Good day, everyone, welcome to the pivotal AGAVE-201 top line axatilimab data conference call. Today's call is being recorded. At this time, I would like to turn the call over to Sharon Klahre, Head of Investor Relations at Syndax Pharmaceuticals. Thank you, operator. Welcome. Thank you all for joining us today. I'm Sharon Klahre. With me this morning to provide a review of top-line results from the pivotal AGAVE-201 trial of axatilimab in adult and pediatric patients with chronic graft-versus-host disease, following 2 or more prior lines of therapy, are Michael Metzger, Chief Executive Officer, and Dr. Neil Gallagher, President and Head of R&D. Joining us on the call today for the question and answer session are Dr. Peter Ordentlich, Chief Scientific Officer, Dr. Anjali Ganguli, Chief Business Officer, and Keith Goldan, Chief Financial Officer. This morning, we issued a joint press release with Incyte, reporting top-line data for the pivotal AGAVE-201 trial of axatilimab, which can be found on the investor page of Syndax's website. Please turn to our forward-looking statement disclosures on slide 2. Before I begin, I'd like to remind you that any statements made during this call are not historical, are considered to be forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995. Actual results may differ materially from those indicated by the statements as a result of various important factors, including those discussed in the Risk Factors section in the company's most recent quarterly report on Form 10-Q, as well as other reports filed by the SEC. Any forward-looking statements made on this call represent our views as of today, July 24th, 2023, only. A replay of this call will be available on the company's website, www.syndax.com, following its completion. I am pleased to turn the call over to Michael Metzger, Chief Executive Officer of Syndax. Thank you, Sharon. Thank you all for joining the webcast on this very exciting day for Syndax. This morning, we are thrilled to announce that all three cohorts in the AGAVE-201 pivotal trial of axatilimab, our monoclonal antibody targeting the CSF-1R, met their primary endpoint of overall response rate in patients with refractory chronic graft-versus-host disease. These responses were durable and accompanied by a reduction in symptom burden in a notably advanced and heavily pretreated patient population. Furthermore, axatilimab was generally well tolerated, and the most common adverse events were consistent with on-target effects in prior trials, and we feel confident that these results will provide the necessary data for optimal dose selection. With these positive results now in hand and pending agreement from the regulatory authorities, we, along with our partners at Incyte, continue to expect to submit a BLA by year-end, with potential commercial launch in 2024. We and Incyte are extremely excited to be one step closer to bringing axatilimab to patients suffering from this devastating underserved condition. Before we turn to the trial results, let me just remind you on slide 4 why we believe axatilimab will bring an effective and differentiated option for the 14,000 patients in the U.S. that suffer from chronic GvHD. Axatilimab has the potential to be the first approved treatment for chronic GvHD to target the disease-modifying macrophage. The graphic on slide 4 clearly demonstrates how the activation, proliferation, and survival of these macrophage populations is regulated through the CSF1 receptor. Through its ability to directly bind the CSF-1R, axatilimab is designed to decrease the proliferation and function of CSF-1R and dependent monocytes and their associated macrophages and has now demonstrated robust monotherapy activity in heavily pretreated patients. We believe axatilimab's differentiated mechanism may also offer the advantage of being an ideal combination partner with standard of care therapies available for the management of this disease. Axatilimab's ability to suppress macrophages allows it to have a significant impact on both anti-inflammatory and anti-fibrotic pathways, both of which are involved in driving the progression of chronic GvHD. Axatilimab is administered as a short 30-minute infusion in the clinic, allowing clinicians to have control over compliance as well as better treat patients experiencing any absorption issues, such as those with gastrointestinal manifestations. Based on its compelling clinical profile, which Neil will go through in the following slides, supported by the positive feedback we have received from numerous key opinion leaders and treating physicians, we firmly believe that if approved, axatilimab will become an important addition to the chronic GvHD treatment armamentarium. I will now ask Neil to walk us through the AGAVE-201 results. Neil? Thank you, Michael. Turning now to slide 5, the global pivotal AGAVE-201 trial enrolled 241 adult and pediatric patients at 121 sites across 16 countries. The trial evaluated the efficacy, safety, and tolerability of axatilimab in patients with active chronic graft-versus-host disease, whose disease had progressed after at least two prior therapies. The primary endpoint of the trial was an overall response rate by cycle 7, day one, C7, D1, using the 2014 NIH Consensus Criteria for chronic GvHD. Patients were randomized to one of three treatment groups, each investigating a different dose of axatilimab. These were 0.3 mg/kg every two weeks, 1 mg/kg every two weeks, and 3 mg/kg every four weeks.... Patients were treated until progression, after six months on trial, patients at the 0.3 mg/kg and 1 mg/kg doses had the option to switch to an equivalent once-monthly dose. Patients were stratified at baseline based on prior exposure to ibrutinib, ruxolitinib, or belumosudil, as well as by disease severity. Because macrophages play an essential role in maintaining physiological homeostasis, these regimen were chosen to allow time for recovery of the macrophage population, thereby potentially minimizing adverse events while maintaining robust efficacy. The demographics on Slide 6. Here we present key baseline demographic data for patients included in the trial. The median age of patients enrolled, excuse me, in the trial was 53 years. The median time since diagnosis of chronic GvHD was four years. 