Good day, and thank you for standing by. And welcome to the second quarter 2021 Kura Oncology Inc. earnings conference call. At this time, all participants are in a listen-only mode. After the speakers' presentation, there will be a question and answer session. To ask a question during the session, you will need to press star one on your telephone or touch tone key. If you require any further assistance, please press star zero. I would now like to hand the conference over to your speaker today, vice president of investor relations, Mr. Pete De Spain. Thank you. Please go ahead, sir. Thank you, operator. Good afternoon, and welcome to Kura Oncology's second quarter 2021 conference call. Joining me on the call are Dr. Troy Wilson, our President and Chief Executive Officer, and Dr. Marc Grasso, our Chief Financial Officer and Chief Business Officer. Before I turn the call over to Dr. Wilson, I would 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 Dr. Troy Wilson, President and CEO of Kura Oncology. Thank you, Pete, and thank you all for joining us this afternoon. I'm extremely proud of the progress our team has made across the pipeline over the past several months, underscoring our focus on operational execution. This progress is highlighted by the first patients dosed in the phase I-B expansion cohorts with our menin inhibitor, KO-539, a clinical collaboration with Novartis to evaluate tipifarnib in combination with the PI3 kinase alpha inhibitor, alpelisib, in head and neck squamous cell carcinoma, and nomination of KO-2806 as the lead development candidate in our next-generation farnesyltransferase inhibitor program. Let's take a closer look at the progress within each of our programs, beginning with our menin inhibitor, KO-539. We continue to have strong conviction in KO-539 and its potential to be both a first-in-class and a best-in-class menin inhibitor. This confidence is supported by the results from the Phase I-A dose escalation portion of KOMET-001, our Phase I/II clinical trial of KO-539. These data showed promising single-agent activity in an all-comer population of patients with relapsed or refractory AML, including patients with NPM1 mutations and KMT2A rearrangements. We're also encouraged by the clinical activity observed in patients with other co-mutations, including a complete remission in a patient with a SETD2/RUNX1 mutation. We believe these patients may represent a potential third expansion cohort, a differentiating feature of our program. KO-539 also demonstrated a favorable safety and tolerability profile with no evidence of QTc prolongation, another important differentiating feature of the program. Given the wide therapeutic window KO-539 demonstrated in the phase I-A dose escalation portion of the study, we've now advanced to two phase I-B expansion cohorts, a lower dose of 200 milligrams and a higher dose of 600 milligrams, each comprising NPM1 mutant and KMT2 rearranged relapsed and refractory AML patients. These two doses demonstrated preliminary evidence of activity and were determined to be safe and well-tolerated in the dose escalation portion of the study. The phase I-B is designed to determine the lowest dose of KO-539 that provides maximum biologic and clinical effect in keeping with guidance from FDA relating to targeted therapies in oncology, now known as Project Optimus. The first patient was dosed in the 600 milligram cohort of the phase I-B in late June. We've now enrolled patients in each expansion cohort and have a queue of patients in screening. Approximately half of an estimated 20 U.S. sites are actively screening patients in the phase I-B, with sites pending across five European countries, a demonstration of the strong execution of our clinical operations team. Our base case is that we should complete enrollment of the 12 evaluable patients in each cohort by the first quarter of 2022. We will assess these patients for safety and tolerability, pharmacokinetics, and efficacy in order to determine the recommended phase II dose. The study protocol gives us the flexibility to enroll up to 30 patients in the selected cohort. This enables us to continue enrolling patients in the phase I-B at the recommended phase II dose while we transition into the subsequent registration-directed portion of KOMET-001. Importantly, we believe data from all patients treated at the recommended phase II dose will contribute to the registrational patient population. Thus, our phase I-B not only helps us to gather a more robust data set in our target populations and to refine the selection of a recommended phase II dose, but it enables us to start our path toward registration and maintain an aggressive development timeline for the program. Although it's early and results are still preliminary, we're encouraged by observations of early signs of clinical activity in the phase I-B. We intend to provide an update on both the phase I-A and the phase I-B at a future medical meeting, pending determination of the recommended phase II dose. In addition, we'll seek to provide qualitative updates on the progress of the phase I-B in the months ahead as appropriate. In the meantime, we're preparing to conduct a comprehensive