Good morning, and welcome to Cogent Biosciences webcast. I will now turn the call over to Christi Waarich, Senior Director of Investor Relations. Thank you, operator. Today's call will review the SUMMIT and APEX data evaluating bezuclastinib in patients with non-advanced and advanced systemic mastocytosis. These data were presented and released in a press release over the weekend and earlier this morning. You can find the press release in the Investors and Media section of our website at cogentbio.com. Before we get started, please be reminded that remarks made during this call may be forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995. These may include statements about our future expectations and plans, clinical development timelines, including future presentations of clinical data and financial projections. While these forward-looking statements represent our views of today, they should not be relied upon as representing our views in the future. We may update these statements in the future, but we are not taking on an obligation to do so. Please refer to our most recent filings with the Securities and Exchange Commission for a discussion of our certain risks and uncertainties associated with our business. With that, it's my pleasure to turn the call over to Andrew Robbins, President and Chief Executive Officer. Andy? Thanks, Christi, and good morning, everyone. Thanks for joining us today. As Christi mentioned, my name is Andy Robbins. I'm the CEO of Cogent Biosciences. I'm very excited today to share with you the most recent clinical updates from the development of bezuclastinib for systemic mastocytosis patients, which were presented this weekend at the annual meeting of the American Society of Hematology. Before we begin, I'd like to set the stage for today. Along with myself and our Chief Medical Officer, Dr. Jessica Sachs, we're joined by two distinguished experts in the field of mastocytosis. First, we welcome Dr. Frank Siebenhaar, who joins us from Charité – Universitätsmedizin. And second, we are also pleased to welcome Dr. Pankit Vachhani from the University of Alabama at Birmingham Dr. Siebenhaar will help us walk us through the SUMMIT data that was presented on Saturday afternoon, and Dr. Vachhani will take us through the APEX data announced this morning. After their presentations, we'll have time for a question and answer session, at which all four of us will be available. Turning in the presentation now to slide four, I'd like to take just a couple minutes to review Cogent Biosciences. We're a growing biotech company focused on the discovery and development of targeted therapies for patients with genetically driven diseases. Our lead program, bezuclastinib, is a potent and selective KIT mutant inhibitor that is currently in active development across three separate clinical trials. First, based on the strength of data you will see presented from APEX part 1, the registration-enabling APEX part two study is actively enrolling patients with the advanced form of systemic mastocytosis. Second, we announced recently that all 54 patients on SUMMIT part one have been enrolled, and based on the quality of initial clinical data you'll see today, we've already announced plans to move rapidly into the registration-enabling part two of the SUMMIT study, commencing in the first half of 2024. Finally, based on the strength of results from two separate phase I/II clinical trials, near the end of 2022, we embarked on a global phase III study of bezuclastinib in combination with sunitinib for patients with gastrointestinal stromal tumors who have previously progressed on imatinib treatment. The enrollment for this trial is going as forecast, and we are on track to complete enrollment by the end of 2024. Turning briefly to our research pipeline, we have now announced three novel programs, including a reversible pan-FGFR2 mutant inhibitor, an EGFR-sparing, highly brain-penetrant ERBB2 inhibitor, and our newest announcement, an H1047R mutant-selective PI3Kα inhibitor. We look forward to discussing these programs in depth on a future call. Now, moving to slide five, let's spend a few minutes on bezuclastinib, a molecule we believe has the potential to become the best-in-class KIT mutant inhibitor. First, bezuclastinib has demonstrated in vitro and in vivo a degree of potency across several mutations in the KIT gene, including D816V driver mutation present in the vast majority of patients. Secondly, bezuclastinib is highly selective for these KIT mutations without inhibitory activity against many other closely related kinases. Finally, bezuclastinib demonstrates a profile of very limited exposure in CNS tissue, suggesting minimal brain penetration. Taken together, bezuclastinib has the potential to demonstrate activity against these mutations without the off-target toxicity seen with other molecules in the class. Before turning over the call to our expert guests, I'd like to describe systemic mastocytosis at a high level. Systemic mastocytosis is a disease of overactive and proliferating mast cells, which are immune cells that play an important role in the inflammatory cascade. In the vast majority of systemic mastocytosis patients, a particular mutation in the KIT gene, known as D816V, is the underlying driver of the disease. It is estimated that as many as 25,000 people in the U.S. suffer from systemic mastocytosis across a number of subtypes. By far, the most common form of the disease is indolent systemic mastocytosis, which represents about 85% of these estimated patients. While patients with this disease have a normal life expectancy, their quality of life is often severely impacted due to a wide variety of symptoms associated with mast cell mediator release. On the other end of the spectrum, approximately 10% of SM patients are diagnosed with a collection of diseases known as advanced systemic mastocytosis. This is a serious, life-threatening form of the disease that leads to uncontrolled proliferation of mast cells in the body. At Cogent, we are conducting clinical trials in both patient settings and are ready to share more about the exciting data presented this weekend. To help us first understand the initial data presented from the SUMMIT Part 1a study, I'd like to turn the call over to Dr. Siebenhaar. Yeah. Thank you, Andy, for this brilliant introduction to the disease and its background. It's my great pleasure to walk you through the initial results from the SUMMIT trial, which is currently ongoing, and we look at the Part one data here. If you please go to slide eight, you see here the study design of the SUMMIT trial, Part 1a and Part 1B. There were two doses compared to placebo, carried forward in Part 2A, and there were patients with indolent systemic and smoldering systemic mastocytosis, both based on the 2016 WHO classification. Eligible for this trial when they had moderate to severe symptoms despite being treated with one or two or more anti-mediator therapies that failed to control their symptoms. The primary objective was to determine the recommended dose of bezuclastinib. This is still an ongoing analysis, and the endpoints were safety, PK biomarkers, and symptom improvement on the PRO measures that were conducted in this clinical trial. All patients that completed Part 1a were then further treated in an extension phase, so patients are still on drug in the open label extension. If you please move to slide nine, then you here see the patient characteristics. 