54% of patients had 4 or more organ systems involved at baseline, including 45% of patients with lung manifestations. Patients had received a median of 4 prior lines of therapy, frequently consisting of recently approved therapies, as demonstrated by the fact that 74% of them had received prior ruxolitinib, 31% had received ibrutinib, and 23% had received belumosudil. 80% of patients enrolled were classified as having severe chronic GvHD based on the NIH criteria. Now turning to Slide 7. The AGAVE-201 trial met its primary endpoint of ORR by Cycle 7, Day 1 across all dose cohorts, represented by the teal-colored columns on the chart. The response rate was assessed using the 2014 NIH Consensus Criteria for chronic GvHD for each dose. A cohort met the primary endpoint of the trial if the lower bound of the 95% confidence interval exceeded 30%, which corresponds to meeting or exceeding an approximate 40% ORR for an 80 patient-sized cohort. The overall response rate by Cycle 7, Day 1, was 74% in patients treated at 0.3 mg/kg every two weeks, 67% in patients treated at 1 mg/kg every two weeks, and 50% in patients treated at 3 milligrams per kilogram every four weeks. As you can see, the lower bounds of the confidence intervals for all cohorts exceed the minimum requirement. In addition, we have included the best overall response achieved on trial, represented by the dark blue columns. These results further support the consistency of effect observed within each dose cohort. The response rates were higher in the 0.3 mg/kg and 1 mg/kg cohorts than in the 3 mg/kg every four week cohort. The highest overall response rate was achieved in the 0.3 mg/kg cohort at 74%, as I mentioned a little earlier. While we've not yet analyzed exposure response relationships, these data may support our belief that lower doses provide a greater opportunity for macrophage function recovery between dosing intervals, and that this may be key to higher response rates and improved tolerability, particularly at the 0.3 mg/kg dose level. I'd like to reiterate that patients enrolled in the AGAVE-201 trial had a longer time since diagnosis of their disease, 4 years, received more prior lines of therapy for chronic GvHD, and had a higher proportion of lung disease involvement than patients included in prior pivotal trials for approved agents. Although the trial was initiated in early 2021, before either ruxolitinib or belumosudil had been approved for the treatment of the disease, a high% of patients in the AGAVE-201 trial had previously received these therapies. This highlights the robustness of the clinical activity of axatilimab observed in the study, and the value of targeting this disease directly by inhibition of macrophages rather than through targeting T or B cells. On Slide 8, there were several secondary endpoints included in the study, including duration of response, validated quality of life assessments using the modified Lee Symptom Scale,% reduction in daily steroid use, and organ-specific response rate. Slide 8. We include positive results from some of these secondary endpoints, and we look forward to presenting the full set of data that further speaks to the robustness of the outcome of the AGAVE-201 trial at a future medical meeting. At the time of the data cutoff in April 2023, the median duration of response, based on the Kaplan-Meier estimate, defined as the time from initial response until progression or death, had not been reached in the 0.3 mg/kg cohort. Among responders treated at 0.3 mg/kg, 60% of patients maintained response at 12 months. Importantly, clinical responses were also accompanied by a reduction in chronic GvHD symptom burden, with 55% of patients treated in the 0.3 mg/kg cohort experiencing a clinically meaningful improvement in symptoms, as measured by at least a 7-point improvement in the modified Lee Symptom Scale score. Responses were observed in patients previously treated with ruxolitinib, belumosudil, and/or ibrutinib, which is meaningful as physicians will want to understand the outcome for real-world treatment for their patients with refractory chronic GvHD. Moving to Slide 9, axatilimab demonstrated a manageable safety profile in this refractory and heavily pretreated population. The most common adverse events observed were consistent with on-target effects of CSF1R inhibition and prior results from axatilimab trials. Patient, amongst the patients treated at 0.3 mg/kg, 18% experienced a grade three or greater treatment-related adverse event, and only 6% of patients discontinued treatment due to an adverse event. Fatigue was the only adverse event of any grade that occurred in over 20% of patients. In slide 10, we show the adverse event profile for all patients treated in the trial. A higher proportion of patients discontinued therapy at the higher doses, and overall, a higher proportion of patients at higher doses experienced adverse events of any grade. Laboratory adverse events that occurred in over 20% of patients included expected on-target events, such as increases in enzymes, aspartate aminotransferase, blood creatine phosphokinase, lipase, blood lactate dehydrogenase, and alanine aminotransferase, as well as fatigue. Overall, the safety profile of axatilimab was as expected. In summary, the data from the AGAVE-201 trial