clinical development plan for KO-539, pending determination of a recommended phase II dose. Additional development opportunities include combination studies, other genetic subtypes, pediatric development strategy, and other indications such as acute lymphocytic leukemia and myelodysplastic syndrome. Efforts are already underway to support some of these larger opportunities. For example, encouraging preclinical data has been generated through one of our research collaborations, showing evidence of synergistic activity of KO-539 in combination with venetoclax in KMT2 rearranged and NPM1 mutant AML models. We expect to have more to say regarding these data potentially later this year. Although our Menin program continues to capture much of the attention, we remain just as excited about the opportunities for farnesyltransferase inhibition in oncology. The most advanced of these opportunities is focused on patients with head and neck squamous cell carcinomas, or HNSCC, that carry mutations in the HRAS gene. Earlier this year, tipifarnib was granted Breakthrough Therapy Designation from FDA for the treatment of patients with recurrent or metastatic HRAS-mutant HNSCC. The Breakthrough Therapy Designation was based upon data from our phase II RUN-HN trial, which was published a month later in the Journal of Clinical Oncology. We continue to be motivated by these data, by the BTD award from FDA, and the potential for tipifarnib to represent the first approved small molecule-targeted therapy in HNSCC. As such, we remain focused on our AIM-HN registration-directed trial and bringing tipifarnib to market as quickly and as efficiently as possible. In addition to addressing an unmet need for patients, we believe the opportunity for tipifarnib in HRAS-mutant HNSCC provides a beachhead to the development of rational combinations and expansion to larger genetic subsets. Among these potential combinations, we've identified, as a priority, the combination of tipifarnib and a PI3 kinase alpha inhibitor. Our preclinical data suggests that HRAS and PI3 kinase alpha are codependent oncogenes in HNSCC, and that combining tipifarnib with a PI3 kinase alpha inhibitor has the potential to provide meaningfully better antitumor activity relative to inhibiting either target alone. We believe this combination has the potential to increase the total addressable population for tipifarnib to as much as 50% of patients with HNSCC. Last month, we announced a clinical collaboration with Novartis to evaluate the combination of tipifarnib and the PI3 kinase alpha inhibitor alpelisib in patients with HNSCC. Alpelisib is approved to treat patients with PIK3CA mutant breast cancer, and it has demonstrated encouraging evidence of clinical activity in patients with HNSCC. Given the strong preclinical rationale and data, we look forward to evaluating the two drugs in combination. We're now actively preparing for a phase I/II study of tipifarnib in combination with alpelisib in HNSCC, which we call the KURRENT trial. The initial cohort will include patients who have PIK3CA-dependent HNSCC. These patients can be identified using next-generation sequencing, which will allow us to identify a recommended phase II dose and schedule for the combination. Under the terms of the collaboration agreement, we will sponsor the KURRENT trial and supply tipifarnib, and Novartis will supply alpelisib. We expect to initiate this study in the fourth quarter of 2021, and we look forward to sharing our progress with you. Meanwhile, through our own internal efforts and our network of academic collaborations, we've uncovered some exciting opportunities for farnesyltransferase inhibitors in combination with other targeted therapies. Last year, we initiated a discovery stage program to develop a next-generation farnesyltransferase inhibitor designed to target innovative biology and address large oncology indications of high unmet need through rational combinations. Our goal for this program was to deliver a drug candidate that has improved potency, pharmacokinetic, and physical chemical properties relative to tipifarnib. Our team identified multiple advanced lead compounds, and I'm pleased to report we've nominated one in particular, a compound we call KO-2806, as our lead development candidate. We're now conducting IND-enabling studies and expect to submit an IND application for KO-2806 by the end of 2022. We believe farnesyltransferase inhibition in oncology has the potential to deliver multiple opportunities for large indications, and we look forward to sharing an update with you as this story continues to evolve. With that, I'll now turn the call over to Marc Grasso for a discussion of our financial results. Thank you, Troy, good afternoon, everyone. I'll provide a brief overview of our financial results for the second quarter 2021, along with guidance for the full year 2021. I invite you to review our 10-Q file today for a more detailed discussion. Research and development expenses for the second quarter of 2021 were $21.1 million compared to $13.7 million for the second quarter of 2020. The increase in R&D expenses was primarily due to increases in clinical trial costs, development and