20 patients were enrolled in the Part 1a. 75% were female. Median age was about 50 years. Their ECOG, see that these patients are have disabilities due to their symptoms, ECOG one and two, 85% of them. The vast majority, 90%, was indolent systemic mastocytosis patients, as this is the most prominent form of the disease, and also 10% patients with smoldering systemic mastocytosis, representing patients with a very high mast cell burden and high tryptase levels. Their symptoms were measured at baseline of the study, using one of the patient-reported outcome tools, which is called the Mastocytosis Activity Score, MAS, and they had a total score at eligibility time in median 45.56, in a range from 26-70, which means that all the patients that were enrolled in the study had moderate to severe symptoms. Their mast cell burden was measured by several biomarkers. First of all, the KIT D816V mutation in whole blood, which was present in most of the patients with a range from 0-32%. Bone marrow mast cell infiltrates were also detected pathologically on a median 22%, and their tryptase was measured. Most of the patients had tryptase levels higher than 20, which also counts as a minor criterion for the diagnosis of systemic mastocytosis. But we know patients, and 50% in this study also had lower tryptase levels at baseline. When we look to their previous treatments, there was 1 patient previously treated with avapritinib, and all patients were on best supportive care medications. On median, they had three different drugs, but up to seven different drugs they were treated with. All failed to control their symptoms. Among those, histamine 1 and 2 blockers, leukotriene antagonists, proton pump inhibitors, cromolyn, omalizumab, and corticosteroids, all drugs that are frequently used in the attempt of controlling the symptoms of indolent and smoldering systemic mastocytosis patients. So at the data cutoff, which was end of October, there was a median time on study for the patients, Part 1 and open label extension of seven months, up to 16 months at that point. All patients completed Part 1a at that time, and at the data cutoff, there were still 18 patients on the trial. Two discontinued, one due to an adverse event and another one by self-decision. If you move to the next slide, please, then we see from the core study, the safety profile of 100 and 200mg bezuclastinib, which looks great. So there's, in the majority, only grade one and two. Very minor grade three events were detected, and they're all among good to manage, and they were all reversible. So, the majority of the treatment emergent adverse events were low grade. No SIEs reported, which is very good. Most of note, no bleeding or cognitive impairment events were reported, and dose reductions were necessary due to fatigue and one patient due to elevated liver enzymes, but that patient was on a high dose and was reduced. The fatigue also could be possible that it's not treatment emerged because fatigue also is a symptom of mastocytosis, which we will see later on. For your information, there was one patient actually on a higher dose with 400 mg, which was in the previously a group of smoldering patients, and due to amendment, this enrollment was closed. This patient showed on cycle four neutropenia and decrease of white blood cells and anemia, but all this was also reversible in that patient. If you please move to the next slide, then you see how the safety profile continued to be very well in the open label extension phase. All the patients that kept on treatment didn't show any further higher grade adverse events, which is very good. And also the patients that changed from placebo to active treatment in the open label extension phase had a very similar favorable safety profile. So if we go to the next slide, please. So here you see the PK profile. So you see that treatments with 100 and 200mg bezuclastinib showed a very good and sustained levels of exposure to the drug. You also see the 400mg that were discontinued, and you see one outlier, and that outlier was the one that needed the dose reduction due to liver enzyme elevation. Most likely, this was a failure of drug intake, therefore, the PK levels were much higher than in the other patients. And go to slide 13, please. Here you see the very promising and very exciting reduction of the disease biomarkers. We look at serum tryptase, the KIT mutation, allele burden in the peripheral blood, and at mast cell infiltrates in the bone marrow. And you see that already at week 12, all patients that were treated with bezuclastinib showed a 50% or higher reduction in these markers. So serum tryptase, which is a marker of mast cell burden in the peripheral blood, nicely reduced. Also, the D816V, the mutation burden measurable in the peripheral blood, as well as the mast cell infiltrates in the bone marrow, showed a very good and prolonged reduction. So as a takeaway, 90% of the patients with baseline serum levels over 20 achieved levels below 20. So basically, this criterion of the disease was gone, and also 67% of patients with a baseline level of tryptase below 20, but above 11.4, also achieved reduction of tryptase to normal ranges, which is a great result. Please go to slide 14. Here you see the different patient-reported outcome tools that were used in the clinical trial. Let me briefly introduce you. So besides the mast cell activity score, which I already mentioned on the baseline assessments, there was the quality of life MC-QoL tool, which is the disease-specific quality of life tool developed and validated in patients with cutaneous and indolent systemic mastocytosis. The score ranges from zero to 100 points, and there's four different domains related to quality of life, which are symptoms, social life, functioning, emotions, and skin. And the MC-QoL quality of life were measured in the SUMMIT trial at baseline and every four weeks. Then again, you see the mastocytosis activity score, which is also a disease-specific patient-reported outcome measures to assess symptom severity, also evaluated and validated in the patients with cutaneous and indolent systemic mastocytosis. Here also, we have a range from 0 to 100 total score. And also here we have domains looking specifically at symptom sets in skin, in the gastrointestinal tract, and others including muscle pain, joint pain, fatigue, headache, and concentration difficulties. And we measured symptom in the SUMMIT trial at baseline and at week 12. Then there were two more measures included in that study, Patient Global Impression of Severity, which is an anchor measure, also targeting patients with non-advanced systemic mastocytosis on a four-point Likert scale from none to very severe. Patients could rate their overall impression of severity of their symptoms. The domains were overall, dermatological symptoms, gastrointestinal symptoms, pain, fatigue, and cognitive, also measured at baseline and every four weeks. And a Patient Global Impression of Change, also for non-advanced systemic mastocytosis, by which the patients rate or rated on a seven-point scale from -3, very much worse, to +3, very much improved, how they rate the change on treatment, also in the four symptom domains: overall, dermatological, gastrointestinal, pain, fatigue, and cognitive. And also this was measured at baseline and every four weeks. Then go to slide 15, and here we see very exciting results on the improvement of quality of life, as assessed by the mastocytosis quality of life tool. You see that all the patients at baseline, on drug and placebo patient had a major impairment of the quality of life, moderate to severe. You see that on the active treatment group, which is the straight line in dark blue. There was a very rapid improvement already at week 4, which was on sustained over the time of treatment up to week 24. Which was not seen in the placebo patients. So placebo patients, they stayed impaired until they switched to the active drug in the open label extension phase. You also see, again, a very rapid improvement within the first four to eight weeks. Most important to see that all the patients reached an improvement from moderate to severe to a mild impairment of their quality of life. This is a great result. If we look into the numbers more in detail, then the median best percent improvement in patients treated with bezuclastinib was 37% in Part 1a, and even more improved in the open label extension to 57%. As said, the placebo crossover shows very nicely how the active drug improved quality of life in these patients. When we look to the symptoms assessed by the mastocytosis activity score, then we see a similar result. Also, all patients virtually on bezuclastinib showed improvement, 35 points in median, compared to only 27 point in placebo. There was a larger range here, which is due to the tool, because the tool measures the nine most prominent symptoms in patients, and not all patients have all symptoms, and not all symptoms improve the same