demonstrates a robust clinical activity and manageable safety profile of axatilimab in patients with recurrent or refractory active chronic GvHD, and confirm our belief that axatilimab, with its differentiated profile and unique mechanism of action, is poised to provide a meaningful benefit to patients and change the paradigm of the treatment of chronic GvHD if approved. I'll now turn the call back to Michael. Yeah. Thank you, Neil. Slide 11 provides an overview of the chronic GvHD market. We estimate that approximately 14,000 U.S. patients suffer from chronic GvHD, 50% of whom require treatment beyond second line due to disease progression, inadequate response, or disease manifestations that aren't fully addressed with current treatments. This population is expanding due to a rising prevalence of blood cancers, as well as an increase in the number of stem cell transplants, and is expected to continue to grow beyond the $2 billion-$2.5 billion market estimate for 2022. There are, unfortunately, no cures for this advanced population of chronic GvHD patients. Following initial treatment with corticosteroids, many patients are cycled through a variety of additional therapies. We believe there is a broad clinical and commercial opportunity for axatilimab. As outlined on slide 12, the treatment paradigm for these patients is evolving with the recent approvals of therapies specifically for the treatment of chronic GvHD. Until recently, most chronic GvHD patients were managed with off-label generic agents. However, Jakafi and Imbruvica are now approved second line treatments for chronic GvHD, while Rezurock is approved as a third-line agent. Despite these approvals, there remains a significant unmet medical need for a disease-modifying treatment, and chronic GvHD continues to cause significant morbidity and mortality among patients following transplant. Importantly, the successful commercial launches of Incyte's Jakafi and Sanofi's Rezurock speak to the unmet need in chronic GvHD that translates to a large commercial opportunity. Chronic GvHD can manifest very differently across patients, and there is no one-size-fits-all therapy for these patients. As physicians gain experience with the recently approved drugs for chronic GvHD, they may choose their treatment option based on ability of a given agent to manage specific disease manifestations. We believe axatilimab's unique mechanism of action and clinical and safety profile will provide a differentiated option for the treatment of chronic GvHD, if approved. On slide 13, I want to reiterate a few key points that we covered in the presentation. First, axatilimab is the only investigational agent to target disease-causing macrophages and impact fibrosis and inflammation as a way to treat chronic GvHD. We believe the data shows that axatilimab has a best-in-category profile at the 0.3 mg/kg every two week dose. In the AGAVE-201 trial, patients experienced a high overall response rate, which was durable and accompanied by a meaningful reduction in symptom burden, as measured by the modified Lee Symptom Scale. axatilimab is a monoclonal antibody, it is less likely to cause drug-drug interactions than small molecule competitors, it has been very well tolerated throughout the chronic GvHD clinical experience, especially at the 0.3 mg/kg dose. We feel confident that this trial reflects real-world treatment, given how many patients were treated with recently approved standard of care agents prior to entering this trial. axatilimab's ability to target monocyte-derived macrophage development, activation, and proliferation may provide a more comprehensive control of the disease as compared to targeting of individual enzymes or signaling pathways. This could be a key differentiator and suggests a benefit for moving axatilimab earlier in the treatment regimen to help prevent organ damage before it occurs. Combinations in earlier settings, both in adults and pediatrics, as well as the opportunity to expand to the ex-US markets, could build significant additional value for axatilimab in chronic GvHD. The impact of axatilimab across all organ manifestations in chronic GvHD, as demonstrated in the published phase 1/2 data, also supports expanding into other fibrotic diseases. Specifically, the data we presented in chronic GvHD-related bronchiolitis obliterans syndrome, or BOS, at the American Thoracic Society conference earlier this year, coupled with the fact that we had a high percentage of patients with lung manifestations enrolled in this trial, provides further support that axatilimab may provide a substantial benefit in other diseases of the lung, where the monocyte macrophage lineage is thought to play a key role, such as idiopathic pulmonary fibrosis, or IPF. Slide 15 lays out the near-term milestones that we anticipate will enable us to realize the full potential of axatilimab for patients and maximize growth for Syndax. We expect to present the full data set from AGAVE-201 at a future medical meeting, which would allow us to further present on axatilimab's compelling clinical profile and the overall benefit it can bring to chronic GvHD patients. Along with our partners at Incyte, we intend to discuss these data with regulatory authorities and pending agreement to submit a BLA for axatilimab in relapsed or refractory chronic GvHD by the end of 2023. While Incyte will be leading these regulatory activities, we will be collaborating with them closely to ensure timely and successful submission. We are looking forward to the initiation of two clinical trials by year-end 2023. In chronic GvHD, we expect that Incyte will initiate a phase 1/2 combination trial of axatilimab with Jakafi in treatment-naive patients. Moving axatilimab earlier in combination could potentially reduce steroid use and