manufacturing activities related to our KO-539 program, clinical trial costs related to our registration-directed tipifarnib trial, non-cash share-based compensation, personnel costs, and other expenses. General and administrative expenses for the second quarter of 2021 were $12.6 million, compared to $7.5 million for the second quarter of 2020. The increase in G&A expenses was primarily due to increases in personnel costs and non-cash share-based compensation. Net loss for the second quarter of 2021 was $33.7 million, or $0.51 per share, compared to a net loss of $20.5 million or $0.40 per share for the second quarter of 2020. As of June 30th, 2021, we had cash equivalents and short-term investments of $567.5 million, compared with $633.3 million as of December 31st, 2020. The cash balance as of June 30th reflects the spend of $6.6 million to repay in full our existing debt facility at a reduced prepayment fee, leveraging our strong cash position. Looking ahead, we anticipate our operating expenses for the full year 2021 to be in the range of $130 million-$140 million as we continue to invest in the clinical and pre-clinical development of our pipeline, important drivers for our future growth. We expect our net cash used in operating activities for the full year 2021 to be in the range of $105 million-$115 million. Based on our current plans, we continue to believe that our cash equivalents, and short-term investments will be sufficient to fund current operations into 2024. With that, I will now turn the call back over to Troy. Thank you, Marc. Before closing, I'd like to take this opportunity to welcome Carol Schafer and Dr. Helen Collins to our Board of Directors. Carol brings more than 25 years of experience as a trusted strategic and financial advisor to the leadership teams of growing biopharmaceutical companies, most recently as Vice Chair of Equity Capital Markets at Wells Fargo Securities. Helen joins with more than 25 years of medical experience, most recently as Chief Medical Officer at Five Prime Therapeutics, where she oversaw the development of bemarituzumab, a first-in-class anti-FGFR2b antibody for the treatments of patients with gastric cancer. Carol and Helen each bring a unique perspective to the board, and we look forward to their contributions as we work to bring our oncology drug candidates to market, expand their use to larger patient populations, and create value for patients and our shareholders. I also want to take this opportunity to express my sincere appreciation to Robert Hoffman for his many contributions throughout his six years on the Kura Board of Directors. We're deeply grateful for his service as a board member and as chair of our Audit Committee. On behalf of everyone at Kura, we wish Robert well in his future endeavors. Now, before we jump into the question and answer session, let me lay out our anticipated milestones for the remainder of the year. Initiate the KURRENT Phase I/II study of tipifarnib in combination with alpelisib in the fourth quarter of 2021. Complete enrollment of 24 evaluable patients in the KOMET-001 Phase I-B expansion cohorts by the first quarter of 2022. Determine the recommended Phase II dose of KO-539 by the first quarter of 2022. Submit an IND application for KO-2806 by the end of 2022. With that, operator, we're now ready for questions. As a reminder to ask a question, you will need to press star one on your telephone. To withdraw your question, press the pound or hash key. Please stand by when we compile the Q&A roster. Your first question comes from the line of Jonathan Chang from SVB Leerink. Your line is now open. Hi, guys. Thanks for taking my questions. First question, can you provide more color around how the dose levels were selected for the KO-539 expansion cohorts? Sure, Jonathan, thanks for the question. The guidance from FDA that is now sort of colloquially known as Project Optimus, instructs sponsors or guides sponsors to identify the lowest dose with maximum biologic and clinical activity. In its guidance, FDA is moving expressly away from maximum tolerated dose in the context of targeted therapies in oncology. The push is toward lower doses, not higher doses, MTD being kind of a relic, if you will, of the old chemotherapy days. With that being said, it was pretty clear that the low dose of 200 milligrams once daily was right because we saw robust activity. That activity was highlighted at ASH. In particular, a couple of responses among NPM1 mutant patients, one with a CR that was MRD negative, the other being an MLFS. When it comes to the higher dose, we really faced a choice. Was it 600 or 800? Given the limitations of the Phase I-A study, the fact that it wasn't genetically enriched for KMT2A and NPM1 mutant patients, we didn't really see a difference between those two doses, a difference enough to justify going with 800 versus 600. Those two doses looked sort of consistent. Per the FDA's guidance, if that's the case, you go with the lower dose. We're now at a point and we're actively enrolling in the Phase I-Bs, as I mentioned in the prepared remarks, at doses of 200 and 600. We expect that both of those doses have good safety and tolerability. They're