way, as you will see on the following slides. But the good message is that there was a 49% median decrease in the Mastocytosis Activity Score for all the patients treated with bezuclastinib 100mg. Okay, then we go to slide 16. Here you see the patient global impression of severity, and this is also a very encouraging result. You see from baseline, patients on active drug showed a rapid improvement in their overall impression on their symptom severity, which also was sustained when they stayed on the drug, and even more improved in the open label phase, as seen at week 16. The placebo patient didn't have that impression. They stayed unchanged unless they were changed to active drug, and then also they showed a very rapid improvement in their global impression of severity of their symptoms. This is great. At week 20, at least 78% of all patients on bezuclastinib had a higher than 1-point improvement in their global impression severity scale. During the open-label phase, four out of six patients that started bezuclastinib also showed more than one point improvement in the overall symptom severity, four weeks after they have changed to active drug. So it's a very rapid, and it's a very sustained, response to active drug as seen in these patients. If you go then to slide 17, please. Here we look at the overall symptom improvement by using the patient global assessment of change, and this is also very notable what we see here. So the overall symptom assessment by the patient showed an overall improvement on the active treatment group, which were not seen in the placebo group, but was seen in the patients again when they switched to bezuclastinib in the open-label extension phase. So overall, at week 12, 63% of patients reported on a symptom improvement, which is better or much, much better or very much better compared to baseline. And after 8 weeks of bezuclastinib in the open-label extension phase, this even further increased to 78% of patients that rated themselves much better or very much better. So this is a very straightforward result. If we then look on the single symptom domains, again, you see here dermatological symptoms, pain, gastrointestinal symptoms, fatigue, and cognitive symptoms. You see more or less the same picture. Very good response in the dermatological domain, in which virtually all patients treated with bezuclastinib showed improvement much better or very much better. Most of them, not so in the placebo group, but then again, in the open label extension phase, most of the patients reported on much or very much improvement. Also the pain resulted, well, the gastrointestinal symptoms and fatigue and cognitive. You see that for some symptoms, it takes a while. So even though there is a fast response in many patients starting at week 4 and are sustained at week 12, there's further improvement in the open label extension phase and also in the crossover placebo to bezuclastinib, you see that patients start to improve when they be switched on the active drug. Good. And then I will close with a very impressive case on slide 19. Here you have the case of a 46-year-old woman that was treated in that clinical trial. She had indolent systemic mastocytosis. She had moderate symptoms despite using two anti-mediator therapies. She had a baseline MAS of 32 and MC-QoL of 38, which again translates to moderate to severe symptom and impairment of quality of life. And when you look at these pictures, you see not only improvement of symptoms that we can measure by the PROs, you see a very good improvement on the skin lesions that come together with mastocytosis. So again, to your note, these lesions are continuously with the patient, so they start to develop and they never fade, they never go away. Usually these lesions stay with the patient for the rest of her or his life. But with bezuclastinib treatment, you see these lesions fade. They have already disappeared at week 24 in this patient, and very nicely resembles the reduction in mast cells and the reduction in skin symptoms and skin lesions, which has a very high impact on the quality of life of patients, because living with these skin lesions is, it's not a good thing. You also see on these lines that her quality of life improved tremendously. And with the fading of the skin lesions, you see that also the serum tryptase levels and the bone marrow mast cell burden decreased under the treatment with bezuclastinib. So she had a -23% change from baseline in her mastocytosis activity score and a 36% change in the skin domain. And also, if you look under the lines, you see that she changed in her global symptom severity rate from moderate to mild throughout the study, and was rating herself much better compared to baseline, starting all from week four. So again, here in this patient, we see the very rapid onset of action and the very rapid control of symptoms and improvement of quality of life in these patients. So to wrap this up, we see that there was yeah, basically no severe adverse events reported by the patients. Even on long treatment, they were not emerging, and the treatment-emerging adverse events, they were all low grade, they were reversible, and they were well manageable. So it means we have a very favorable safety and tolerability profile also in the open-label extension, which sets the stage for a long-term treatment, even with this with bezuclastinib, which is fantastic. Then at week 12, and this is very exciting, virtually all patients achieved a more than 50% reduction in markers of mast cell burden, serum tryptase, KIT D816V allele burden, peripheral blood, and bone marrow mast cell burden. The patients all reported on a very rapid symptomatic improvement with bezuclastinib, which was sustained and even further improved over time. The quality of life improvement was very great, and also the symptom improvement as measured by the patient global assessments were fantastic. So, taken together, bezuclastinib shows a very promising potential in disease-modifying therapy for patients with non-advanced systemic mastocytosis. So, I'm allowed to say that that additional clinical data from the Part 1B, which works with a different formulation, are expected for early next year. And we all hope, and our patients hope, that we can continue with part two in the first half of next year. So thank you for your attention, and with this, I turn back to Andy. Thanks, Dr. Siebenhaar, for your excellent presentation. Now I'd like to invite Dr. Vachhani to review for us the data presented from APEX Part One, the clinical trial announced this morning. Fantastic. Thank you, Andy, and also thank you, Dr. Siebenhaar, for that nice presentation. I'm Pankit Vachani from UAB, and we have a poster today showing us the updated results with regards to the safety and efficacy of bezuclastinib from the APEX study. So let's move on to slide 22. In this slide, as you are seeing the study design of this APEX phase II open label, multi-center study of bezuclastinib in advanced systemic mastocytosis. Patients who are being enrolled are the ones with advanced SM, which includes all three major subtypes: that's aggressive SM, SM-AHN, which is the most common one of these three subtypes, as well as mast cell leukemia patients. Now, there is no restriction on prior therapy, so some of these patients could have received avapritinib or midostaurin, and not to mention many other therapies, depending on what they received before. The platelet count at entry level is 50,000 or more. And the study has two parts. Part one is the dose optimization part, and part two is the expansion part. And the results that we'll talk about today are from part one, which uses formulation A, much like what Dr. Siebenhaar was talking about. And in part one, there are four dose doses that were being explored: 50 BID, 100 BID, 200 BID, and 400mg once daily. So the primary endpoint was incidence of adverse events, serious adverse events, PKs, biomarkers, the overall response rates. Part two, which is not what we are so, so much going to talk into, it has its own endpoints as well. Of course, there are many additional endpoints as listed below on the left side of the screen, which include safety, tolerability, efficacy analysis as measured