benefit morbidity and mortality. In IPF, we plan to initiate a phase II trial with the goal of generating proof of concept for axatilimab on top of standard of care treatments, along with clinical information to better guide the long-term development in IPF. We remain keenly focused on preparing for potential commercialization of axatilimab with Incyte, a clear leader in the GvHD space. They bring significant experience and expertise that will help to appropriately message and position axatilimab in the evolving treatment landscape using its differentiated mechanism of action and the positive results from AGAVE-201 to delineate axatilimab's value proposition to both physicians and patients. The positive AGAVE-201 pivotal data that we've reviewed today continues to support our belief that axatilimab will be a differentiated, effective, and practice-changing intervention for this underserved population. This is an exciting time for Syndax. I look forward to providing future updates on the axatilimab program, as well as top-line data for our AUGMENT-101 pivotal trial of revumenib in patients with KMT2A rearranged acute leukemia later this quarter. Before we turn it over for questions, I would like to take a moment to extend our gratitude to the patients, their families, the investigators, and site staff who participated in AGAVE-201, as well as earlier axatilimab trials. We would not be at this exciting juncture today without your valuable contributions. Additionally, I would like to thank the teams at Syndax and Incyte for all of their hard work and collaboration, which made this trial and the positive data readout possible. With that, let's open the line for questions. At this time, if you would like to ask a question, please press the star and one on your touchtone phone. You may remove yourself from the queue at any time by pressing star two. Once again, if you would like to ask a question, please press star one. Our first question comes from Salveen Richter with Goldman Sachs. Hi, thanks. Good morning. This is Matt on for Salveen. Could you just go a little more in detail on the market opportunity in the US? You said 14,000 patients, 50% pass beyond corticosteroids. You know, you have those 7,000 patients. How many pass beyond, you know, Jakafi treatment? How many are you looking at in terms of this, you know, third line plus? Thanks. Great. Thanks so much for the question. I'm actually going to ask Anjali to take that, the question, please. Yeah. Thanks for the question. We actually believe that it's close to, you know, 80%-90% of patients will need treatment beyond Jakafi. I think there's an evolution of this paradigm that's changing because of the fact that now these physicians have agents that they can really believe will help their patients, and I think they're more likely to try additional treatments rather than, you know, potentially give up or send them to hospice. You know, the ability to move beyond to new therapies once something stops working, and know what to look for and know what to expect with the, you know, in terms of safety and efficacy and potentially even specific impact on organ manifestations, I think will really change the game for physicians, and we're really excited to be bringing this novel treatment to the marketplace. Got it. Thank you. Thanks for the question. Thank you. We'll take our next question from Phil Nadeau with TD Cowen. Good morning. Congratulations on the data. A few follow-up questions from us. In terms of the better response out of the 0.3 dose versus the higher doses, in your prepared remarks on the slides, you suggest maybe it was due to adverse events. It did seem like there were higher dropouts at the 1 milligram dose versus 0.3. Did those dropouts happen early in treatment before the primary endpoint was assessed? What was the time course of the adverse events and when patients discontinued therapy? ... Yeah, Phil, thanks for the question. I'm actually going to ask Peter Ordentlich, our Chief Scientific Officer, to address that. Yeah, thanks. Happy to take that question. You know, I'll start by saying obviously, that the data are new, and we are still in the process of looking at the exposure response and exposure safety analysis, which will address that question. To understand, how and when patients are coming off the study. Of course, from the data that we presented, it is plausible that the adverse event profiles at the higher doses may play a role, in the lower response rates observed. From a scientific perspective, we really do want to emphasize the point that Neil had made in the presentation, where our hypothesis is that macrophage recovery in between doses is an important feature of our strategy for blocking CSF-1R. It's certainly possible and likely that the lower doses allow for a greater recovery period than the higher dose. That certainly may translate to the differences in response rates and safety and tolerability we've observed so far. That's very helpful. Statistically, how would a dropout be handled in terms of the primary endpoint? If they had obtained a response before cycle seven, but discontinued therapy, would that response, well, that's observation carry forward, be carried through cycle seven, or would that be considered a non-response if the patient was no longer on therapy at cycle seven? Yeah, Peter, maybe just follow up for Phil on that one as well. Yeah, the primary endpoint of the study is response rate by cycle 7, day 1. If a patient had a response and discontinued, that will still count as a response. Got it. Okay. In terms of the FDA filing, what doses will be filed? Realizing it's early days, would you file just the 0.3 milligram dose, or are you contemplating filing any of the others? Yeah, let me ask Neil to address that. Yeah. Thanks for the