very clean. We think either dose could potentially be a good going forward dose. The phase I-B study is now explicitly an efficacy study, and it will allow us to both select an RP2D and begin to compile patients who we believe are gonna be eligible to be included in the population for registration. Understood. Thank you. Second question, how should investors be thinking about the cadence and the substance of KO-539 updates for both the escalation and expansion portions over the remainder of 2021 and in 2022? Yeah, great question. The way we're thinking about the phase I experience is, the phase I-A, excuse me, is a safety study. The phase I-B is really an efficacy-driven study. The phase I-A is now closed to enrollment. We got out of it, I think, what we were expecting. The molecule is safe and well-tolerated across the range of doses. We're seeing anecdotal activity, but there are limitations. The limitations are, it's not genetically enriched. A number of patients are not efficacy evaluable. Despite that, we continue to see encouraging signs of activity, including in patients who had progressed on a prior menin inhibitor. We thought that was noteworthy. The phase I-B is explicitly in the KMT2A and NPM1. Our goal, Jonathan, as we said in the prepared remarks, is to have the phase I-B cohorts fully enrolled by the end of the first quarter of next year, and to be in a position where we have identified the recommended phase II dose. We'll do everything we can to meet or exceed that timeline. Given what we're seeing in the screening queue and the pace of enrollment, we think that's a good base case projection. Our intent is to provide qualitative updates on the study throughout the remainder of 2021. You've gotten some sense of that today from the commentary. Initially, you're focused on site activation. You're focused on the screening funnel. You're talking about, are we actually recruiting patients to the two arms? We are. I think we'll be able to give guidance both on enrollment and qualitatively, what are we seeing, right? I don't think we're going to be able to call out specific patients for the very reason that it's our hope and our intent that this data will be considered for registration by FDA. We have to treat it with some sanctity. I think we'll be able to provide guidance on enrollment and on activity. Are there differences between the arms? That's our intent, is to provide qualitative guidance, and we'll look to present the Phase I-A and the Phase I-B together as the full Phase I experience at an upcoming medical or scientific meeting. Understood. Thank you. If I can just sneak in one more, mostly because I don't think you'll be able to [audio distortion] this, but in the chance that you can, can you expand on what you mean by the early signs of clinical activity in the Phase I-B expansion cohorts for 539? Thank you. Sure. I mean there are a number of measures of that, including disease stabilization, improvement of performance status. But the most notable one, Jonathan, is reduction in blast counts. And I should just leave it at that. Again, we don't want to be cherry picking data. What we want to do is to leave you and the others on the call with an understanding that from our perspective, the fact that what we're seeing, it's early, it's preliminary. But what we're seeing in the Phase I-B reinforces that the dose selections of 200 and 600 were the right dose selections. Got it, thank you. Your next question comes from the line of Peter Lawson from Barclays. Thanks for taking the questions. Troy, just on kind of data disclosures that we may get this year, would we get anything around durability from any of the previously treated patients where we've seen them? Peter, I think we're going to have to wait until we disclose the full Phase I experience. We have been thus far impressed with the durability, but it's early days. This is a handful of patients. The data's preliminary. I think, we don't want to pick and choose. We need to look at durability in the context of the full clinical package, and it's our intent to enroll the Phase I-B as quickly as we can and be in a position to talk about both the safety and tolerability and the efficacy profile of 539 as quickly as we can at an upcoming future medical meeting. Got you. You'd mentioned a patient that progressed on a prior menin inhibitor, so you kind of are seeing signs that you can potentially re-treat with menin inhibitors. Yeah. A couple of comments, Peter. Yeah, it's actually plural, patients, not just one. I think what we're seeing is evidence of clinical activity. Just to be clear, right, let's draw a distinction between the mechanism of action and then what one might do in a registrational context. That gives us confidence that, just as you say, even in patients who have progressed upon treatment with a prior menin inhibitor, you're still seeing evidence of clinical benefit. That's fine for phase Ia. We're not expressly excluding those patients from the phase Ib. In all likelihood, they will be excluded from the registrational study. It goes both ways, right? You don't want to bias in favor of patients who might be more likely to respond. You also don't