using different response criteria, PK/PD analysis, biomarkers of mast cell burden, et cetera. While we are at this slide, let's also just quickly take a look at the part two expansion optimized using the formulation B. So that part, which is currently enrolling, although we are not gonna look at those results right now, that part, part two, has 65 patients who are being dosed at 150mg once a day dose. That's the formulation B, which is an optimized formulation with improved bioavailability. Now, there are some additional planned cohorts, as you can see, and in particular, I want to draw your attention to the second of those, the middle one, which says that there are 20 high-risk AHN patients who will be dosed at 150mg once a day with concomitant associated hematologic neoplasm-related therapies. That's a very nice cohort that will, in effect, test the safety and efficacy of the combined approach of, let's say, using a hypomethylating agent plus bezuclastinib. After all, these patients are at high risk for progression, and we need to have data on the use of combined therapies, which is currently lacking in literature, and I'm very excited to see that that cohort has also been planned here. All right. So once again, we'll focus on the part one as we go into the next slide. So coming to slide 23, 33 patients have been enrolled, and the median age is 68, ranging from 33 to 87. There's a lot of data on this slide. I would focus more on the total, all the patients, that's the total green colored column. And there, what you will see is 72% of patients had SM-AHN, which is very much in line with what one would expect of the advanced SM category. They had. Some of them had received prior therapies for advanced SM. In particular, avapritinib, for example, was used by 16% of patients. Midostaurin was used previously by about 31% of patients, while the remaining ones, so 69%, were TKI naive at the time of going on the study. You may see that there are some mutations reported, SRSF2, ASXL1, RUNX1, found in almost 60% of patients. These are some of the high-risk mutations, which connote bad prognosis with advanced SM, and 60% of the patients had one of these. A KIT D816V mutation was found in the very significant proportion of patients. As you can see, the median VAFs were higher than what Dr. Siebenhaar talked about. The median VAF for all patients put together was 6%. And a very high mast cell burden as expected in this patient population, and as you will see, the tryptase levels are significantly high. So 153, if you look at all the patients put together with, you can see in tryptase. Now let's go to slide 24, which gives us information with regards to the safety profile of the drug. So first and foremost, the majority of adverse events were low-grade and reversible. Very, very importantly, I have to t here's no cognitive impairment or bleeding events were reported. I don't know if you are aware or not, but the current therapies which we use either have adverse events or in particular have intracranial bleeding events and cognitive issues, which are of significant concern both to the providers and to the patients. So this is a very important bullet point, which is no related cognitive impairment or bleeding events reported from the patients thus far. Coming to the third bullet point, so the majority of heme adverse events were low-grade, reversible, and did not require dose reductions. Now, yes, there were some related serious adverse events reported in four patients, and those are listed there. For example, grade four thrombocytopenia. There was a hypersensitivity reaction. There was a grade three drug-induced liver injury case, and also a grade three leishmaniasis. The grade 3 DILI, I just want to add some information as it's also noted in the slide, that there was a mixed cholestatic pattern of injury, but the patient was actually found to have biliary outflow tract obstruction, which caused a picture that looks like liver injury, that may be attributed sometimes by a physician to the drug. But in reality, having biliary outflow tract obstruction is going to cause, for example, bilirubin elevation. And it is my understanding, actually, that the hepatologist and many other members of the STM committee actually don't think that this was truly a DILI. Regardless of all of that, it's there, and nine out of 32 patients required dose reduction due to adverse events, right? Six of whom were actually receiving the 400mg dose, and only three out of 32 discontinued due to adverse events. The paper that people saw, the green columns again, the rates of treatment-related adverse events in more than 10% of patients are shown. These are more or less in line with what you would in an advanced SM patient population that is receiving a c-KIT inhibitor. The rates of peripheral edema and periorbital edema are low overall. Yes, there are cytopenias, as again, one would expect in patient population. Slide number 25. So these are some fantastic results. Okay, so what we are seeing are three sets of graphs. These are graphs for tryptase, mast cell burden, and the KIT D816V variant allele frequency from peripheral blood. Put together, these are the three biomarkers of disease burden, of mast cell burden in a patient. Starting with serum tryptase, what you will notice is 94% of patients achieved a 50% or more reduction. And in fact, if you look at these, waterfall plots, these are in serum tryptase decreases. In fact, 100% of patients who got at least two cycles with of treatment had a 50% or more reduction in their serum tryptase. Just the depth of these serum tryptases are worth noting. In that same vein, the mast cell burden graph is shown on the right, and you will notice once again that 97% of patients with baseline mast cell burdens and at least one post-baseline assessment achieved a greater than 50% reduction in mast cell burden. Generally speaking, these mast cell burden improvements continue over time, so we usually see deeper responses happen over time. And last but not the least, the KIT D816V variant allele frequency. That's the mutation, that's the driver of this condition, systemic mastocytosis. Those levels were decreasing as well. 93% of patients achieved a 50% or more reduction. So what all these three things put together tell us is that the drug is hitting the target, it is hitting it deep, and although not mentioned here, is the fact that these are, in many ways, durable responses. All good things that we were seeing and hoping to see as expected. Now, let's go to slide 26. Slide 26 is talking about the responses observed from the patients that we enrolled in this part one study. There are a lot of numbers over here, and one can sometimes get lost, or maybe if I can help to focus on certain numbers. If we look at the table at the top and maybe look at the column number four, that's talking about the modified IWG-MRT-ECNM criteria, looking at patients who were TKI therapy naive. If you look at that CR, CRh, PR, plus CI, that's row number 1, that's showing you a 61% response rate. The one right below it, which is CR, CRh, and PR, that's also an impressive 56% response rate. Now, where things do get interesting when we take a small patient population so far, for example, the 27 patients from whom the assessments are happening for the entire population is sometimes having a heterogeneous patient population, including three subtypes and further subtypes based on the particular AHN and these SM-AHN disease subtype. So then that can create some issues where you can have CR, CRh, PR, CI responses, which have too many factors at going. So when I look at this data, I also like to focus especially on the PPR number. That's in table. The bottom table, and if you look at the TKI therapy naive column, that's the middle column, the one with the 22 patients, you will see that the overall response rate, the CR plus PR in that TKI therapy naive as per the PPR assessment, was 86%. Now, why is this important? It's important because, well, number one, it's again, a high percentage of patients who are responding, but also in particular because that is what the number that tells us that, again, the drug is hitting its target, it's doing what it's supposed to do, as we also saw from the previous slides, where we saw the mast cell burden markers coming down. So definitely tells you about the activity of the drug. Now coming to slide number 27, that's the conclusion slide. As we saw before, bezuclastinib has continued to demonstrate a differentiated safety profile. In particular, no intracranial bleeds, no drug-related neurocognitive issues. Majority of the adverse events were low-grade and reversible. 