Good day, and welcome to the Kura Oncology First Quarter 2022 Earnings Conference Call. All participants will be in a listen-only mode. Should you need assistance, please signal a conference specialist by pressing the star key followed by zero. After today's presentation, there'll be an opportunity to ask questions. To ask a question, you may press star, then one on your telephone keypad. To withdraw your question, please press star, then two. Please note this event is being recorded. I'd now like to turn the conference over to Mr. Pete De Spain, Senior Vice President of Investor Relations. Please go ahead. Great. Thank you, Ian. Good afternoon, and welcome to Kura Oncology's First Quarter 2022 C onference C all. all. Joining me on the call are Dr. Troy Wilson, our President and Chief Executive Officer, and Tom Doyle, our Senior Vice President of Finance and Accounting. Dr. Stephen Dale, our Chief Medical Officer, is also with us and available to answer questions. Before I turn the call over to Dr. Wilson, I'd like to remind you that today's call will include forward-looking statements based on current expectations. Such statements represent management's judgment as of today and may involve risks and uncertainties that could cause actual results to differ materially from expected results. Please refer to Kura's filings with the SEC, which are available from the SEC or on the Kura Oncology website for information concerning risk factors that could affect the company. With that, I'll now turn the call over to Troy. Thank you, Pete, and thank you all for joining us this afternoon. Despite what continues to be a challenging broader market environment, we continue to operate from a position of strength here at Kura, armed with three independent drug development programs, a strong, experienced team, a well-designed clinical development strategy, and a cash runway through 2024. Now, as we approach a series of important catalysts driven by completion of enrollment in the Phase 1b study of our menin inhibitor, ziftomenib, and culminating in top-line data next quarter and a full data presentation in the fourth quarter. As mentioned, I'm pleased to report we recently completed enrollment of the patients in the Phase 1b portion of KOMET-001 required to identify a recommended Phase II dose for ziftomenib. Recall the study was designed to enroll two expansion cohorts, 200 milligrams and 600 milligrams, with each cohort comprised of patients with NPM1 mutant or KMT2A rearranged relapsed and/or refractory acute myeloid leukemia. The goal of the Phase 1b is dose optimization consistent with FDA's guidance around Project Optimus, and the two doses were selected based on the encouraging clinical activity, safety profile and tolerability demonstrated in the Phase 1a portion of the study. We're now assessing the patients in each expansion cohort for safety and tolerability, pharmacokinetics and exposure, as well as efficacy. We remain on track to identify the recommended Phase II dose for ziftomenib and to report top-line data from the Phase 1b study in the third quarter with a more complete data set from KOMET-001 reserved for presentation at a medical meeting in the fourth quarter. As a reminder, the study protocol gives us flexibility to enroll additional patients in the Phase 1b, enabling us to maintain momentum while we transition into a subsequent Phase II registration-directed portion of KOMET-001. We believe data from all patients treated at the recommended Phase II dose will have potential to contribute to the registrational patient population. Meanwhile, we remain enthusiastic about the encouraging safety and profile tolerability and clinical activity we are observing in the Phase 1b study as we continue to add sites in the U.S. and Europe in anticipation of the subsequent Phase II portion of KOMET-001. We also intend to conduct a comprehensive development strategy that builds upon the potential to register ziftomenib as a monotherapy while giving us flexibility to access larger opportunities through combinations and in earlier lines. We look forward to sharing much more regarding our global development strategy for ziftomenib later this year following identification of the recommended Phase II dose. Now let's turn our attention to our farnesyltransferase inhibitor programs. We continue to view farnesyltransferase inhibition as a potentially valuable therapeutic and commercial franchise, one with potential to deliver multiple opportunities in oncology. One of the first examples of the use of FTIs as a targeted therapy was demonstration of the potential for tipifarnib to drive durable responses in recurrent and metastatic HRAS mutant HNSCC, and our ongoing AIM-HN registration-directed trial continues in that indication. More recently, we've begun efforts to build upon the initial monotherapy activity of tipifarnib with two goals. Number one, to drive deeper and more durable responses, and number two, to expand the potential patient population. Toward this end, we're pursuing the KURRENT-HN