want to bias in favor of patients who you may have exhausted that mechanism of action. I think that data's anecdotally important, and it's one of the pieces that gives us confidence that we have a best-in-class menin inhibitor. I think, as we go forward, I wouldn't be expecting us to enrich in a lot of patients who've been on prior menin inhibitors, is the way I would say it. Great. Thank you so much. Sure. Thank you, Peter, for the question. Your next question comes from the line of Tiago Fauth from Credit Suisse. Your line is now open. Thanks for taking the question. I guess just to follow up on tipi, if you could provide any commentary on AIM and how enrollment trends are tracking there. Related to that, how much has genetic screening in that indication has evolved over time, and how that may play a role in the future combination studies. Since we're kind of in the same topic, if you could provide any detail on how 2806 could actually differ from tipi in a sense that will be able to address more indications, explore additional combination approaches. What are some of the features that you expect to improve upon? Thanks. Sure, Tiago. Thank you. Three good questions tucked in there. Let me take those in turn. AIM-HN, just to remind everyone on the call, we made a major amendment to the protocol last year, where we did two things. We removed some of the impediments to enrollment, and we expanded the patient population to include all HRAS mutant patients. That meant we have to enroll up to 100 evaluable patients to fully meet the registrational total. We also did this, I should say, in the context of the pandemic. We did see a very significant dip primarily in screening of patients during the pandemic. Now that at least the first wave of COVID is behind us, and we've had the chance for these protocol amendments to work their way through, we've seen an improvement, an uptick, Tiago, in enrollment. We're still not at a position where we can give guidance. One of the things that we've been experiencing is we have a conversion rate on the study of approximately 30%. That means, out of 10 HRAS mutant patients identified, we can get three of them on the study. That really relates to the fact that these patients are pretty fragile in the second and later lines of head and neck squamous. Similar to any trial, you want to put good, high-quality patients on, but that means we have to screen and thus identify many more patients. The team is doing a terrific job of that. The study's just kind of quietly marching along. To your second question, which relates to the first, one of the challenges in head and neck, in contrast to AML or, say, lung cancer, is that genetic screening is not standard of care. Typically, physicians do not conduct genetic screening until a patient has exhausted, now, typically, the checkpoint inhibitors plus or minus chemo. By the time that happens, the patient may or may not be in a position where they're actually able to receive benefit from another therapy. We're working to raise awareness. We're working with the KOLs and the physicians to increase the awareness of genetic screening. That's a big driver and part of what we're so excited about by combining alpelisib and tipifarnib. This is all sort of laid out in our corporate presentation. The combination of tipi plus alpelisib goes from 5% of the head and neck population to potentially up to 50%. That 50% comprises four genetic subtypes, HRAS mutant, HRAS overexpressed, PIK3CA amplified, and PIK3CA mutant. We're going to start the KURRENT study, which is the combination of alpelisib and tipifarnib in the PIK3CA dysregulated population. That's one where it's quite a bit larger. It's 20%, maybe even 25% of head and neck, so you have more patients from which to choose. If you have now one out of three or one out of two patients that may be an eligible patient for your combination, we think that will help to drive genetic screening, awareness of these small molecule-targeted options. As we think about the program strategically, the combination with alpelisib is an important next step, and it builds on the very significant clinical activity of tipi and the encouraging clinical activity of alpelisib. To your third question about 2806, so we became aware of the tipi/alpelisib combo is a true example of synergy. A lot of people throw that term around, but there are specific algorithms to measure synergy. You see clear synergistic activity with tipi and alpelisib in different genetic subtypes of head and neck squamous cell carcinoma. What's interesting, and again, this is in the corporate presentation, you see synergy of tipi plus other drugs as well, cisplatin, CDK4/6 inhibitors, just to mention a couple of examples. What we have found is that farnesyltransferase inhibitors offer the potential to go pretty impressively beyond where other small molecule-targeted therapies can go. We're being kind of circumspect about exactly what is the biology, exactly what are the indications, because this is obviously a very competitive field. We have a publication pending. We have intellectual property pending. It was part of that initiative, Tiago, to target 2806. Tipi is a very good