Good afternoon, ladies and gentlemen, and welcome to the Q1 2024 Kura Oncology Financial Results conference call. At this time, all lines are in listen-only mode. Following the presentation, we will conduct a question-and-answer session. If at any time during this call you require immediate assistance, please press star zero for the operator. This call is being recorded on Thursday, May 2, 2024. I would now like to turn the conference over to Pete De Spain, Head of Investor Relations. Please go ahead. Thanks, Chris. Good afternoon, and welcome to Kura Oncology's first quarter 2024 conference call. 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. 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. Let's jump right in. Last week, we were proud to announce that ziftomenib is the first investigational treatment to be granted breakthrough therapy designation for the treatment of NPM1-mutant AML. The FDA granted BTD for ziftomenib based on data from our ongoing KOMET-001 clinical trial in patients with relapsed/refractory NPM1-mutant AML. NPM1-mutant AML is a disease of significant unmet need for which there is no approved targeted therapy, and it represents approximately 30% of new AML cases annually. BTD is awarded for a drug that treats a serious or life-threatening condition and may demonstrate substantial improvement on one or more clinically significant endpoints over available therapies. The designation is intended to expedite development and review of drugs, including an organizational commitment by FDA senior managers and experienced review staff, as well as eligibility for rolling review and priority review. We're highly encouraged by FDA's decision to grant breakthrough therapy designation for ziftomenib, recognizing its potential as an innovative medicine for patients with NPM1-mutant AML. We look forward to working even more closely with FDA to bring ziftomenib to patients in urgent need of effective treatments as quickly as possible. Meanwhile, we're on track to complete enrollment of 85 patients in our ongoing KOMET-001 registration-directed trial of ziftomenib in relapsed/refractory NPM1-mutant AML by the middle of this year. Ziftomenib is also being evaluated in combination with current standards of care, including venetoclax, azacitidine, or cytarabine plus daunorubicin, commonly known as 7+3, in patients with NPM1 mutant or KMT2A rearranged AML. In January, we reported top preliminary clinical data from the first 20 patients in the dose escalation portion of the KOMET-007 trial, including five newly diagnosed patients with adverse risk AML and 15 patients with relapsed refractory AML. Ziftomenib demonstrated an encouraging safety and tolerability profile in combination with 7+3 and with venetoclax plus azacitidine, enabling continuous administration of ziftomenib while effectively mitigating the risk of differentiation syndrome. Notably, no differentiation syndrome events of any grade were reported among the first 20 patients. Furthermore, no dose-limiting toxicities, QTc prolongation, drug-drug interactions, or additive myelosuppression were observed. As of the January eleventh data cutoff, all 5 newly diagnosed patients with adverse risk NPM1 mutant or KMT2A rearranged AML, treated with ziftomenib and 7+3, achieved complete remission with full count recovery for a CR rate of 100%. The overall response rate among the 15 relapsed refractory patients treated with ziftomenib and venetoclax was 53%, including a 40% ORR among the 10 patients who had received prior venetoclax, a setting with very limited effective treatment options. The CR/CRh rate among the 9 relapsed refractory patients who were menin inhibitor naive was 56%. As of the data cutoff, 16 of the first 20 patients remained on trial, including all 11 NPM1 mutant patients. Continuous daily dosing of ziftomenib at 200 mg QD was well tolerated, and the safety profile was consistent with features of underlying disease and backbone therapies. I'm very pleased to say that our team continues to demonstrate outstanding execution. The 400-milligram dose of ziftomenib has now been cleared for both the NPM1-mutant and KMT2A-rearranged relapsed/refractory venetoclax cohorts, and enrollment for both of those subsets at the 600-milligram dose is ongoing. We've also cleared the 400-milligram dose of ziftomenib in the frontline adverse-risk NPM1-mutant 7+3 cohort and have escalated to the 600-milligram dose. Enrollment of the 400-milligram dose in the frontline KMT2A-rearranged 7+3 cohort is ongoing, and we anticipate clearing that dose cohort shortly. At this rate, we expect to identify the recommended phase 2 dose for ziftomenib in combination with venetoclax and in combination with 7+3 by the middle of this year. Concurrently, we plan to initiate a phase 1b expansion study with a number of combination cohorts, including venetoclax in newly diagnosed NPM1-mutant or KMT2A-rearranged AML. Venetoclax in relapsed/refractory NPM1-mutant or KMT2A-rearranged AML, venetoclax in relapsed/refractory NPM1-mutant AML, and 7+3 in newly diagnosed NPM1-mutant or KMT2A-rearranged AML, removing the qualifications for high-risk disease. Each phase 1b combination cohort is expected to enroll independently with approximately 20 patients per cohort. In the meantime, we continue dosing patients in our KOMET-008 study of ziftomenib in combination with additional standards of care, including the FLT3 inhibitor gilteritinib, FLAG-IDA, or low-dose Ara-C, for treatment of relapsed/refractory NPM1-mutant or KMT2A-rearranged AML. Roughly half of all patients with relapsed/refractory NPM1-mutant AML have co-occurring FLT3 mutations, and the prognosis for these patients is poor. Preclinical data for ziftomenib in combination with FLT3 inhibitors demonstrate strong synergistic effects compared to either single agent alone. We believe a best-in-class safety and efficacy profile, as well as optimal pharmaceutical properties, will enable ziftomenib to become a cornerstone of therapy for patients with acute leukemias. This belief is backed by increasing