28% of patients required dose reduction due to AEs. Only 9% of patients discontinued due to AEs, though. The second bullet point talks about some of the very encouraging signs of clinical activity. We noted the 56% overall response rate, and we also talked about the very high 86% PPR-based response rate. Very high percentage of patients are achieving the reductions in serum tryptase, KIT D816V variant allele frequency, and bone marrow mast cell burden. This suggests that on target as expected from the drug. The exposure that is achieved with the 100 mg twice daily, which is equivalent to like 200 mg per day dose, that resulted in optimal efficacy and safety outcomes. All patients receiving the 100 mg BID dose achieved PR or better and remain on trial with three patients at more than 20 cycles. The dose of the 100 mg BID was well-tolerated, with the majority of patients reducing patients who got higher doses, like the 400 mg daily. As I indicated right at the beginning, the enrollment to Part two is ongoing. 150 mg once a day using the optimized formulation that's expected to deliver the same optimal exposures in line with the 100 mg BID of the original formulation, the results of which we just saw. Again, this brings to an end the evaluation of the combined therapy, and concomitant agent therapy is also open for enrollment. Thank you. Great. So thanks very much, Dr. Vishwani, for your excellent review of the APEX data. Now, before I turn the call over to the operator for questions, I'd just like to make a few additional remarks. First of all, I'd like to thank Dr. Prithviraj Bose and his colleagues at MD Anderson for recognizing the SUMMIT bezuclastinib presentation as one of three highlighted clinical data presentations this weekend at ASH. I encourage you to read their press release that MD Anderson issued about the data from SUMMIT on Saturday afternoon. It's very encouraging. Next, I'd like to address a few, shall we call them misunderstandings, about the SUMMIT trial that we've heard about over the weekend. Starting at number one, the patients participating in SUMMIT Part 1B remain in the blinded, placebo-controlled portion of the trial, and Cogent will not unblind these data until at least the middle of January next year to prepare for presentation of these data at the 2024 Quad AI annual meeting in February. Secondly, when reporting results in this initial presentation of SUMMIT Part 1a, we've worked closely with our group of external authors to ensure we are describing the data accurately and fairly. In the case of small datasets that include individual outliers, medians are often a more accurate way to show central tendencies than means. But to alleviate any concerns around methods of measuring averages, on the MC-QoL data presented by Dr. Sievenpiper, you may recall the impressive data that showed within the first 12 weeks of bezuclastinib treatment reported we reported a median best improvement of 37%, which increased to 57% by week 20. Using means on these same measures generated analogous values of 38% and 55%. So hopefully, we can put that concern to bed. Number three, there remains a concern about the new PRO tool that Cogent is creating for this patient population. Based on our careful diligence in conjunction with our outside PRO expert partners, along with a great deal of learning from the prior summary basis of approval document, which outlines several methodological and technical concerns raised by the FDA about their ISM SAF tool, we believe with 100% confidence that we will deliver on time a novel PRO tool that reflects the breadth of symptoms impacting ISM patients and will be acceptable for use in assessing the primary endpoint of SUMMIT Part 2. Once this tool and its scoring system has been finalized, we plan to report the results from Part 1 patients. So great. Now that we've cleared up any confusion, I'd like to turn and specifically address the community of physicians, patients, and families living with systemic mastocytosis. We at Cogent are committed to rapidly developing bezuclastinib because we know you deserve more than one choice to help you in your fight against this disease. Based on the data presented this weekend, we believe that bezuclastinib has clear potential to become the treatment of choice for patients with both advanced and non-advanced forms of the disease. Thank you for partnering with us to demonstrate what bezuclastinib can do. With that, I'd like to turn it over to the operator for questions. Thank you. If you'd like to ask a question, please press star one one. If your question has been answered and you'd like to remove yourself from the queue, please press star one one again. Our first question comes from Chris Raymond with Piper Sandler. Your line is open. Yeah, thanks. Maybe two questions, maybe first for Andy. You know, there's been a lot of chatter, you know, over the weekend about your data, from docs and other market participants, if you will. So, you know, a lot of us have been struggling to try to understand how to, how to comp this to avapritinib, just given all the different measurement tools that are out there. Maybe just, Andy, if you could step back a little bit, talk about the key one or two aspects of this data that illustrates that, that bezuclastinib is, is helping patients? And offers a, you know, an advanced over standard of care, especially in ISM. Then maybe for Dr. Vachani and Siebenhaar, there's been a bit of controversy around the relevance of biomarkers in this disease, especially in non-advanced SM, you know, correlating symptomatic with symptomatic improvement. I think this came up during the oral presentation also on Saturday. Just would love to hear your views on this, especially with your experience treating patients and the correlation between baseline disease and severity and biomarker readings. I guess, you know, long and short, are serum tryptase, is that a relevant disease biomarker in your view? Thanks. Great. Thanks, Chris, and I'll certainly let our expert guests address your second question. To get back to your first question, obviously, a couple of things. Number one, this is the initial readout of bezuclastinib in ISM, so we freely acknowledge that it's a small sample. And, you know, while, of course, we're always interested in how are we doing for patients in their journey to health, it's admittedly sometimes hard to compare a early-stage small registration-sized 230-patient phase three trials. But what was most encouraging to us from the data when thinking about the impact to patients, number one, I think obviously the very impressive PD results across all the commonly used biomarkers of the disease. So just as a reminder, 100% of our patients achieved more than a 50% reduction across all three commonly used biomarkers, including 90% of patients getting their tryptase back below 20 nanograms per ml. So that certainly stood out to us. And then when we look at the patient-reported outcome data, one thing that we're y ou know, of course, we understand why people like to look at relative improvements to do cross-trial comparisons, but in the real world, what physicians and patients care about is: how, how do I feel at the, you know, after 12 weeks, 24 weeks, 48 weeks? How good can I feel by taking a drug? And so we also look at things like the absolute performance, the absolute scores on these scales. And what struck us is that, you know, referencing back on MC-QoL, because it is probably the most robust scale that you can use to comp across drugs that have been developed, within 12 weeks, within 20 weeks, using some of the open label extension, within eight weeks of the placebo patients crossing over onto active, what we're seeing is that the average scores for our patients on bezuclastinib are down