drug. 2806 is even better. It is more potent. There is less inter-patient variability. We've largely eliminated the first pass effect. It's not meant to compete with tipifarnib in HNSCC. As you'll see through the rest of this year and into next year, it's meant to go into new disease indications that represent significant patient populations, and we've to this point, not disclosed them. That's something that I would think we will disclose. It'll depend on the timing of the publication, it'll be disclosed either later this year or early next year. In the meantime, we are doing steps to lay the groundwork for both preclinical and clinical studies, to now build on those rational combinations of FTIs plus other targeted therapies. Did I answer your three questions? You did. You answered them all. I appreciate the reply. Yeah. Thank you so much. Appreciate it. Your next question comes from the line of Reni Benjamin from JMP Securities. Your line is now open. Hey, good afternoon, guys. Thanks for taking the questions. Congrats on getting the dosing started for the phase I-B expansion. Maybe just two questions from me, Troy. One, piggybacking off a previous question regarding the patients who progressed on prior menin inhibitor. I guess I typically would think that maybe they couldn't stay on the drug due to toxicity issues as opposed to resistant mutations coming up. Am I thinking about that correctly since they're responding to another menin inhibitor, or are there key resistant mutations that maybe KO-539 may be inhibiting at the same time? I think, Reni, this is still an evolving story. We're not aware of mechanisms of resistance to menin inhibitors in the form of point mutations. These are not like tyrosine kinase inhibitors where you can develop a gatekeeper mutation or something. It's important to note the patients who come onto our study have active progressive disease at the time they come on the study. It's not that they were discontinued from another study due to tox, it's that they actually progressed and then came onto our study. This is still kind of an open question in our mind, right? Is will patients respond to one menin inhibitor when they perhaps progressed on another? I think what it potentially does is it reinforces this notion that given the wide therapeutic window, we can push the dose very hard on this compound. That's been demonstrated both by These are anecdotal reports. We don't want to make too much of them, but also the fact that we have seen activity outside of the MLL-r and the NPM1 mutant context. That ultimately may best be addressed through combinations. We've said very consistently, we believe we've got the best-in-class safety profile. We believe we've got the ability to push the dose. The biology is evolving, but I think we're encouraged, and we'll get a much better read on this in the phase I-B, which is actively enrolling and setting us up for registration. Got it. Just my final question on the phase I KURRENT study. Can you just give us a little bit of color on the trial design here? Do you have to start re-dosing tipi with a fixed dose of alpelisib, or are both changing in dosing? About how many patients per phase, if you will, for the phase I dose escalating as well as the phase II? Yeah. Good question. In fact, I'll draw your and everyone's attention. We've added a new slide to the corporate presentation that is a schematic of the current study. It doesn't speak, Reni, to your question of specific numbers of patients, but it does at least show you the initial schematic for the doses. What you'll see is that alpelisib is held constant, it's dosed continuously, and tipi is dosed every other week, both being dosed as they typically are. I'll just remind everyone that the preclinical studies that were conducted showed synergistic activity at doses that were below the dose of each drug as a monotherapy. We dialed them both down by, I believe, to approximately 70% of the monotherapy dose, and you're still seeing better activity of the combination. It might take some tinkering, Reni, in the study to get the dose and schedule right. You don't know until you try it. It's difficult to model these toxicities. Our team has done a significant amount of work preclinically to show that there are a number of different doses and schedules. You can give them both continuously, you can give them both intermittently, that will drive activity. That will give our clinical team and the investigators the flexibility to be able to go in there. The trial is a very elegant design. Mollie Leoni, our VP of Clinical Development, took the lead on developing it, and Stephen Dale also weighed in on it. It allows you to change the dose of both drugs, and it relies on the extensive safety databases of both drugs. We're hopeful it gives you a fairly efficient a chance to get to a recommended dosing schedule for the combination. Given, Reni, that we're in the genetically selected population, namely either PIK3CA mutant or PIK3CA amplified, we might get some early indications of activity, although the study is not explicitly designed to have an efficacy endpoint. Similar to KOMET, any efficacy at that point would just be anecdotal