investigator enthusiasm, as evidenced by rapid enrollment across all of our ongoing ziftomenib studies and further bolstered by breakthrough therapy designation by FDA. Ultimately, our mission is to develop ziftomenib across the continuum of care for all patients with acute leukemias whose disease is driven by the menin pathway. We also have a growing body of preclinical data that supports attractive opportunities for menin inhibitors beyond acute leukemias. Based on internal preclinical data, we believe there may be a role for ziftomenib in the treatment of certain solid tumors, and we're working towards submission of an investigational new drug application for the first of these solid tumor indications in the second half of this year. We look forward to sharing some of the preclinical data that support this opportunity at a scientific or medical meeting later this year. Meanwhile, we continue to make progress toward a next-generation menin inhibitor, which we intend to direct toward an additional, soon-to-be-disclosed indication. And we remain in a strong financial position, enabling us to invest in research, development, and pre-commercial activities to maximize the value of ziftomenib and support our other pipeline assets. Now let's turn our attention to our farnesyltransferase inhibitor programs. We continue to build upon the impressive clinical benefit we've demonstrated with tipifarnib as a monotherapy in patients with recurrent and metastatic head and neck cancer. We have been evaluating the combination of tipifarnib with the targeted therapy alpelisib in PIK3CA-dependent head and neck squamous cell carcinoma in a phase 1 dose-escalation study that we call KURRENT-HN. We remain pleased by the manageable safety and tolerability profile of tipifarnib in combination with alpelisib, and we are encouraged by the clinical activity observed at multiple dose levels. We expect to complete enrollment of two dose expansion cohorts to help inform selection of the optimum biologically active dose for the combination by the end of 2024, and we look forward to presenting preliminary clinical data from the KURRENT-HN trial of tipifarnib and alpelisib at a medical meeting in the first half of 2025. We believe the manageable safety and tolerability we've observed with the combination of tipifarnib and alpelisib also significantly de-risks development of our next generation farnesyltransferase inhibitor, KO-2806, as we begin to evaluate it in combination with other targeted therapies. Despite the success of targeted therapies such as tyrosine kinase inhibitors and KRAS inhibitors, a considerable need remains to drive enhanced antitumor activity while addressing mechanisms of innate and adaptive resistance. We are developing our next generation farnesyltransferase inhibitor, KO-2806, to address this need. KO-2806 was designed to improve upon the potency, pharmacokinetic, and physicochemical properties of tipifarnib. Last year, we presented compelling preclinical data supporting the rationale for combining KO-2806 with distinct classes of targeted therapies, including tyrosine kinase inhibitors and KRAS inhibitors. In October, we began dosing patients with KO-2806 as a monotherapy in a phase 1 dose escalation trial that we call FIT-001. That trial uses an innovative design that enables us to begin dose escalation of KO-2806 in combination cohorts very early on in the study, while continuing to dose escalate concurrently as a monotherapy. In fact, we dosed the first patient with KO-2806 in combination with cabozantinib in clear cell renal cell carcinoma in February, just 4 months after KO-2806 entered the clinic. We are on track to dose the first patient in combination with adagrasib in KRAS G12C mutated non-small cell lung cancer by the middle of this year. As a reminder, the study of KO-2806 and adagrasib is supported by a clinical collaboration and supply agreement with Mirati, now part of Bristol Myers Squibb. While our focus with KO-2806 remains on renal cell carcinoma and KRAS-driven tumors, its rapid development progress provides us with further flexibility as we consider potential development paths forward in head and neck squamous cell carcinoma. If successful, we believe KO-2806 could become the ideal combination partner for multiple targeted therapies in large solid tumor indications. 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 of 2024. Research and development expenses for the first quarter of 2024 were $36.3 million, compared to $25.2 million for the first quarter of 2023. The increase in R&D expenses was primarily due to increases in clinical trial costs related to our ziftomenib and KO-2806 programs. General and administrative expenses for the first quarter of 2024 were $18.2 million, compared to $11.4 million for the first quarter of 2023. Net loss for the first quarter of 2024 was $49.5 million, compared to a net loss of $34.1 million for the first quarter of 2023. This included non-cash share-based comp expense of $8.5 million, compared to $6.8 million for the same period in 2023. As of March 31, 2024, we had cash, cash equivalents, and short-term investments of $527 million, compared to $424 million as of December 31, 2023. This includes net proceeds of approximately $145.8 million from our private placement in January 2024. We believe that our cash, cash equivalents, and short-term investments will be sufficient to fund our current operating plan into 2027. 