into the 20s, if you look at the Y-axis. Those are, those are levels of absolute quality of life on MC-QoL that have not been reached by previously studied drugs. So that is very encouraging to us. And then finally, and, and Dr. Siebenhaar highlighted this in his presentation. We look at the mastocytosis activity scale as a very useful tool for assessing the severity of symptoms, which is notably different than assessing quality of life with a PRO instrument. And if you look at the patients on our trial who were dosed with a 100mg dose, within 12 weeks, we showed a nearly 50% improvement from baseline on this scale. Those results are unlike anything seen before at any time point for the competitive drugs on symptomatic severity scales. So what these early results suggest to us is you should continue rapidly developing this drug. It has some very strong potential to help patients live better lives with this disease. Now, I'll let Dr. Siebenhaar and Dr. Vachani maybe opine on your second question. Yeah. Thank you, Andy. I'm very happy to take the biomarker question, Frank, here. And want to just echo what you just said. I totally agree what you said. So, we have this very rapid and very sustained effect, which is really, really of special interest. Let me go into your question regarding tryptase and KIT mutation burden peripheral blood. So there's two things you need to consider when looking at this. So first of all, yes, it is important biomarkers. Why? Because it shows us target engagement. So, mastocytosis is defined by the accumulation of mast cells in different tissues. This is mirrored by increased tryptase and increased D816 mutation burden, measurable in the peripheral blood of patients. So when we see this going down, this is good markers for us to see that we're targeting the mast cell and the mast cells go down, just as we see the skin lesions, fade. Which is true, you can not one by one translate reduction in tryptase, reduction in KIT D816V mutation burden with the reduction of symptoms and improvement of quality of life, because there's more about and why. You know, the PROs that we are using right now, they were developed and validated in patients before we had any treatment, if, effective, like, avapritinib or other tyrosine kinase inhibitors. We just had no drugs that, that are able to do this. So, you know, not most, some of the symptoms we measure by the current PROs, and are associated with mastocytosis, they're believed not being specific for mastocytosis. So we're measuring itch, we're measuring whealing, we're measuring gastrointestinal symptoms like diarrhea and cramping. We're looking at pain, but then we also look at fatigue and concentration difficulties and tiredness and all these things which come with mastocytosis, but which also come with other diseases. So we are just about to learn that some of these symptoms that are associated to mastocytosis may not necessarily be a direct consequence of mast cell activation, but more a consequence of having, you know, a chronic, incurable disease that patients suffering from for, you know, for the last decades. So this is what Andy mentioned. Therefore, it's so important to keep improving and learning on these PROs. And also, and this is done with the data, Cogent is capturing right now in their part one, looking at the response of symptoms and making even the PRO better than it was before, which is now possible, but which wasn't before. So maybe we do see then a better correlation of these biomarkers, but, but as of yet, reduction in tryptase and reduction of D816V not necessarily means that we help the patient. But in the end, and this is what also, Andy said, in the end, it's a matter of, you know, improvement of quality of life, reduction of symptoms, and, this, this needs to come together. Look, those are excellent points by Dr. Siebenhaar and Andy, and I'll just add very quickly that I agree that we didn't really see a complete correlation, right? Between many of these mast cell mediators and symptom improvement. And I also fully agree that symptom burden decrease should be our primary goal in ISM patient population. However, I will say that at the same ASH, that same oral presentation session, we also saw how the mortality rate of ISM patient population is probably higher than what we have been talking about. And one wonders why that happens, right? And maybe that brings into the fact that possibly these patients also have other things ongoing that we are not capturing. Tryptase is just one of many mast cell mediators. There are so many other items as well, and just to throw two or three out, histamine, there's heparin, there's leukotrienes. And while we don't measure these on a routine basis, they have their own cumulative long-term damage on end organs. As an example, histamine, for example, or heparin, for example, can actually cause long-term osteoporosis. So while, yes, we did not see we haven't so far seen with the available data, a complete correlation between these biomarkers, these are not going away. I think seeing deep responses is a great thing because it tells you you are hitting the target, you are controlling the disease nevertheless. And all the caveats about the symptom burden that Dr. Siebenhaar absolutely are true, and they stand as what he just mentioned. Great. So just quickly, you know, obviously this is a complex and robust data presentation. So, you know, if I could be so bold as to ask our guests to maybe stay on a few more minutes, I know we have several other questions in the queue. So we'll try to get to everybody and maybe go over by, you know, 10 minutes or so to handle the remaining questions. Thank you. Our next question comes from Charles Zhu with Guggenheim. Your line is open. A bit early, you're still waiting for the part 1B data, but you showed sort of PK, PK/PD, markers of response, safety. How are you thinking about sort of for the, the recommended phase II dose for part 2? How are you thinking about sort of selecting that with the data that you've seen right now, and, and how are you weighing sort of the, the, the preliminary safety signals versus efficacy? And then I have a, a follow-up after. Thank you. Okay, We missed the first part of your statement, but I think I get the gist of what you're asking. It's about, now that we've announced we're excited to move forward, how do we select dose? Because this is a, you know, fundamentally a classic dose exploration study. The short answer to your question is we are definitely going to wait to see the data from part one B, because we think with 54 patients, with what we predict exposures will be across the doses we studied, in the range of IC50 to IC90 target inhibition on D816V, we're optimistic that we will see a very good mapping of that exposure relationship to things like low grade tolerability adverse events, as well as the where the robust PD markers and PRO improvements take place. The one thing that we know right now is that it looks like what's emerging is a very broad and wide therapeutic index, and so it gives us a lot of flexibility to try to optimize the dose, not just to, you know, minimize safety and maximize efficacy. But what we really look at here is that the measure of efficacy in this disease, the primary endpoint, is definitely going to be improvement on a symptomatic severity scale, is a mixture, in our opinion, of efficacy and safety. Because as you increase the rate of adverse events, you are likely muting or decreasing the potential to score highly for patients on patient-reported outcomes. So, you know, certainly we're going to wait to look for the Part 1B data. It's not that far away. It's literally several weeks around the corner. At Q1, when we present the robust part one SUMMIT data, I think we'll be in a very good spot to opine about what our plans are for take-forward dosing. Great. Thank you. And then maybe just also on the end for the PRO symptomology data. Looks like a lot of the readouts you had around N=8 patients, but I think you had sort of maybe 15 patients that you dosed at 100 or 200 mg in Part 1a. Can you just give us some color on, you know, what happened, you know, why you didn't include those other patients? Is it just follow-up