question. While we agree that, you know, the data at 0.3 mg/kg are pretty compelling, as Peter alluded to, A, we just got the data, B, we're still in the process of analyzing, you know, producing the full analysis. Of course, you know, any discussion around dose will be dependent on that and subsequent conversations with health authorities. Obviously, we'll keep you informed as that evolves, but overall, we're very excited. Great. Then last question from us, what is rate limiting for filing? Is it simply preparing all the documents, or is there anything else that has to be completed? Yeah, thanks, Phil. As you know, filing is an undertaking, but we're very well prepared, and we're working closely with Incyte to make that a reality. I think our timeline is before year-end, that we'll have a BLA filed. Nothing in particular. Now that we have the data, we have work to do to get the filing together, but it's certainly an exciting time for the company to participate in that. Thanks for taking our questions, and congratulations again on the results. Thank you so much, Phil. Thank you. We'll take our next question from Anupam Rama with JP Morgan. Hey, guys! Congrats on the data, and thanks so much for taking the question. Should we be assuming ASH towards the full medical conference presentation? What other analyses are planned to sort of highlight differentiation here? Is, you know, the medical conference where we're really going to understand sort of your macrophage recovery hypothesis and if safety was and played a role in terms of the dose inverse dose response that you're seeing? I have a question here also, just can you remind us how long the administration takes for axicabtagene ciloleucel? Thanks so much. Sure. Thanks for the question, Anupam. First off, your question about whether ASH is the conference. We have a policy of not speaking about, you know, specific conferences and projecting whether or not we'll be presenting at those conferences until we have acceptance of submissions. I'm going to hold off in commenting on which medical meeting we'll present the full data set at. there are a number of options, and so we're thinking about that actively as of now. In terms of analysis, other analyses that we'll be digging into, maybe I'll ask Peter to address that as well. Very happy to. Of course, we have a large number of secondary analyses and endpoints that we will be eager to report, response by organ class, subset analyses and such. You know, that will all help understand our obviously high response rate and durability. Of course, the other areas that we're interested in are these questions around exposure response, exposure safety. Those will be key to understanding the differences between the doses. We do have a number of pharmacodynamic markers that we'll be also looking at, and I think those will go along with the exposure response analyses to help us understand this dose question. Anupam, just to highlight, something that Peter had said earlier, I mean, these are remember, these are different regimens. We dose patients at the 0.3 every two weeks, the 1 every two weeks, and the 3 every four weeks. There's differences in the regimen that. As Peter said, the recovery of the macrophage over the period is important to understand better. I think that's something we'll be digging into. Then relative to the onset of action of the drug is fast. While I don't believe that we gave specifics around the actual time to best response, we had previously disclosed in our published work at JCO with the earlier trials, phase I, phase IB, that it was, you know, within a cycle or two. Of course, this is an IV administration, 30-minute push, which we highlighted in the presentation. Great. congrats again, and thanks so much for taking the question. Thanks so much. Thank you. We'll take our next question from Yigal Nochomovitz with Citi. Hi, guys. Thank you very much for taking the question. Just a few more for me on efficacy. Have you looked at fibrosis yet? Would that be something we would see at a medical meeting? With respect to subset analyses, I'm curious what other subset analyses you have conducted or will conduct, specifically by number of prior therapies, as well as by specific organ involvement locations, such as lung versus scleroderma. Thanks. Sure. Thanks, Yigal. Long list of questions there. Let me actually ask Peter to address the efficacy and subset analysis question, 'cause there is a lot going on. Thank you. No, we have not yet looked at fibrosis in the study or, you know, organs and such. The subset analyses that you already mentioned, of course, are top of the list. We are very keen to understand the differences in responses to the prior therapies and by organ class. Of course, we had already presented from our phase I, II results, suggesting axatilimab has some, you know, clinical benefit in patients with their lung GvHD involvement, which were presented recently. We are, of course, interested to see and confirm those in a larger patient subset. Then certainly the other organ manifestations are, of course, of interest as well. Then again, just getting back to the question of dose and such, you know, just to reiterate this question of exposure, response, and understanding that, and the safety and such, is one of the key things that we'll look at, and that will go along with each of those types of subsets that, you know, we've talked about, baseline demographics, organ subsets, prior therapy, and things like that. We're just so excited to have such a positive study, to be able to look at all of those questions in a fairly large patient set. Thanks. Then with respect to structuring the label and the discussions with Incyte, obviously, this trial was meeting of 4 prior lines. I think even the enrollment criteria were 2 or