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 lay out our anticipated upcoming milestones. For our menin inhibitor programs, complete enrollment of 85 patients in the KOMET-001 registration-directed trial of ziftomenib in NPM1-mutant AML by mid-2024. Identify the recommended phase II dose of ziftomenib in combination with venetoclax and azacitidine by mid-2024. Identify the recommended phase II dose of ziftomenib in combination with 7+3 by mid-2024, and initiate a phase Ib expansion study of ziftomenib in combination with standards of care, including venetoclax, azacitidine in newly diagnosed NPM1-mutant or KMT2A-rearranged AML in the second half of 2024, and submit an investigational new drug application for ziftomenib in a solid tumor indication and present preclinical data at a medical meeting in the second half of 2024. For our farnesyltransferase inhibitor programs, dose the first patients with KO-2806 and adagrasib in KRAS G12C-mutated non-small cell lung cancer by mid-2024. Complete enrollment of two expansion cohorts in KURRENT-HN and identify the optimal biologically active dose of tipifarnib and alpelisib by the end of 2024, and present data from the KURRENT-HN trial of tipifarnib in combination with alpelisib in PIK3CA-dependent head and neck squamous cell carcinoma in the first half of 2025. With that, operator, we're now ready for questions. Thank you. Ladies and gentlemen, we will now begin the question-and-answer session. Should you have a question, please press star followed by one on your touchtone phone. You will hear a three-tone prompt acknowledging your request, and your questions will be polled in the order they are received. Should you wish to decline from the polling process, please press star followed by two. If you are using a speakerphone, please lift the handset before pressing any keys. One moment, please, for your first question. Your first question comes from Jonathan Chang, Leerink Partners. Jonathan, please go ahead. Hi, guys. Congrats on the progress, and thanks for taking my questions. First question, how should we be thinking about the implications of Ziftomenib getting breakthrough therapy designation on the likelihood of success of KOMET-001 and the timelines for potential approval? Yeah, Jonathan, thanks for the question. So in terms of the implications for approval, there was a question out there, you know, in the ether, whether, you know, NPM1 mutant AML was actually, you know, of the same magnitude as KMT2A rearranged AML in terms of unmet need. And, you know, as we indicated in the prepared remarks, this is the agency saying, you know, not only is that a significant unmet need, but this is a therapy that represents the potential for substantial improvement over the standard of care. Now, you know, we haven't commented specifically on our specific engagements with the FDA other than to say, across our various studies, you know, we're engaged with the agency on a regular basis, you know, across different studies, and as we look forward to an eventual NDA submission. I think you have to believe that not only is this a validation of Ziftomenib in terms of this patient population, but it's, you know, it's certainly a de-risking event, as we think about the submission and ultimately an application for marketing approval. That's certainly the way that we view it. It is, after all, the first and only BTD in the NPM1 subset, which is by far and away the larger of the two subsets. In terms of timelines, again, we've said consistently, what matters is that you get it, you know, at or ideally just before you complete enrollment, because what it really does is several things. It recruits the A team from the agency, which is important at a time when the agency has a, you know, has a lot going on, right? A lot of sponsors vying for attention. You get, you know, you get their, their priority and, and, and their expert review. They, they work with you very collaboratively, and they basically open up, you know, other possibilities to accelerate timelines. And we've spelled out a couple of those, including rolling review, priority review. You basically, you know, you get on the shortlist of priority programs at the agency. So, you know, we intend—we've said consistently, we intend to take advantage of every tool and trick and technique we can to accelerate timelines. This is the latest one. I think it puts us in a solid position. We are exactly where we wanna be in terms of enrollment. You know, as we say in the heading to the sub-bullet, enrollment is nearing a close, and now we're looking forward to letting the data mature, and then all the work that goes into the submission, and then looking forward beyond that. So, hopefully, that answers your questions. Great, thank you. And just one more question for me. Can you provide any color on when we might see more ziftomenib clinical data over the course of the year? Yeah, sure. I'm sure this is a question on a lot of people's minds. So, you know, we have kinda multiple things to be looking at. The last update, again, as we alluded to in the prepared remarks, was the January disclosure, where we showed data from the first 20 patients enrolled in the KOMET-007 study. You know, clearly, we can give an update, you know, on those patients. We are just really moving quite quickly and quite aggressively through dose escalation. It'll—I think a lot of people are looking toward what is the recommended phase 2 dose for the different combinations and in the different populations? And then, what does that data look like? Does it, you know, does the trend... We saw, we think, pretty encouraging data from the first 20 patients in terms of safety, tolerability, combinability, and clinical activity. Does that trend continue, right? Are there, are, does everything look good? And then, as we alluded to, obviously, you turn the corner, you move into the expansion cohorts, which will take us into newly diagnosed frontline venetoclax, newly diagnosed 7+3 without the requirements for adverse risk. That'll be sort of another tranche of data. We haven't, Jonathan, to this point, been more specific. We're keeping our options open. You know, people are looking toward EHA. We're not even yet to the late-breaking abstract deadline. We've used corporate events quite successfully. There's always ASH at the end of the year. We may take advantage of one or several of those. You know, when we, when we have more specific guidance that we can give you, we'll say something. But that's the way we're looking at it. We know... We think we know what our audience, our analysts, and investors are looking for, and we're gonna try to come at the right times with the right data