trial to evaluate the combination of tipifarnib and alpelisib, an inhibitor of PI3 kinase alpha, in selected HNSCC patient cohorts. By combining tipifarnib and alpelisib, we believe we can achieve both goals. Our preclinical data suggests the combination has potential to provide meaningfully better antitumor activity relative to inhibiting either target alone. By targeting both PIK3CA and HRAS dysregulated HNSCC, the combination has potential to increase the total addressable population for tipifarnib to as much as 50% of patients with HNSCC. In December, we dosed the first patient in our Phase 1/2 KURRENT-HN trial of tipifarnib in combination with alpelisib in HNSCC. The initial cohort includes patients who have PIK3CA-dependent HNSCC. Screening has commenced in an HRAS overexpression cohort, and we expect to dose the first patient in this cohort by the third quarter. Our goal with the current HN trial is to identify a recommended Phase II dose and schedule for the combination and look for early signs of clinical activity. Our team is making excellent progress, and we look forward to providing an update. Beyond HNSCC, we're beginning to understand FTIs may represent an ideal combination partner for certain classes of targeted therapy in large solid tumor indications. The first of these emerging combination opportunities was highlighted last month in a late-breaking presentation at the American Association for Cancer Research annual meeting in New Orleans. The new findings were generated through a collaboration with Inserm, the French National Institute of Health and Medical Research. The presentation featured pre-clinical data supporting the potential for tipifarnib to prevent emergence of resistance to osimertinib in EGFR mutant non-small cell lung cancer. Several farnesylated targets were identified that appear to control the ability of lung cancer tumor cells to enter and exit a state that makes them tolerant to osimertinib. Using pre-clinical in vivo models of EGFR mutated lung tumors, co-treatment with tipifarnib durably prevented relapse to osimertinib for up to six months with no evidence of toxicity. Collectively, these data strongly support the potential use of an FTI to prevent or delay the adaptive response to osimertinib. We're preparing to initiate a Phase I study of tipifarnib in combination with osimertinib in treatment naive, locally advanced, and/or metastatic EGFR mutated non-small cell lung cancer, and we expect to dose the first patient in that study, which we call the KURRENT-LUNG trial, in the third quarter. We intend to perform initial clinical evaluation with tipifarnib and osimertinib while in parallel advancing KO-2806, the lead development candidate in our next generation FTI program through IND-enabling studies. We remain on track to submit an IND application for KO-2806 in the fourth quarter. With that, I'll now turn the call over to Tom for a discussion of our financial results. Thank you, Troy, and good afternoon, everyone. I'm happy to provide a brief overview of our financial results for the first quarter 2022. I invite you to review our 10-Q filed today for a more detailed discussion. Research and development expenses for the first quarter 2022 were $20.9 million, compared to $20.3 million for the first quarter of 2021. The increase in R&D expenses was primarily due to the increase in ziftomenib clinical trial and personnel cost. General and administrative expenses for the first quarter of 2022 were $11.9 million, compared to $10.6 million for the first quarter of 2021. The increase in G&A expenses was primarily due to the increase in professional fees and non-cash share-based compensation. Net loss for the first quarter of 2022 was $32.5 million, compared to a net loss of $30.7 million for the first quarter of 2021. This included non-cash share-based compensation expense of $6.7 million, compared to $5.1 million for the same period in 2021. As of 31 March 2022, we had cash equivalents and short-term investments of $480.1 million, compared to $518 million as of 31 December 2021. Based on our current plans, we believe that our cash equivalents and short-term investments will fund current operations through 2024. With that, I now turn the call back over to Troy. Thank you, Tom. Before we jump into the question and answer session, let me just lay out our anticipated milestones for 2022. For our menin inhibitor program, identify the recommended phase II dose of ziftomenib and report top-line data from the Phase 1B study in the third quarter, present updated data from KOMET-001 at a medical meeting in the fourth quarter. For our FTI programs, dose the first patient in the HRAS overexpression cohort of KURRENT-HN in the third quarter, dose the first patient in the KURRENT-LUNG trial in the third quarter, and submit an IND application for KO-2806 in the fourth quarter. With that, operator, we're now ready for questions. We will now begin the question and answer session. To ask a question, you may press star then one on your telephone keypad. If