or kind of what's the reasoning for not having those patients? Thank you. Sure. It's a great question, and, you know, the answer here is it's a learning curve for Cogent, entering a new disease with PROs. And at the beginning of Part 1a, we admittedly struggled a little bit to implement an effective electronic data capture system for PRO data, which impacted some of the earliest patients enrolled in Part 1a. So the data that you see from PROs, where we denoted the sample size, is reflective of all of the data that was collected in Part 1a. Obviously, where we didn't collect data, especially from the earliest patients, we can't report it. What we can tell you is by the end of Part 1a, the compliance, and that word makes it seem like it was a patient issue. It really, admittedly, was a little bit of a coding issue, getting up to speed on how to collect these data at the beginning of the phase I study. The compliance was up to 94% across these PROs, and we expect the Part 1b data to meet or exceed that level of, of patient compliance. Great. Thank you. Thank you. Our next question comes from Anupam Rama with JP Morgan. Your line is open. Hey, guys. Thanks so much for taking the question. Two quick ones from me. One granular question. We've gotten a couple of questions on the BEZU 100 mg QD patient that saw the AST, ALT elevation in part one. Any color there on the baseline characteristics or considerations for that patient? And then maybe a question for the company and also the KOLs. I guess there are some fears about potential enrollment dynamics in SUMMIT Part Two. As you think about this portion of the study for the KOLs, how do you think about the patient phenotypes that can enroll in part two, given the current treatment landscape and development landscape? Are you worried about enrollment dynamics? And for the company, what are the strategies for accelerating and/or hitting your internal enrollment projections in SUMMIT Part Two? Thanks so much. Okay, great, Anupam. Good to hear from you, and thanks for the question. I'll try to do number 1 and maybe give a couple thoughts on number two and then open it up to our guests to opine as well. So we did report a patient with grade three liver function test elevation who was dose reduced and discontinued. I can give you a little bit of color. That patient was near the end of the 12-week period, had elevated ALT and was dose held, dose reduced and held to allow the liver enzymes to come back did. But at the conversion of week 12 into the open-label extension, because they were on hold, they were ineligible because they weren't at a dose that was translatable into the second part of the study, essentially the open-label extension. Obviously, or maybe not obviously, we know by talking to the investigator, that the patient was devastated because she was experiencing significant symptomatic improvements, and she really did not understand why a number on a piece of paper that was, you know, asymptomatic to her would eliminate her, you know, ability to continue on in the trial. Interestingly and anecdotally, the patient was prescribed subsequently 25 mg of avapritinib and was rapidly discontinued due to high-grade three to four thrombocytopenia. So, as we showed on the PK slide, this patient did have an abnormally high exposure of bezuclastinib. We speculate maybe they had an abnormally high exposure of avapritinib as well, in the subsequent treatment period. So there may be something very specific about that patient's body chemistry that allows for very high levels of exposure of these KIT inhibitors. With regards to enrollment dynamics, of course, we're very interested in Dr. Siebenhaar and Dr. Vachhani opinions on how and whether we can enroll a robust population in SUMMIT Part Two. What I can tell you is that we have created already an incredibly robust patient wait list across the world, including in the US. Dozens and dozens of patients have already said, "I want to participate in your trial. I will wait for you to initiate it." Some of the issues that we've heard of, and I think, you know, Dr. Siebenhaar mentioned this, or Dr. Vachani actually mentioned this in his APEX talk, is potential fears about cognitive issues with other options, which are, you know, actually pushing patients to wait to try bezuclastinib. But certainly open it up to the experts to give their opinion about this. Yeah, I'm happy to start. Frank here. So yeah, I have completely the same impression. Also, we have a waiting list of patients. They would love to participate in the clinical trial, and this is something even typical for patients with mastocytosis. They love seeing things developing finally for their disease. They love to be a part of the development and the clinical trials. So I have not any obstacle that the landscape or the changing of the landscape will hinder including patients in a clinical trial. They want to help. They see the benefit of not having only one. They know that this is not the end of the story. There is issues coming with the treatments, and so they are very, very lucky to help and seeing further options being developed. Can't agree more. I personally have at least eight to 10 patients waiting for, some of them for almost a year at this point, that they want to go on the trial. And, you know, a few things to note over here. Me and my colleagues do bring up the option of using everolimus on-label for these patients, but the concern of intracranial bleed and neurocognitive issues, I can tell you that that factor alone has put off some of the patients, and they want nothing to do with such a thing. They would love to go on a trial, wait six more months if that be the case. So I personally don't see any issues with getting patients onto the study. And I'm not speaking just for myself. I know I'm speaking for my colleagues as well. The concerns for adverse events is one of those issues, and on the other drug, everolimus. And then there's the other part, which is that if we can avoid the intracranial bleeds and neurocognitive issues by using, let's say, bezuclastinib, maybe we can deliver higher doses of the drug, right? More effective c-KIT therapy, more effective targeted engagement. And maybe by doing that, we can improve the symptom burden and the biomarkers further beyond what everolimus does. So these are things that patients keep talking about, and I'm sure maybe if you don't know, there's a very strong community of patients behind, let's say, on Facebook and many other social media. They all are talking about the drug, and they. Some of them have come to me asking specifically for this trial, and they are willing to wait for even many more months. Thank you. Our next question comes from Sam Slutsky with Life Sci Capital. Your line is open. Hey, good morning, everyone. Thanks for the questions. I guess first for Dr. Siebenhaar, can you just talk about the unmet need in ISM currently with everolimus on the market, and then just the growth of patients coming to the clinic following its approval? I have one follow-up question for Dr. Vachani. Yeah. So I mean, the unmet needs will not change because there's a lot of patients, a lot of patients need treatment, and, as said, patients rather like to be part of a clinical trial. So the number of patients in line is still a lot, and, you know, it will also, our patient will not cover everything, I believe. For example, we see also in that study that patients with smoldering systemic mastocytosis are treated in the Cogent program, which is of major importance because these patients have the highest mast cell burden. Those patients are the highly symptomatic, and those patients have not been treated in the everolimus trials. This is one unmet need, which continues to be an unmet need and which hopefully will be met by the upcoming clinical trials with bezuclastinib. Okay. And then, for Dr. Vachani, just how important will the bezuclastinib combination data be in SM-AHN patients as you think about potential use of the drug? And then I guess also for Cogent, anything on the prior TKI patients, which ones were a, but ended any prior aid response? Hey, thanks. I definitely heard the first question, maybe not the second part of your question. Let