that will help give everyone confidence that we're going in the right direction. Got it. Thanks for taking the questions. Sure. Thank you. Your next question comes from Jason Zemansky, Bank of America. Jason, please go ahead. Good afternoon. Thank you so much for taking our questions, and congratulations on the progress thus far. I was hoping maybe you could shed some light into the patients who have remained on the trial. You mentioned 16 of 20 patients, including all 11 NPM1 patients, are still in the study. What happened with the four, or did... You know, was it disease progression or something else? What dose were they being treated with? Yeah. Jason, thanks for the question. So maybe just to take a step back, those numbers that I cited to you were as of the January 11 data cutoff. So I was basically, you know, restating the results from that data cut of the 20 patients. We had, as we said, we had all five patients in the newly diagnosed 7+3 cohort respond. We had a significant number in the relapsed refractory. You know, we are just to sort of set everybody's expectations, that all of that data for those 20 patients was taken at a 200 mg dose. And I think it was an open question in many people's minds as to what to expect at a 200 mg dose. I had more than one investor say to me, "Well, you know, it wasn't really active at 200. I hope you get to 600." You know, it's actually active at all the doses. We did determine that the 600 mg dose is the optimal dose as monotherapy. And the point of this experiment, this escalation, is to determine what is the optimum dose in combination. In terms of... I don't know that we gave a lot of detail at the time, Jason, of that data cut. We did have, you know, I'll just... Something that we did call out at the time, we had one patient who crossed over from the frontline 7+3 to the relapsed refractory venetoclax, had a CR, actually, in both arms. We had another patient who, Mollie, I think at that time, cited, who had unfortunately had a small bowel obstruction before the patient ever even got on ziftomenib. So, you know, in these heavily pretreated, particularly relapsed refractory, it's not evidencing a high rate of progressive disease. It's more often that they have, unfortunately, Jason, some clinical sequelae that just are associated with having advanced leukemia. Got it. Well, maybe just to kinda touch a little bit more on the KMT2A patients that dropped out of the trial. Was there homogeneity among the group, and does this read through to your expectations for ziftomenib within the, I guess, entirety of the KMT2A population? So I wouldn't. So again, staying on that, 200 milligram data set of 20 patients, I think it's too small to draw any kind of conclusion. We do, we do, you know, we did say and we do say, 200 milligrams of ziftomenib is an active dose. There's no question. Is that the optimal dose? I would say stay tuned, right? We'll find out. Our view is if you can push the dose as monotherapy to 600, you should. Something that we are, that we've talked about is the potential for whole body exposure. And we think that's important in terms of both getting patients into response, Jason, and keeping them there. And obviously, that improves as you're able to go to higher doses. You get higher whole body exposure. You know, we'll, at the appropriate time, be able to walk you through the 200-mg dose as well as the higher doses, and then we can, you know, we can draw some conclusions as to what we're seeing. What I can say to you, and you can just tell it from enrollment, is, you know, we don't have any toxicities. We don't have any real DDIs to speak of. That's part of, we think, why enrollment is going so quickly. Ziftomenib is, once you've mitigated differentiation syndrome, it's actually a very easy drug to work with, with these various combination regimens. So we're looking forward to updating that data. I wouldn't, other than the drug is, it has, you know, manageable safety and tolerability and good early evidence of clinical activity. I'm not sure I would overinterpret that 200 milligram data. Got it. Perfect. Thanks for the color. Sure. Thank you. Your next question comes from Roger Song, Jefferies. Roger, please go ahead. Great. Congrats for the progress, and thank you for taking the question, Troy. Maybe start with one clarification question and one follow-up question. For clarification, just to confirm, for the RP2D you about to declare, that is in all of those four cohort first line and relapsed refractory in both venetoclax and the 7+3, but your phase 1b trial or the phase 1b expansion trial, you plan to do only in first line venetoclax, is that correct? Roger, I'm not sure I understand the second part of your question. Let me answer what I think is the first part, and then you can ask me the second part again. For the RP2D, each cohort is enrolling independently of the others. Remember, for everybody's sake, the way the protocol is written, we don't have to go back to the agency to initiate the expansion cohorts. We need the safety monitoring committee to make a determination that our recommended Phase 2 dose has appropriate safety and tolerability to move forward into an expansion cohort. We don't have to go back, in other words, to the FDA and ask for permission. We will... So those cohorts are. They're roughly all enrolling at the same rate, but there's a little bit of variability, as you can tell. The KMT2A 7+3 cohort is lagging just a little bit behind the other 3. We will be validating that RP2D and gaining more experience in the expansion cohorts. You're really, you know, as I said, well, as you move from escalation to expansion, you're actually going into healthier – quote, unquote, "healthier patients." They still have AML, but patients who do not have adverse risk, for example, in the case of 7+3, or frontline patients in the case of venetoclax, you'd like to understand the profile of the drug in that set, so that you can then make the appropriate considerations and decisions on registrational trials going forward. So