you are using a speakerphone, please pick up your handset before pressing the keys. To withdraw your question, please press star then two. At this time, we will pause momentarily to assemble our roster. Our first question comes from Jonathan Chang of SVB Leerink. Please go ahead. Hi, guys. Thanks for taking my questions. Jonathan Chang at SVB Securities. First question on ziftomenib. Can you please refresh our memories as to what investors can expect in the top line third quarter data versus the medical meeting presentation in the fourth quarter? Sure, Jonathan, thanks for the question. The focus of the top line data will really be around the safety, tolerability and clinical activity at the recommended Phase II dose, Jonathan, with a particular focus on the CR/CRh rate in the patients that were enrolled in the dose that we've identified as the recommended Phase II dose. That's what you should look for in the top line. In the data, that'll be reserved for a little bit later in the year at a medical meeting. There you should look for a much more fulsome presentation of the data from the KOMET-001 study, and that's where we'll get into you know, the breakdown between the specific genetic subtypes, more detail around both the safety and tolerability as well as the efficacy, you know, potentially, you know, specific anecdotes around patients that are interesting and just a much more comprehensive data set. The top line is really intended, as we've guided consistently, just to communicate that we've identified the recommended Phase II dose and to help inform investors that we continue along the path toward what we believe will be the start and ultimately the execution of a successful Phase II. Got it. Thank you. Second question: With enrollment completion in the Phase 1b expansion cohort, can you provide any color on how many patients in the cohorts have NPM1 mutation versus KMT2A rearrangement? Yeah, it's a good question, Jonathan, and thank you for it. Without getting specific, you know, what I can tell you is we actually see a pretty good balance between the two populations. I you know, I'm gonna hold off on the specific numbers until we get to the data presentation in the fourth quarter. Suffice it to say, we didn't see a sort of a disproportionate enrollment to one genetic subtype or the other. We see good balance. That you know that gives us confidence that as we've said all along, from our perspective, we think there's going to be one recommended Phase II dose to treat both patient populations, and we're seeing you know, we're seeing what we wanna see in both populations. You know, hopefully that helps give you a little bit more color on your question. Great. Thank you. Thanks for taking the questions. Sure. Thank you. Our next question comes from Peter Lawson of Barclays. Please go ahead. Mr. Lawson, your line is now live. Hey, thanks so much, Troy. First question is just around safety. Just how much safety data we'd see in the 3Q update. Have you seen any further cases of Differentiation Syndrome, and how's the management strategy going with that? Thank you, Peter, for the questions. Given that it's gonna be a top line cut of the data, we'll probably give some color around the safety and tolerability. I can tell you what we've seen thus far. Ziftomenib appears to have a very encouraging safety and tolerability profile. To the second part of your question, really the one thing of note is we have continued to see Differentiation Syndrome, but as we discussed on prior calls, we now have what we believe to be a very robust and enhanced mitigation strategy, and it seems to have given the investigators the toolkit that they need to manage it. To that end, you know, neither we nor the investigators run away from Differentiation Syndrome. To the contrary, if you see it's usually an indication of clinical activity. The key is, can you manage it effectively, and can you keep the patient safe? At this point, I can tell you the enhanced mitigation strategy appears to be, you know, doing exactly what it was designed to do. We'll probably have some very, you know, high-level color around it in the top-line release with much more data to follow. But, you know, there shouldn't, it should be very consistent with what we've said all along. Gotcha. Thank you. I may have missed this, I apologize, but the current head and neck trial, when do we see the first kind of readouts of that? Yeah. You didn't miss it, Peter. We were a little bit vague, but let me answer your question. This trial is intended to determine the recommended Phase II dose and schedule for the combination. It's a Bayesian design that allows us to adjust the levels of both of the two drugs, tipifarnib and alpelisib. The primary focus is safety and tolerability, but we are looking for clinical activity. I think at this point, Peter, we you know, in the prepared remarks, I commented that the trial's going well, and we are encouraged. You know, there may be an opportunity. I hope there'll be an opportunity in the not too