more prior lines. What are you thinking in terms of how you would frame that on the label, in terms of the patient population? Thanks. Thanks, Yigal. I'm gonna turn it over to Neil to address that. Thanks. Well, the study was designed, I mean, the study eligibility criteria allowed patients to enter if they had, two or more prior lines of therapy, and our intention would be to file, or to submit with the, with the objective of getting an equivalent label. In other words, for patients who had failed at least two prior lines of therapy. Okay, cool. Thank you. Welcome. Thanks, Yigal. Thanks. Thank you. Our next question comes from Brad Canino with Stifel. Hi, congrats on the results from me as well, thanks for providing some detailed elements in the top line. I do have two additional data questions, though, that I hope can be answered, at least qualitatively. The first is: did a lot of the 0.3 mg/kg patients move to the Q4-week higher dose? In your view, did the increased toxicity impact the durability of response in this trial at all? Yeah, maybe the first part of the question, I think, Brad, I think we, you know, we don't have the data today to suggest or to support the amount of patients who actually went on to the extended dose. Meaning the, you know, we're able to switch one stable at six months, moving on to the monthly dosing. We do, we do believe that'll be fairly significant in terms of the number of patients who did go on to the monthly dosing. Again, that'll be reserved for the future presentation. Maybe the second part of your question, I'll ask Peter to follow up on that. Yeah, thanks. I mean, in terms of durability, it, you know what? The data are still evolving, so it's a little hard to answer that question. All we can do is point to the data in the slides, which the median duration of response has not yet been reached for the 0.3 mg cohort. What we're reporting is that 60% of patients responding, maintained their response at 12 months. Again, as Michael mentioned, we don't have yet the information for the patients who, you know, changed their dose regimen and such like that. All we can look at so far is the data that we've, you know, presented and suggest that duration of response seems to be quite robust for that cohort. Okay, great. Then second, on safety, you've been clear on the mechanistic effect for the transient liver enzymes, but did you see any events less than 20% in frequency of stuff like bilirubin increase or organ damage, particularly at the higher doses? Thank you. Thanks, Brad. I'll ask Neil to take that question. I'd just like to reiterate the point that I made during the scripted part of the call, which is that the safety profile that we've observed, based on the information that we have to hand, caveat being that we continue to generate the additional analyses, but we have all the key safety outputs, is that the profile is, as has been previously observed, right? It's consistent with what we saw in prior studies. Obviously, we'll present the full safety analyses at a forthcoming medical meeting. We're not seeing anything that's unusual. Brad, was that... Do you have a follow-up question, or was there anything specific that you're asking about? Sorry. No, that's it. Thank you. Appreciate the comments. Thank you very much. Thank you. We'll take our next question from Michael Schmidt with Guggenheim. Hey, guys. Congrats on the data from me as well. Maybe just a follow-up. Obviously, realizing that some of the subset analyses are still pending, but anything that you're seeing by means of, you know, differentiating from Rezurock around the organ response across different tissue types, is that consistent with what you've seen before? Anything that jumps out in terms of a differentiation from a, you know, organ distribution perspective? Yeah, Michael, thank you for the question. I think, you know, unfortunately, this will be a little less satisfying than you'd like. I think we're still waiting on, you know, to be, you know, really specific around how we, how we've done on an organ-by-organ basis. I think that's subsequent analyses. I think the way we see the data, and certainly the 0.3 seems to be, I would call it, best in category, overall profile relative to efficacy, safety. Remembering, of course, that, you know, four prior lines of treatment for, you know, the median for this patient population. We're treating extremely sick patients who have multiple organs involved, who have received other therapies, and because of that, you're seeing, you know, sort of patients who have the most difficult characteristics to treat: lung involvement, GI, eye, I mean, it goes on, the list goes on. This is a very sick population. As we expect to see the data at a medical meeting, I think we'll come to realize that we do have differentiated characteristics based on how the mechanism works on both inflammation and fibrotic effects that will have a, you know, a profile that is not only competitive, but highly differentiated versus some of these other agents. All right, super. Thank you. That's it for me. Thanks, Michael. Thank you. We'll take our next question from Peter Lawson with Barclays. Great. Thank you so much, and congrats on the data. I guess the first question would just be around the response rates and durability and what they look like, kind of pre- and post-Rezurock, and anything in the side effect profile that would or could potentially preclude you from using the drug in combination. Thanks for the question, Peter Lawson. In terms of response rates, obviously, this is, you know, we'll have more data on how the breakdown looks like in patients who have received prior treatment with Rezurock. They were represented in the trial. I think we showed roughly 20% or so had prior Rezurock. We also shown patients