particularly in venetoclax, we're not yet in the frontline. We need to get there. So that will help us clarify safety, tolerability, combinability, and activity. Enrollment's going so fast, Roger, that, you know, that's not gonna be, you know, that should be well underway, you know, here after we reach the RP2D around midyear. The team is just crushing it in terms of enrollment. Did I answer your questions? Yeah, I think you answered the first part. The second part really is just to clarify, what is the phase 1b expansion cohort? Because you mentioned the- Ah. First line, first line Venetia- Yep. combo. Yep. How about the relapsed refractory and the 7+3? Thank you. Oh, I see. Okay, got it. Yeah. So, so the way to think about it is, we will continue to evaluate the, the genotypes separately. So you have effectively 7 arms. You have venetoclax, frontline venetoclax, NPM1, and KMT2A. You have relapsed refractory, again, NPM1 and KMT2A. Same thing with 7+3, frontline, now no longer adverse risk. And then one cohort you might have picked up on, which is ziftomenib plus venetoclax, only venetoclax in the relapsed refractory setting. And that's one where we get a lot of interest from investigators asking the question, "Do you really need azacitidine?" And you clearly need ven, but do you need azacitidine, given that menin inhibitors are epigenetic, you know, their mechanism is an epigenetic modifier? We'll test that in the clinic and see. So when you consider each of two genotypes, times those, you know, three, essentially three plus the venetoclax ziftomenib combo, that gives you seven arms. That's what we're describing, Roger, as the phase 1b. We will not necessarily move forward with all of those into registrational. We're gathering the safety data, the activity data. We're already working on what does the first registration enabling study look like, the second, et cetera. We'll provide more color on that, you know, likely later this year. ... Excellent. Okay, so that's, that's clear now. Actually, you already partially answered my last question, follow-up question, is the registration passed? Maybe can you give us a little bit, you know, in terms of timeline guidance, when you will start to think about the, the registration, for either of those cohorts? Yeah. So we're already thinking about it. We're already planning for it. Even though, you know, we're learning—we're continuing to learn about ziftomenib as we dose escalate. And to some extent, you know, what you're waiting for is, you need to be able to say to health authorities, "This is the dose in the combination, and this is the data that supports that dose selection." That's the point of this exercise. But you can leave that dose, Roger, in brackets and say, "This is what the design of the trial looks like, pending this dose." And, you know, our team is working quite intensely already to map out what do those registration trials look like? And obviously, you look at our emerging data, you look at the competitive landscape, you look at what are the regulators looking for in terms of endpoints, you do the commercial considerations. All of that gets folded in. What I can say to you is, so far, you know, our belief is that ziftomenib has the potential to be the best-in-class menin inhibitor, and there's nothing we're seeing thus far that takes us off of that view. In terms of safety, tolerability, combinability, absence of toxicities, QTc, drug-drug interactions, everything's looking good. So at this point, we have a wealth of options. We clearly won't do them all or won't do them all at the same time. We need to prioritize, and we're doing that important work now, Roger. We'll talk more about the design. We'll probably give you a view on the design after we've gotten some input from the health authorities, 'cause we wanna make sure that we bring them along, you know, as is appropriate, when you're considering registrational studies. Excellent. Thank you, Troy, for all the comments. That's it from us. Thank you. Thank you. Your next question comes from Li Watsek, Cantor Fitzgerald. Lee, please go ahead. Hey, good afternoon, and congrats on the progress. Just a couple questions from me. Troy, I wonder if you can provide any color on whether the FDA has seen additional data for the breakthrough designation, potentially from the ongoing pivotal study as well? Yeah, Lee. So, you may find this answer unsatisfying, and for that, I apologize. We can't really give you specifics on our engagement with the agency. You know, suffice it to say, they are very familiar with the benefit risk for ziftomenib. I mean, they've been great partners with us from the beginning. As I say, we are in active discussions with them, already beginning to put the pieces in place to make sure that the modules of the NDA are lining up with their expectations. I can't speak specifically to your question. You know, I think it. You know, they don't frequently award a BTD unless they're reasonably confident that the drug's actually going to deliver. Of the drugs that get breakthrough therapy designation, 90% of them go on to get approval. The ones that don't, it's typically, like, a manufacturing issue or something else, which obviously won't be the case of a small molecule. That gives you some guardrails, you know, but we were, you know, we're obviously thrilled by the BTD designation, and particularly to be the first menin inhibitor and maybe the only one to actually get it. Okay, thanks. And then for the 100 400 mg dose, it sounds like it's been cleared. So I wonder if you can share any maybe early indication whether you're seeing a dose response here relative to the 200. I understand the patient population is slightly different, but any color there will be helpful. So, we cleared it. For those of you who, you know, who listen regularly, the last time we had the, I had the microphone in a Reg FD compliance setting, I said that one of the three cohorts was open at 600. Here we are, I think it's two weeks later, 10 days later, now three of the four are open. My point, Lee, in telling