distant future to share some more data with you, but we haven't put any specific guidance around what that data would be or the venue. Once we have it, we'll be sure to share it with you and others on the call. Great. Thank you so much. Sure. Thank you, Peter. Our next question comes from Tiago Fauth of Credit Suisse. Please go ahead. Hi, guys. Jonathan on for Tiago. Thanks for taking our question. We already know a lot about the differentiation between ziftomenib and the main competitor you're frequently compared to, but there are now several other menin inhibitor trials running. You know, with that in mind, it looks like you're likely ahead of those, but from what you've seen from those trials so far, is there anything you could say about the relative differentiation between those programs or anything pre-clinically or even from the standpoint of trial design? Thanks. Yeah. Jonathan, thanks for the question. You know, I'm gonna defer on addressing our competitors. I'll let them speak to their data and their designs. I'll maybe highlight something I think that a year ago was perhaps viewed as a negative, and now I view very much as a positive, and that is the Phase 1b design for which we've just completed enrollment. You know, at the time, the concern was that you've lost time, why is the FDA making you do this. This was very early in the dawn of Project Optimus. What it's provided us is a significant amount of experience at two different doses, one of which will be our recommended Phase II dose. As we now look to transition from Phase 1b to Phase II, I think we have a very solid understanding of the safety, the tolerability, the PK, the exposure, and the efficacy at ultimately what will be the recommended Phase II dose. That perhaps wasn't fully appreciated by everyone at the time, but what it means is you're gonna get a very full picture at the RP2D in Q3, and it should give everyone much more confidence that those parameters are gonna follow through, not only through the medical meeting presentation in Q4, but on into the Phase II. That's probably the most significant difference, Jonathan, that we've seen between what we're doing and others. I think it positions ziftomenib, you know, very competitively relative to the others' drugs in the landscape. Very helpful. Thank you. Sure. Our next question comes from Roger Song of Jefferies. Please go ahead. Great. Thank you for taking the question. Maybe, Troy, can you just comment on so far the regulatory interaction? Have you discussed with the FDA about your RP2D plan and when you will discuss the pivotal. Will that be after the top line data in 3Q versus the full data in 4Q or maybe later? Yeah. Roger, so I wanna be careful here on specifics. We interact with the agency pretty regularly across all of our programs. You know, we very much work in partnership with the agency, and we've found them to be very, very productive partners. I don't wanna speak to the specifics, just given the timing and some of the sensitivities. Suffice it to say, you know, today it's significant in that we've completed enrollment of the 24 patients needed to support the Phase 1b. We are in the process of collecting and analyzing that data ultimately to identify the recommended Phase II dose. Then that's gonna require a package that needs to be submitted to the FDA. That hasn't happened yet, that is, you know. The team knows exactly what it needs to do, and it's very much focused on that. I don't wanna be a lot more specific as to the timing, just out of respect of, you know, for the agency and for their process. I will tell you, I think the team is not only doing everything they need to do, but I hope as is clear, is executing with the diligence and the urgency that's needed for this program, you know, to really be competitive. Got it. Yeah. I think last time we removed the clinical hold on the DS seems pretty promptly as well. Okay. Got it. Maybe just another question from us. For tipifarnib this combo trial, can you just remind us where are you at the monotherapy, the pivotal study, and also if the combo data looks good, how you're gonna strategize this combo versus monotherapy moving forward? Thank you. Right. Yeah, Roger, thanks for the question. Roger, let me just pick up on something that you said because I can't resist, if you don't mind. You know, we—It wasn't that long ago that the clinical hold was lifted, and at the time, shortly thereafter, we said we were seeing high interest and high engagement among the investigators in the AML community for ziftomenib. I hope now that we've come back exactly on schedule with the cohorts enrolled and enrollment ongoing, that underscores, you know, what we said back then. There is a very high level of interest and engagement in this compound and in this class in the AML community. Just wanted to round out the answer to that. On your FTI question, yeah, we find ourselves at an interesting point. Enrollment in AIM, which is the monotherapy registration-directed study for tipifarnib in HRAS-mutant head