and tell you you're going directly in the right direction. That's summarized in our corporate presentation, and over the next few months, as we lead up to the kickoff of KURRENT, which again, we're expecting in Q4, we'll give more color on exactly the sizing of the study. It's going to be pretty typical with what one would expect. Terrific. Thanks for taking the questions. Happy to do it. Once again, if you would like to ask a question, you will need to press star one on your telephone. Your next question comes from the line of Phil Nadeau from Cowen and Co. Your line is now open. Good afternoon, congrats on the progress, and thanks for taking our questions. First, one question on KO-539's Phase I-B. The cohorts, do they have a minimum requirement for the number of MLL-r patients that are enrolled, or will it just be first of all patients, and whether it's NPM1 or MLL-r, it doesn't particularly matter? Yeah. Phil, thanks for the question. It's actually the latter of the options. There is no explicit requirement of either NPM1 or MLL-r. The trial has a mechanism to ensure that the two arms are balanced so that you don't end up with all the NPM1 mutant patients in one arm and the MLL-r in the other arm. It's going to largely be what we get. If the early indications continue, we're seeing a good mix of both populations. Quite a bit different than what we saw in the Phase I-A, of course, we're now operating at potentially many more sites, and everybody is expressly looking for these patients. I think that's the kind of color, Phil, we might be able to provide a bit more qualitative updates in the months ahead. Perfect. Second question is a follow-up to an earlier one. When you were choosing the doses to advance into the expansion cohorts, you talked about the safety and clinical efficacy. Were you also able to look at things like the leukemogenic gene expression, for example, MEIS1 gene expression, and was there any difference between the various doses that were tested in the phase I-A? We've looked at that as an exploratory endpoint, Phil. It's a good question. The answer is we're looking at it. It really didn't factor into the dose decision. The dosing was driven first and foremost by safety and tolerability, and then secondly, by clinical efficacy. We didn't use any kind of surrogate biomarker to factor into that decision. That is work that we're doing both to help inform the development in MLL-r and NPM1 mutant subtypes and also to understand how do you think outside of the MLL-r and NPM1 mutant populations, and where else could you go? Those are exploratory and not really gating at all, either on the selection of the two doses for the phase I-B or I think ultimately what will come out in terms of the determination of the RP2D once we have the 24 evaluable patients enrolled. Got it. Last question is actually on that determination of the recommended Phase II dose. With 12 patients in each cohort, each patient's approximately 8% of the cohort, what is a clinically meaningful difference in response between the cohorts? Can you give us some sense of how you're thinking of what would differentiate 600 milligrams versus 200 milligrams, given the relatively small size of the cohorts? It's a really good question, and it's one that I've asked both Mollie Leoni, who's now leading this program. She's now the clinical lead for the Menin program, as well as Stephen Dale. The short answer, Phil Nadeau, is you kind of know it when you see it. There isn't an explicit difference that one needs to see. If you don't see a meaningful difference, they look roughly the same, FDA's very strong guidance will be go with the lower dose. That being said, you will have the ability to either dose up or dose down as you need to. Only if you really see a striking difference, either one way or the other, will you select it. If the two cohorts run out and they look comparable in terms of CR, CRh, and safety and tolerability and the other parameters, I think the consensus is you're going to go with the lower dose. I will say, I'll reiterate this again. I say it whenever it gets asked. I think we have good confidence that either of these doses is a good going forward dose. This is really now a question of refinement and what is the optimum dose, not only for this study, but this dose will then set the starting point for all future studies, which is why it's important to take the 24 patients and really get it right because it becomes the cornerstone of the program, and the entire development plan rests on it. I think the team has it well in hand. Perfect. Thanks for taking our questions. Happy to do it. There are no further questions at this time. I will turn it back over to Dr. Wilson for any closing remarks. Thank you, operator. Thank you all once again for participating in the call today. We're going to be at the Wedbush PacGrow Healthcare Conference next week, and we'll look forward to speaking with many of you then. In the meantime, if you have any additional questions, please feel free to contact Pete, Marc, or myself. Thank you and have a good evening, everyone. This concludes today's conference call. Thank you for participating. You may now disconnect.