of up over 70% had prior Jakafi, as you'd expect, the second-line treatment, and also Imbruvica as well. We'll have those breakdowns, you know, at a future medical meeting as we present the data. We you know, as we've shown, a very high response rate across the board. Reminder, all of the doses met the primary endpoint of overall response rate, highly significant, as well. I think you have the, you know, the underpinnings, if you will, that even in prior-treated patients with all these different agents we've done, the drug has performed very well. In terms of combinations, I would just point out that it's an antibody and drug-drug interactions we expect to be at a minimum relative to small molecule drugs. There is no reason in our mind, with non-overlapping mechanisms of action, that we would expect not to be able to combine our drug with Jakafi, for instance, or others. That's an advantage of this drug that perhaps others don't have. There's nothing today that would preclude that, and we're actually excited to get going with some of our trials, as I pointed out in the remarks, that we'll be inside we'll be initiating a trial by the end of the year in combination with Jakafi to kind of move this upline into the frontline setting. I guess final question would just be around the dose-response relationship you have, or inverse relationship. Thoughts about exploring lower doses? Would you need to do that? Are you thinking about doing that? Maybe I'll make a comment, and then I'll pass it to Peter. I think, look, the way this trial was designed, it was designed with three different regimens, right? Two different, every two week regimens and a four week regimen. If you look at the 0.3 and the 1, they're very similar in terms of efficacy, as you see in the presentation. Safety may be differentiating for the 0.3, and we see some separation at the 3, but they're different regimens, right? I think with Peter's earlier comments around macrophage recovery is very important over a longer dosing interval. I think that's some of the dose-response relationship work that we're going to be doing to be looking at that. I think we're, you know, quite pleased with the profile that emerged at the 0.3, and, you know, and the 1 as well. I think one looks good, too. Again, remember, all 3 doses met the primary endpoint, highly statistically significant at those doses. We feel quite good about meeting the benchmark, and obviously, we're looking for best overall profile, which I think we achieved here. Dose ranging was a major objective of this trial, right? That's why you have a low dose, 0.3, a 1 mg every two weeks as well. We were trying to differentiate between the two of those and looked at a convenience dose at once a month. We were trying to cover a number of bases. We think we worked very collaboratively with the agency in order to design this trial and put forth a result that gets at the best optimal. We call it the optimal dose. Great. Thanks so much. Thanks, Peter. Thank you. We'll take our next question from Kalpit Patel with B. Riley Securities. Yeah. Hey, congrats on the data set, and thanks for taking the question. We saw that 60% of responding patients maintained their response at 12 months with the 0.3 mg/kg dosing schedule. Do we have the data for the other two dosing cohorts? Also the same question for the modified Lee Symptom Scale. Thanks for the question, Kal. Yeah, it's an important, you know, set of data that we're going to be, you know, holding back, but putting forth at the medical meeting. I think we this is top line. Unfortunately, we can't get everything into a top-line release. We certainly wanted to highlight the 0.3 as being, you know, sort of the, what we think could be an optimal dose here. The rest of that data, in terms of duration of response and all the sub-analyses we've talked about, will be presented at a future medical meeting. Again, just to reiterate, the endpoint was reached on all the doses, so it's a matter of finding, you know, showing you the other, you know, important indicators, which, again, we'll have at a medical meeting. Okay, great. One on the safety. In the Phase II, we saw the enzyme elevations, the CPK increases, lipase increases, AST increases, but none of those were grade 3 or higher, in that Phase II. Was that also consistent in this trial as well? Yeah, maybe I'll ask Peter to address that on safety. Yeah, thanks for that question. Trying to think. I'm not sure we've done that full comparison yet between those results. Yeah, I don't, I'm not sure I have that answer for you. We'll obviously look at that. We've been looking closely. We just got the data at those types of things, but just don't have an answer for you on that. Yeah, I think just to... Okay. Just to answer your question, maybe from a higher level, Kalpit, is, you know, I think the results, as Neil pointed out in his, in his description, the results on the safety side were highly consistent, you know, with what we've seen in previous trials. There was nothing that, you know, opt out, that said, "Okay, we're at a higher rate," nor a new frequency that we saw in this trial that we didn't see in previous trials. Certainly at the 0.3, that was, you know, the best profile from a efficacy and safety perspective on all of these measures. We feel quite confident there, but there's really nothing I think we would point to in terms of safety as something that's emerging, as more significant or different. Okay, got it. One last maybe from me. Do we have a median time on treatment for this trial, specifically for the 0.3 mg/kg dosing cohort? Why don't ask Neil to take that please? Yeah, good question. you know, it's being calculated. We haven't disclosed it yet. We will include all of the- Okay. These are just all of the additional data points