and neck, enrollment is continuing. We know the drug is active. You know, you've seen the data from the Phase II RUN-HN. We continue to see monotherapy activity. The challenges that we faced is that the patients coming to that study have typically coursed through both platinum and IO. As a result, you know, a large majority of them are just not sufficiently fit to go on to a study. It sort of is what it is. You know, the team is working very hard to execute against that, but that's the reality of that patient population. KURRENT really addresses that in three different ways. The first is by combining alpelisib and Tipi, you open up the potential population from, you know, 4%-8%, which is the HRAS monotherapy to as much as 50% when you look at HRAS dysregulated and PIK3CA dysregulated populations. Nearly a tenfold difference in the potential patient population. The second, of course, is by providing additional biomarkers, you're giving physicians more reasons to do screening. You heard us say in the prepared remarks, the HRAS overexpression cohort is open, and in screening, we of course have patients who are being screened for both PIK3CA mutations and amplifications. That helps just open the funnel up, if you will. The final point is the preclinical data suggests that, you know, there's really a strong potential for drug-drug synergy with this combination in these genetically selected populations in head and neck. We see synergistic activity that's greater than what you could do with either drug as a monotherapy. Obviously, if you can offer patients better efficacy with acceptable safety and tolerability, that's a win. It's a very good question, how do you integrate those two development streams, AIM on the one hand, KURRENT on the other. Stephen and the development and regulatory teams at Kura are very much engaged in that right now. I don't have a lot more to tell you, but it is very much top of mind, and we'll share additional updates as we have them. You can tell we're quite encouraged by the progress that the team is making on Kurrent, and we'll share more progress as we have it. Great. Thanks for the comprehensive comments. Thank you. Sure. Thank you. Our next question comes from Reni Benjamin of JMP Securities. Go ahead. Hey, good afternoon, guys. Thanks for taking the questions. Maybe just starting off with ziftomenib. Troy, when we're when I think in the past, we've talked about, you know, the potential combination studies. Venetoclax was one of the potential partners. There were some others. I'm just kinda curious, as you know, continue to progress through both preclinical and clinical development, have there been any kind of changes to your thoughts? Are you still looking. You know, what are the top, call it top two, you know, combination studies that you'd like to get started, and when do you think that might get started? Yeah. Reni, thanks for the question. There's a lot sort of packed in there. Let me see if I can unpack it. Combinations are of high interest to us. Ultimately, that's probably going to be the highest best use for menin inhibitors, if you wanna serve the most patients and provide the greatest unmet need. I continue to believe, you know, there's a very strong case to be made for the monotherapy registration, but AML will be a disease of well, the treatment paradigm will be one of combinations. The predicate to any of those combinations, of course, is identification of a recommended Phase II dose so that you know where to start. With the combo, we are, you know, moving toward that goal with all due speed. We've just, you know, now completed enrollment, and we're looking forward to giving the top-line data next quarter. There are a lot of activities, Ren, going on in the background on to support the combination studies, both in the front line and in earlier lines of therapy. We haven't said a lot yet about timing because, again, we wanna be respectful of interactions with the agency. I can assure you that those activities are going on very actively in the background, and we'll say more when it's appropriate and, you know, the studies are underway. In terms of prioritizing them, I mean, you put your finger on at least a couple of them. Venetoclax continues to be a very attractive combination partner. There's strong evidence for potential synergy between venetoclax and ziftomenib. You know, there are some suggestions clinically that synergy may carry over into patients. Obviously, you know, that's not a substitute for running a study, but I think there's a very strong rationale to do that. The other, of course, is FLT3. FLT3 is you know, a very large patient population. When we unveil our development strategy, I think you'll find it's a continuation of what we've done well. It's efficient. It's meant to be comprehensive. It's meant to target both patients in the two genetic subtypes as well as looking for expansion opportunities outside of those genetic subtypes. You know, we're looking forward to sharing it with you probably a little later in the