beginning, it wasn't so favorable, or else they wouldn't have relapsed. That's number one. In terms of the tolerability of SNDX-5613, what I can tell you is that all of the patients that I have personally treated have not had any tolerability issues. They have not had any symptomatic toxicities related to SNDX-5613. I think the overall feeling that my patients have are that it's kind of miraculous, right? Here they're taking an oral pill. A lot of these patients, by the way, get referred in from places who've told them to go to hospice care. They're being told they should go to hospice. They're calling us as like a last-ditch effort, maybe we'll have something, and then we give them this pill. Obviously, the ones who respond think it's a miracle. They're at home taking a pill, and they're in remission. Overall, that's dramatic, but it's true, and the tolerability is very, very good. Great. Thank you for taking the question. Your next question comes from line of David Lebowitz with Morgan Stanley. If you could break down the MLLR responders between ALL and AML patients. Similarly, could you possibly break down responders based on what dose they received, if they received the CYP3A4 dose level or the non-CYP3A4 dose level? Yeah. Hi, David. Thanks for your question. As Eytan pointed out, there are responses both in ALL and AML. Again, I just want to put some context. This is an ongoing phase I trial in which 30 patients have been treated, I think it's a little hard to give too much of dissecting of rate of responses in the various subcategories. Obviously, that's what phase II is for. We have a dedicated ALL trial in phase II and a dedicated AML trial in phase II. Similarly, I think for the dose responses, as you saw from the way the trial progressed, relatively small numbers of patients at each dose on each arm. The numbers are just very small. I think I missed the last part of that. Have there been responses, I guess? Can you at least give some sort of qualitative data as to did you see some specific responses in the ALL population? Did you see a certain level of, I guess, responses at the lower dose in the CYP3A4 dose as well? Yeah. As Eytan pointed out, we have seen responses both in ALL and in AML. At the recommended phase II dose, we've seen responses both in Arm A and in Arm B. Oh, thank you very much for taking my questions. Thanks, David. Your next question comes from the line of Colleen Kusy with Baird. Yeah, good morning. Thanks for taking our question, and congrats on the news this morning. Maybe for Eytan, if you can speak to the Grade three adverse events seen in the trial so far beyond QT prolongation and how manageable those are in your experience. Yeah. The Grade 3 adverse events that we saw outside of the QT are all very, very manageable. They are things that we commonly see in patients with acute leukemia, even if they were casually related by the study investigators. They are easy to deal with and not a big issue. The rates of those are very low. I don't think that's an issue. I guess the one thing you might be thinking about is the differentiation syndrome. The differentiation syndrome, as I mentioned in the talk, is something that's good. It means that your leukemia cells are going away. Differentiation syndrome is seen with a wide variety of drugs now in acute leukemia. The prototype for differentiation syndrome that caused it was ATRA and arsenic trioxide for acute promyelocytic leukemia. The IDH inhibitors can cause a differentiation syndrome. The gilteritinib can cause a differentiation syndrome. Leukemia docs and oncologists in general know to look out for it. The good thing about differentiation syndrome is that when it's recognized, it's easily shut off by giving steroids. You see it, I had a patient on a different drug a few weeks ago who I recognized differentiation syndrome. I started steroids, it went away, and that was it. It's increasingly recognized, and I think recognized by all oncologists and easy to deal with. The other grade three events, I think are very low and not of any clinical significance. They're not something that we can't deal with. Great. Thank you. Maybe for Briggs, for the phase II expansion cohorts, are there initial thoughts on the expected size of those cohorts and what the bars might be in the separate enrollment cohorts? Yeah. There are initial thoughts. I think the size of those will in part depend upon the statistical design of what is the bound the response rate would have to exclude. Then there'll also be a question particularly of how much for overall safety at the time of filing. Those are discussions that Michael and his team will have with the agent at our end of phase I. Great. Thanks so much. We do have a follow-up question from the line of Peter Lawson with Barclays. Great. Thanks for taking the follow-up. I may have missed this, Briggs. Just do we get a sense of the NPM1 patients? Were those CRs? I've got a quick question for Dr. Stein, just around the kind of real-world use of azoles and whether patients are complying or not, and if an approval would kind of require an azole on board. Thank you. Yeah. Thanks so much for the follow-up questions, Peter. The third vignette that Eytan presented was a patient with NPM1 relapsed refractory disease, went on to have a CR and so that's one of the two responses to NPM1. I will just mention that in NPM1, the additional NPM1 population, we have seen evidence of, I guess one might call anti-leukemic activity. It didn't reach the criteria for a CR, but it's clear to us we're seeing evidence of activity off the revumenib. Eytan, you probably can't detect azoles. Yeah, I'm not sure I got the entire question, but I'll answer what I think I understood, which is that, I think the question was around the use of azoles in the real-world setting in patients with acute leukemia. In patients in many places, not all places, but in many places, in patients who are neutropenic with acute leukemia, they go on azole antifungal prophylaxis. There are three azole antifungals that we use most commonly. Two of them are strong CYP3A4 inhibitors. One of them is not a strong CYP3A4 inhibitor. Which azole the patient gets is often dictated by insurance and not by what the doctor wants to do necessarily. I think one of the good things, there are many good things about how azacitidine and venetoclax has been approved, but one of the things that that approval has done is it's given oncologists and hematologists a lot of experience with modifying dosages of medications because of concomitant azole prophylaxis. You know that with venetoclax, without a concomitant strong CYP3A4 inhibitor, the dose is 400 milligrams once a day. With a concomitant strong CYP3A4 inhibitor, it's either 100 or 70 milligrams once a day. We have a lot of experience with these sort of dose reductions, and luckily a lot of us have, and I think most of us have pharmacy staff that we can talk to if we have any questions about this. To summarize, yes, azoles are used in real-world practice in most places around the country. Some are strong CYP3A4 inhibitors, some are not. When they are strong CYP3A4 inhibitors, we know how to dose adjust for that drug interaction. There's no problem with compliance for the azoles. I guess I'm just kind of thinking through the idea of needing or not needing a strong CYP3A4 inhibitor to change the dose level of the azole. Oh, no. There are no compliance issues. There are no compliance issues. All the patients are deathly afraid of getting an infection because they know that the infections are the things that are the most serious complication of acute leukemia. They're told, You really need to take this. This is going to prevent a fungal infection, which could be very bad. I have not encountered in my practice or talking with colleagues, people that don't want to take azoles. Great. Thank you so much. It's really helpful. There are no further questions at this time. Great. Well, thank you, everybody. We're right on the hour. Again, I want to thank Eytan for taking an hour out of his very busy schedule to help put this data in context, and we thank him again for his leadership with the file. Thank you all. I think it should be clear that we're quite excited about what we're seeing. I will say our excitement really stems from the excitement of Eytan and the other principal investigators for treating these patients. They tell us they're excited, we can't help but also be excited. Thank you very much for your time this morning. We'll talk to you later.