you that is this data is like evolving in real time. What is encouraging is, you know, again, nothing really of, to be concerned about, in terms of safety, tolerability, drug-drug interactions. I wanna be careful not to get too far ahead of the data. The monotherapy data, Lee, clearly says 600 is better than 200. We didn't test 400, obviously, but 600 was clearly better than 200. You would expect, Lee, that same relationship to apply in the combination setting. And so the real question is, is the safety and tolerability manageable at 600? If that's the case, then you would expect, you know, improved activity to pull through in both populations. But I'll answer you that, the question that way, rather than sort of trying to give you an early peek at the 400 milligram cohort. Okay, thank you. Sure. A pleasure. Thank you. Your next question comes from Brad Canino, Stifel. Brad, please go ahead. Great, thank you. It's nice to be able to focus on just your call this evening. I just want to check in on the BTD. Can you help me understand when you submitted for that designation and why it ended up at that submission date? Yeah. So, not really, Brad. I mean, you, just to answer the question in a general sense, in our experience, the way that BTD works is you have a pre-submission, you know, if the agency wants you to put in a full application, they'll indicate it at that time. Otherwise, they might indicate, you know, that they'd like to see you answer questions or provide additional data. If they invite you to submit the full application, they typically get back to you in about 60 days. That's again, that's the general course. You know, one of the questions that I think was out there in the community was, what exactly is the unmet need in NPM1 mutant AML? You know, I think we were very successful in convincing the agency of the view of many of the docs, which is it's, you know, particularly once you're in the relapsed refractory setting, there's no difference in unmet need between KMT2A and NPM1. So, you know, we've had a very constructive dialogue with the agency all the way back to I hate to say it, but, you know, the agency was very helpful in terms of our navigating our partial clinical hold. They have been great partners ever since. I think they see the promise of menin inhibitors. I think, you know, they're quite excited. I don't wanna speak for them, but they have been a great partner to work with. Okay. Maybe if I can ask one more, Sure. As you're progressing through the combo dose escalation, have the enrollment rate across the different cohorts mutations come in line with your expectations headed into the trial? Thank you. Yeah. So the enrollment has actually been pretty even across the cohorts. It ebbs and flows, you know, as you go week to week. I'm not sure, Brad, we had really... You know, I'm not sure what our expectations necessarily were going in. Certainly, we are seeing very, very strong engagement. I'll just remind everybody that, you know, for each of these arms, if you will, it's six patients per dose. Now, some of these doses are actually over-enrolling because sometimes you have patients who have cleared screening and, but you're not yet ready to put them in the next highest dose. So there may be, rather than six, we may have seven or eight or even more at a given dose. But at a minimum, when all is said and done in the escalation, we'll have at least 72 patients, and I'm telling you now, it will be more than 72. Think about how fast that enrollment's gone. We started in July, and look at it relative to, you know, other comparables out there. There's just been incredibly strong engagement. The lag in the KMT2A frontline 7+3, Brad, is probably just reflective of the difference in the incidence. Again, NPM1's 30%, KMT2A is probably five, it's 10% if you include all of leukemia. It's probably, you know, 3%-5% in AML. That's probably what you're seeing. But it's, you know, again, it's, it's lagging behind, only, you know, only very, very briefly. We should, as we said, we should be clearing the 400 milligram cohort in the 7+3 KMT2A here imminently, and we expect that that one will go to 600 as well. Thank you. Sure. Thank you. Your next question comes from Peter Lawson, Barclays. Peter, please go ahead. Hey, thanks for taking the question. Just around the 200 milligram dose in combination, are there any trends emerging from the duration on therapy between the KMT2A versus the NPM1 patients, Troy? It's early, Peter. It's early. I mean, maybe just to take a step back, it's too early. If you look at these patients in general, though, Peter, the KMT2A are often younger, more typically, more frequently go to transplant. The NPM1s, you know, the median age is, like, 60, so they, and they, you know, oftentimes they're older, a little bit more frail. They perhaps don't go to transplant as readily as the KMT2A. I think it's too early to say. What we saw from the 200 milligram data, Peter, was, you know, even at that dose, which again, in our view, was a non-optimized dose, you saw meaningful clinical activity, I think, better than many people expected. You know, it certainly gave us confidence to continue escalating. A big part of the KMT2A, Peter, of driving clinical benefit there, is going to be this concept of whole body exposure. We think that's critically important. We think it gives the patients the best chance of really differentiating all of the extramedullary disease, and that's the advantage that ziftomenib has as we look out across, you know, the competitive landscape. It's highly tissue penetrant, it's extremely well-tolerated, it has, you know, doesn't have any other toxicities, and in combination, the DS is very well managed, very well mitigated. So I think we're optimistic, Peter, that as we go higher in dose, that may provide a benefit to both sets of patients, and whether those patients go on to transplant or not. Obviously, you know, we'll be able to say a lot more when we show you, show you the next data installment here. ... Gotcha. And then are you seeing anything