year as we get closer to the medical meeting. Hopefully that gives you some color and much more to share, I think, you know, in the second half as which we're very close, very quickly approaching. Got it. Oh, that's just perfect. Maybe just switching gears too from the KURRENT for Tipi. The KURRENT, you know, head and neck study in combination. You know, you're gonna be starting enrollment of the HRAS overexpression cohort. Outside of it being a target for Tipi, is there any other rationale? Is it a bypass mechanism for patients who, you know, get exposed to PI3Kα or are they kind of a patient population that has a much worse prognostic factors? How should we be viewing this overexpression cohort? It's a great question, Reni, and you have two questions in there, and I'm just gonna tease them apart and answer each of them. There are at least two populations in that current trial that relate to farnesylated targets. I'll just draw everybody's attention. We updated our corporate presentation this afternoon in connection with this call, and there's a very nice graphic that shows both the relevance of tipifarnib to HRAS overexpression, where HRAS is the farnesylated target, and then a second major mechanism, which is Rab farnesylation. Reni, in your question, you mentioned a bypass resistance. That's exactly what you see with PI3-kinase inhibitors. Once you inhibit the oncoprotein, oftentimes you'll see upregulation at mTOR, which is the next node down. You know, I'm personally I worked on this 12 or 13 years ago in the context of mTOR kinase inhibitors and PI3-kinase alpha, but that is one of the principal resistance mechanisms, and tipifarnib silences that. It deletes the farnesyl group off of Rab and potentially blocks that bypass resistance. That's why we think there's a strong rationale in the HRAS overexpressers, where you're just removing RAS, which is a bad actor for a lot of reasons, even if it's not mutated. In the PIK3CA populations, you're directly addressing mTOR through Rab. Again, I would direct everyone, if you're interested, to the graphics in our corporate presentation. For those reasons, Ren, we think, you know, we think it's a very strong rationale for combination. You know, the team's doing a terrific job, and we look forward to sharing, you know, results with you in the future. Terrific. Then my final question is just the current lung trial. I really like the preclinical work that was highlighted at ACR. Can you talk a little bit as to the mechanism of action? You know, how might it actually prevent resistant mutations, kind of the goals of the study and what might be kind of go, no-go decision matrix metrics that you might be looking at? Would it be progression-free survival mainly, or would you be looking at things like overall response rate primarily? Right. Yeah. Great question, Ren. Again, sound like a broken record here, but I would direct everyone to our revised corporate presentation that's available on our website. There are three or four slides now in there that speak to KURRENT-LUNG and that, you know, really distill it down to its essence. Ren, let's just quickly, you know, jog through your questions. The mechanism of action is it is now well understood that there are a subpopulation of cells that are drug-tolerant cells when you treat lung tumors, EGFR mutant lung tumors with osimertinib. A small fraction of those tumors are so-called drug-tolerant cells. The reason those cells are drug-tolerant is they actually rewire their cellular architecture. They actually dedifferentiate, and they become DTC cells, drug-tolerant cells. The process by which they enter that drug-tolerant state depends on a farnesylated protein. The process by which they exit that state depends on a farnesylated protein. If you block the entry and exit, essentially, you've barred the door. Now you don't allow those cells to enter their DTC state, and they then become susceptible. They eventually die off under pressure from osimertinib. It is those DTC cells, Ren, to your next question, that are believed to seed the molecular origins of adaptive resistance. In that drug-tolerant state, they can sit there essentially and cook and find a way around osimertinib. You don't allow the cells to ever get there, and the consequence of that, and again, I'll point you to the cartoon and then the data on the next slide in the corporate presentation. In the case of osimertinib alone, eventually you see the tumor relapse. You get little seeds of resistance, they grow out, and boom, the tumor comes back. In the case where you're adding tipifarnib to the osimertinib, you see an extended delay on that resistance. In some cases, you know, a prevention, nearly a complete prevention. These are preclinical data. To the third part of your question, Ren, what are you looking for? What are we looking for in KURRENT-LUNG? You're looking, of course, at safety and tolerability. You need to establish a recommended Phase II dose for the combination. PFS is the primary endpoint, but we're gonna be looking