me address that first part first, which is about the how the importance of concomitant AHN therapy plus the bezuclastinib. This is very important because the patients with advanced SM have a detriment in their quality of life, but also they face higher mortality, right? So we are talking about survival in the range of, what, maybe a few months to three or four years. And that survival low survival rate is driven especially by the SM-AHN population, meaning that they have mastocytosis, and they also have another clonal neoplasm, so another blood disorder or blood cancer. Now, when we get into the biology of these additional, the associated hematologic neoplasm, those neoplasms are not just driven by the KIT mutation. They are additionally also driven by other mutations. The bezuclastinib, for example, would not cover that. Everolimus alone would not cover that. So what we have seen is, and we realized is we very likely need to use concomitant therapies to slow down the progression of these SM-AHN patient populations. The problem right now, however, is that if we do combinations with midostaurin, for example, well, midostaurin is not a great, a drug in terms of its KIT inhibition. And everolimus, although it is good, has concerns with regards to cytopenias. We cannot use it in patients with platelet counts less than 50, or maybe even the whereabouts of 50 at the optimal doses. Why? Because, again, of the concern for intracranial bleeds, neurocognitive issues. These are the same patients. The SM-AHN patients are the same patients who also have low counts, partly driven by SM, partly by the KIT therapy, and partly by the AHN per se. So the associated hematologic neoplasm comes with low platelet counts. So it is very important to be able to deliver safely a combination of drugs which slows down the progression of these SM-AHN populations. So far, we have not been able to do combination therapies with avapritinib in any safe manner, and I tell all my colleagues across the country not to do that. It would be unsafe. And that is where the importance comes in of treating SM-AHN with two drugs. And we also at the poster, we didn't show it in the slides today, but in the poster, there's also a preclinical data that suggests that the combination of bezuclastinib and hypomethylating agents would not have a non-permissive thrombocytopenia. So that goes in line, that also supports the use of these two drugs. And I didn't really hear about your second question, so maybe if you can repeat, I'm happy to address. Oh, yes. So just looking at baselines, it looks like there's five patients who had received prior avapritinib for Advanced Systemic Mastocytosis. I guess, did any of those patients end up responding to treatment or, or what were outcomes like in those groups? So, yes, let me w hile we are doing this, I'm also pulling up the exact thing that you were asking for. The prior avapritinib-treated patients. Right. So there were TKI-exposed patients. I'm not sure if they were necessarily avapritinib exposed patients who had responses that we had shown both by PPR and the modified IWG ECNM criteria. If anyone from Cogent knows if these were prior midostaurin or avapritinib-treated patients, and if you can jump in and say, please. Yes, we do know that there were prior avapritinib patients who achieved response both on modified IWG and PPR criteria. To be fair, this is probably unlike resistant mutation following, you know, deep response on avapritinib. Many of the prior avapritinib patients who enrolled into the study discontinued avapritinib due to significant toxicities associated with that drug. So it's one of the reasons we're interested in studying that population, because we know that there is troubling adverse events related to that drug at the ASM dose, and offering those patients who can't tolerate avapritinib a choice, we think is important for the advancement of the field. So, to be respectful to the time of Dr. Siebenhaar and Dr. Vachani, I think we're going to limit this to one last question from the field. Operator, if you can go to the next individual. Thank you. Our last question comes from Eun Yang with Jefferies. Your line is open. Thank you very much for squeezing me in. I have a couple of questions. One is, fatigue is a part of Mastocytosis Activity Score domain, but then it also appears as a side effect. Question to the KOLs is that, is the fatigue indeed treatment-related? And what do you think causes this symptom, this adverse event in patients? Second question is to Andy. Obviously, we have to see all the data earlier next year, but when you start the pivotal Part 2 study, is it your goal to define just one dose, or is there a potential that you could take two different doses in pivotal study? Thank you. Great. Thanks, Eun. I can answer the second question first. I think our goal, you know, based on how drugs are developed in this field, is to find an optimal dose, and we are confident that, at following the completion of Part One, we will be able to... Our goal is to take a dose into SUMMIT Part Two. With respect to fatigue, and then, you know, maybe I'll invite Dr. Siebenhaar to comment as well. I know he brought it up in his comments. There are these treatment-emergent adverse events, which are sometimes difficult to pinpoint to related to drug versus related to disease. It is certainly something that we're going to continue to monitor, and we will have a more robust data set to see if this truly is, you know, a low-grade adverse reaction to bezuclastinib or sort of a background symptomatology associated with the disease. But Dr. Siebenhaar, I don't know if you want to add anything. Yeah, very happy. So, yeah, completely agree. We need to be, we need to be careful here. So I think it's, it's too early, and we need to follow this up in, in more patients. I also would rather think it's not treatment emerged. It's probably, you know, since the fatigue also is a symptom of mastocytosis, and among the symptoms which, you know, probably do not respond as early, as quick, and as good as the more related symptoms to mast cell activation, it could be also, just, disease-related rather than drug-related. So, it was seen yet only in, in single, in a single patient or in two. And we also see in mastocytosis patients without treatment, that their fatigue, you know, gets worse and gets better. It's a little bit also depending on how they feel in general, what's their surroundings. So for me, this is not compromising anything. I would rather believe it's disease than treatment-related, and as Andy said, we definitely need to follow up this, but don't take home that fatigue will be a prominent side effect of bezuclastinib. I would rather think it will not. Great. Thank you. So thanks very much for all the questions. Once again, I want to thank very much Dr. Siebenhaar and Dr. Vachani for joining us today, presenting the data, and for staying over an additional 20 minutes to answer questions. We certainly appreciate your support on the call today and in general for the development of this asset. And while we are, do notice, because we do read a lot, that there are, you know, investors and analysts that want to focus on sort of arbitrary single data points and compare them to other drugs and decide yes or no. What we take away from this weekend at ASH is in interactions with dozens and dozens of investigators, the excitement about the positive data that we presented on bezuclastinib, and in the field, the support that we're getting from both the investigators and the patient community to continue developing this drug, as it does represent at least a very important treatment option, if not the potential for becoming the standard of care long term. We are committed to doing that and certainly want to thank the patients and their families for participating in our trials and trusting that bezuclastinib is going to help them feel better and live longer. So with that, I'm going to close the call and one last thing. Thanks so much to my Cogent colleagues for helping getting us to this point. We are looking forward to a very, very exciting 2024. Thanks, everybody. Thank you for your participation. You may now disconnect. Everyone, have a great day.