that we'll have, you know, when we present the full data set at a forthcoming medical meeting. We're looking forward to sharing it all with you, but as Michael said, we have to hold some stuff back. Okay, great. Thanks for taking the questions, and congrats again. Thanks, Kalpit. Thank you. We'll take our next question from Justin Zelin with BTIG. Yeah, good morning. This is Jeet on for Justin. Thanks for taking our questions, and congrats on the data. Just two quick ones from us. Any thoughts on how the once every two-week dosing regimens align with clinical practice and the frequency with which clinicians see patients? The second is, just any thoughts on the sub-Q program and how you plan to advance that in light of this data? Thanks. Sure. In terms of, maybe thank you for the question, Justin. In terms of clinical practice, I'll just make a comment about that. You know, our understanding, we've talked to lots of physicians, and certainly they've enrolled patients in this trial. You know, remind you, it's a 240 patient trial, and certainly the experience from the phase I where we tested different doses, but all two week regimen. Physicians were, you know, obviously very encouraged by what they were seeing, and their patients had tolerated and done really well in the trial and speed of onset and drug comes on board and has an impact pretty immediately. I think they're excited to get patients who are this sick under control quickly. I think that's a differentiator for, and an important aspect of this. They're really concerned about efficacy in this patient population. To have an impact, that is, you know, and they can interact with their patients regularly. These are high-touch patients who need to be seen regularly. It all kind of lines up rather well for treatment, where physicians can have that interaction with patients and monitor them closely. That's actually worked out very well, and we expect that the 0.3 dose every two weeks will be, you know, will be that next new agent potentially for these patients, and the regimen works fine. Maybe the second part of your question, I'll ask Neil, if you could take that? The question was about, sub-Q. Yeah. Yeah. I would say that having the sub-Q formulation is a priority for both Syndax and our partner, Incyte. The conversation is a very active conversation between both companies. Incyte will be leading development of that formulation, and feel very similarly about it to us in terms of prioritization, but we don't have specific timelines that we want to reveal right now. I can assure you that it's, we see the importance of it, so the patients and their caregivers have a choice, as to how the drug can be administered. You know, stand by, and we'll share more information when we can. Lastly, thanks, Neil. Lastly, I'd point out that the, you know, patients were able to transition to a four week dose as well on this trial. More data forthcoming in a medical meeting where we can see that breakout. We are hopeful that we'll have a four week option for patients as well coming out of this trial. Jeet, are you there? Yes, thank you for that. Appreciate it. Sure. Thank you. Thank you. We'll take our next question from Joel Beatty with Baird. Hi, that's on the data. The first question is: Was the response seen in lung and GvHD patients in today's data supportive of plans to move ahead with a proof-of-concept study in IPF? Also, could you discuss if there's milestone payments associated with today's update? Yeah, thanks for the question, Joel. Look, I think, our plans for IPF have been, you know, formulating over some time. I think we've been excited about the mechanistic rationale for patients with IPF. We've been encouraged, physicians as well, have been encouraged by what we've seen in earlier trials, as well as preclinical information that we've generated, in patients who have, you know, lung, obliterans, for instance, and we recently, you know, published some data on that. I think there's the totality of the information that we've generated to date, plus the information coming out of this trial, where you'll see further, you know, breakdown on that data, specifically in patients who have lung involvement. We do, and we did point out that 45% of the patients in the trial had, you know, significant lung involvement. That is, I think, knowing that the overall trial was quite positive, I think it encourages us that we'll have an impact in diseases of the lung, and IPF is obviously a high priority for us to prove that out. In short answer to your well, maybe long answer to your question, yes, we think it's highly supportive of what we'll do in IPF, and we're looking forward to initiating that trial. In terms of milestones, we do have milestones with Incyte that are part of our agreement, which we signed with them a few years ago. Our next milestone is an approval milestone for U.S. approval. We'll be kind of updating that information, giving specifics around that and the timing there. Obviously, therefore, we'll come into focus, in a, you know, future correspondence. Great. Thank you. Thank you, Joel. Thank you. At this time, we have no further questions in queue. I'll turn the floor back to Michael for any additional or closing remarks. Great. Thank you, operator. We look forward to continuing the conversation and updating you more fully on the business at our upcoming quarterly call, which is scheduled for August 3rd. Obviously we're looking forward to seeing many of you at upcoming conferences as well. We appreciate your time and attention on today's call. We're excited about the data, and we look forward to giving you more information, hopefully before the end of this year, as I know many of you are looking forward to seeing that as well. Thank you so much, and we wish you a very good day.