in the side effect profile as you, when you combine, is there anything- No That would be impact in durational therapy or any quirks from particular regimens? If anything, Peter, I think it's actually helping with the backbones. Ziftomenib is so active in these populations that, you know, the people think about, you know, if you think about how do you use this, in the case of 7+3, they're on for about a week, right? On chemo, and then they're on ziftomenib after that. You don't have to hit them with a sledgehammer when you're giving them, you know, a potent differentiating agent, but... And that's both populations. With venetoclax, the protocol follows venetoclax as it's labeled, but, you know, there's an openness among investigators to move patients off of these myelosuppressive regimens as quickly as possible. You may actually see better results. We'll see, you know, when you combine with ziftomenib. It's early days, but Peter, we're not seeing anything in terms of safety, tolerability, side effect profiles, combinability. We're not seeing anything that's giving us any concern. In fact, if anything, it's telling us, you know, what, I... We use these best-in-class language, you know, we mean it when we say it. It- ziftomenib, now that we've put the DS question largely to bed, I think ziftomenib is really going to be able to show you what it can do. Great. Thank you so much. Thanks for taking the question. Pleasure. Thank you. Your next question comes from Phil Nadeau, TD Cowen. Phil, please go ahead. Thank you. This is Ernie Rodriguez for Phil. Thanks for taking our question. I have, we have one with the competitors' menin inhibitor launching, and even though it's in another indication, the KMT2A, is there anything, you know, they're likely launching soon in this year, later this year, is there anything on that launch that you would be looking to, or any metrics or any other aspects that you would expect will be useful or informative to your strategy? Yeah. You know, this may surprise you, but, let me take off my Kura CEO hat for a second and just say, if they're able to get approval and get to market, we're going to applaud, we're gonna congratulate them. Because at the end of the day, we all do this for patients, and, you know, and KMT2A, which is, which is the indication you're talking about, is a disease of high unmet need. I think that, you know, and, and I, I'll let them speak to their process and where they are. It is, it, you know, KMT2A is a much smaller opportunity, but it's a good indicator of the utility of menin inhibition. We'd certainly be happy that they're out educating, physicians and educating the community when we're coming along with what we believe is a better menin inhibitor. And whether you look at their combo data or our combo data, you have to believe that combo is the way to go here. So while we believe that ultimately when we get to market in NPM1 mutant AML, we will be best in class, we also think it sets the stage for us to be best in class in combination and in maintenance, and that's how you drive a multi-billion dollar peak sales potential. So we'll be paying, playing, excuse me, we will be paying careful attention, you know, watching, cheering, learning, not necessarily tracking their key performance indicators because the drugs are very different, but it will be instructive of the utility of menin inhibitors. What is clear to us is that there is... You know, 30% of AML patients are NPM1. We're seeing that in terms of enrollment. It's going like gangbusters. And the fact that we're seeing such strong KMT2A enrollment in the combo, I think really speaks to the potential of those regimens to drive activity. Hopefully, that answers your question. It does, thanks. And another quick one on the preclinical data in solid tumors- Yeah ... that you expect to disclose on H2. What should we expect on that? Should we be, are we gonna be able to determine, like, what, where, which kind of solid tumors would be most amenable or you will be pursuing in on the clinical side? Or is it more like a broad proof of concept in a broader range of solid tumors? Yeah, so what we're talking about really is epigenetic regulator, epigenetic regulation of oncogenes, or potential oncogenes, right? That's what you should be looking for. Are there going to be multiple opportunities? We think so. But each of them is sort of their own. You know, we're all still learning about epigenetic regulation. What's clear to us is that menin, the menin MLL interaction appears to play a critical role, both within and outside of AML. When you see this non-clinical data, and we've been, you know, working on this internally for quite some time, looking not only with our ziftomenib, but with other menin inhibitors as well, you'll know very. It'll be very obvious to you, the first place that we're going. Beyond that, I think we have to continue to be data-driven. We've been very good about putting non-clinical data out there and letting that guide the development. We're gonna continue to do that. So we've really taken our time, gone to school, done the work, and quite excited to share that data with you here in the second half of the year. It'll, you know... If it works the way it works non-clinically, it's potentially transformational for that disease type and can only then, you know, drive the TAM that much larger. All right. Thank you. That's helpful, and thanks again for taking our questions. Sure. Thank you. Your next question comes from Reni Benjamin, Citizens JMP. Ren, please go ahead. Hey, good afternoon, guys. Thanks for taking the questions. You know, maybe I missed it, Troy, in your prepared remarks, but what's happening with the post-transplant program? Has that been initiated? Maybe I missed it, you know, as one of the upcoming milestones. Yeah. Just wanted to know- Yeah How you're thinking about that. Yeah, thanks for asking, Ren. You did not miss it. What I can tell you is, in contrast to 001, KOMET-001 and KOMET-007 and 008, that trial is an investigator-sponsored trial. We've done everything