at a number of endpoints along the way. Given the high activity of osimertinib as a monotherapy, you'd have to have a pretty significant trial for a difference in response rate. If the clinical data recapitulates what we see preclinically, you'll see it in PFS. The trial is designed to look for just that. If we see that, obviously, you know, that's a big deal because you could keep patients on osimertinib then, you know, that much longer and really provide them with a high quality of life. This is, you know, just a final comment I'll make, Ren. This is what you'll see. alpelisib and tipi is the first example, Osi-Tipi is the second. I hope you'll see a third and then a fourth. We're using this concept of precision medicine now to go after much larger patient populations, but using all of the, you know, this real strength of precision medicine. You know, I think it's gonna be an exciting, you know, several years coming up as we see whether the clinical data recapitulates the very strong preclinical data. We're cautiously optimistic and look forward to sharing updates with you in the future. I hope I've answered all the various parts of your question. You definitely have. Thank you very much for unpacking it so nicely. Have a good one. Sure. Thanks, Reni. This is the last reminder. If you have a question, please press star, then one. At this time, our next question will come from Yeva Petrushka of Cowen. Please go ahead. Hi. Thanks for taking our questions, and congrats on completing the enrollment. You mentioned earlier that you've seen additional cases of DF. Just wanted to follow up on that with a few details. What was the severity and at what dose? Thanks, Yeva, for the question. Starting with dose, there doesn't, at least in our experience, between the two Phase 1b cohorts, there doesn't appear to be a dose dependence. You know, differentiation syndrome is, it appears, you know, just to take a step back, one expects to see differentiation with this mechanism. The extent and the severity of Differentiation Syndrome appears to be more patient specific, maybe related to tumor burden, you know, maybe more common among KMT2A. You know, we have such a small number, it's hard to draw really any definitive conclusions, but you know, our experience has been with the enhanced mitigation strategy, the physicians have the toolkit that they need to be able to manage the Differentiation Syndrome. Ultimately, our experience, Eva, has been, again, if you're seeing differentiation and Differentiation Syndrome, that's usually a marker of clinical activity. What we've found with the investigators now is that they're leaning into that. They're making sure that they can get the patients through it, and they have the, and we've talked about in the past, and I can, I'm happy to summarize it again if it's helpful, but we have a very thorough and expert mitigation, enhanced mitigation strategy to give them the tools that they need. It's something to watch out for with this mechanism of action, but it isn't really, we think gonna be any part of the determination of whether 200 milligrams or 600 milligrams is the recommended Phase II dose. Thank you. That's helpful. Just one other point to confirm, so the top line data and nomination of the RP2D, will that be disclosed together at the same time? Yes. Yes. Okay. Can we expect- Yes. Any PK/PD or any additional data along with the, you know, RP2D disclosure to support the rationale? I don't know that we'll get into PK/PD, Eva, because we wanna make sure we, you know, we protect the sanctity of the data set for the eventual presentation at a medical meeting. Suffice it to say, you know, all of the data will line up in support of the ultimate recommended Phase II dose. I think the thing that will matter is, again, you know, does the safety and tolerability continue? I can tell you now it does. Are you seeing a level of clinical efficacy that gives you confidence in a successful Phase II? And, you know, what are the elements of that? This is going to be top-line data. It's probably, you know, there are probably gonna be questions and, you know, I think it'll be a very fulsome presentation at the medical meeting in Q4, where more, you know, we'll be able to get into things more like exposure and the kinds of questions that you're getting to. Got it. Thank you so much. Thank you. This concludes our question and answer session. At this time, I would now like to turn the conference back over to Mr. Troy Wilson for any closing remarks. Thank you, operator, and thank you all once again for joining our call today. We'll be participating in the Cowen Oncology Innovation Summit, the Jefferies Healthcare Conference, and the JMP Life Sciences Conference next month, and we look forward to seeing many of you there. In the meantime, if you have any additional questions, please feel free to contact Pete, Tom, or me. Thank you again, and have a good evening, everyone. The conference is now concluded. Thank you for attending today's presentation. You may now disconnect.