as sponsor, or not as sponsor, but as the drug sponsor, if you will, as the company. We've done everything we can. We've put it into the investigator's hands. They're working through the last few bits of red tape. They have everything they need. As with any investigator-sponsored study, it's their study. They control the conduct, they control the timing, they control the dissemination of data. What I can tell you, Ren, is that the FDA's reviewed it, cleared it. It's really now just in study startup, but it is in the hands of the investigators. So we're not, you know, we're probably not gonna be in a position to guide you on enrollment there, and we're gonna have to rely on them to speak about the trial. But it's going in the right direction, and let me go one step further. It's just to remind everybody, we are assessing the safety and tolerability of ziftomenib in the post-transplant maintenance context, so that we can have the appropriate discussions with health authorities about what a registration-enabling study would look like. Because we can't do everything at the same time, we've actually accepted a proposal to do it as an IST. And at this point, Ren, they're just, I think, dotting the I's and crossing the T's. I will- Great. Thank you for that. One other thing. Yeah, one other thing, Ren. I'll say is, of course, and this, we do get this question, which is why I wanted to add to it. We do have patients in post-transplant maintenance, both in the monotherapy and in the combination setting. So, you know, the way we're doing this is, our studies now permit physicians to put their patients back on ziftomenib post-transplant if they're in the various studies. The IST that I referenced is a dedicated study that you know would be a lead-in to a dedicated post-transplant maintenance study, which would be independent and essentially agnostic to where those patients come from. Those two strategies would then marry up to make sure that you can take patients from the front line all the way through to the maintenance setting without interruption. That's the bigger picture strategy. Got it. Thank you for that, the added clarity. Just switching gears real quick to 2806. Yep. You know, when I look at KURRENT-HN and you know, the potential to complete enrollment in the two expansion cohorts and still identify the optimal biologically active dose in you know, by the end of 2024, is. Can I take that kind of a timeline and apply it to KO-2806? Or is KO-2806 such a unique molecule, you know, and very different from tipifarnib, that maybe that entire enrollment of the combination study is gonna be a lot quicker, and we might see data a lot, a lot faster than we're seeing at KURRENT-HN? Sure. Yeah, so I would be hesitant to draw conclusions across trials about enrollment. The KURRENT- HN trial, the one you're referring to, is, you know, it, it's a handful of sites. It's a signal-seeking study, really intended to, you know, answer the question: Is one plus one equal to three? i.e., tipifarnib one, alpelisib one, do you get better activity than either drug as monotherapy? I'll remind everybody, you don't expect to see really responses from either tipifarnib or alpelisib in PIK3CA mutant head and neck. The work that's been done with alpelisib largely resulted in stable disease, and you wouldn't expect tipifarnib to have activity in that genotype in head and neck. So the fact that we're seeing activity at multiple doses and that we have, you know, manageable safety, tolerability, and activity to justify some dose optimization, I think is a good... It says we may be able to extend beyond the work that we did with Tipi as a monotherapy and open up that patient population, but it's also, I think, highly de-risking of what you should expect with 2806. Because if you can combine with alpelisib, it gives you confidence that you can combine with, whether it's adagrasib, cabozantinib, or something else, it's giving us confidence that, you know, you want 2806 to be a new and improved tipifarnib. The final thing, Ren, is we don't wanna go too fast. I know that sounds counterintuitive. It's actually a very good question. If there's an opportunity in head and neck, do you go with tipifarnib or do you go with KO-2806? I would say our primary focus with KO-2806 right now is renal cell carcinoma and KRAS-driven tumors. There are, you know, I don't even know how many KRAS inhibitors, either in the clinic or streaming into the clinic. They will all have the same issue. They will all have innate and adaptive resistance. We're trying to come up with an approach that basically cuts that off at the knees. If we can demonstrate it without adagrasib, then we're gonna have the high-class problem of which of these solid, solid tumor indications do we pursue? We've been, Ren, very data-driven with KURRENT and just letting the patient experience sort of guide us on where to go. We're encouraged, the physicians are encouraged. The response rate in that setting is, like, 20% in second line. It's 5% or less in third line. You know, it is as bad as pancreatic cancer. So the fact that we're seeing, you know, I think, encouraging clinical activity is a good thing. It's just too early, Ren, to say, what's the development strategy? Is it KO-2806? Is it tipifarnib? I think it does go a ways toward de-risking the overall program. And again, if we can pull this off, you're talking about some big solid tumors. The KO-2806 trial is a dose escalation study. And, you know, those always have their own challenges, but again, I wouldn't draw conclusions of one disease type to the other. Our clin ops team has been exceptional across the board, from ziftomenib to KO-2806, to KURRENT. You know, they're making good progress with the ziftomenib one trial. We'll likely share data next year on that study. I think it's probably a little too early to show anything on ziftomenib here in 2024. Excellent. Thanks for taking the question, Chris. Sure. Thank you. Your next question comes from Justin Zelin, BTIG. Justin, please go ahead. Thanks for taking the questions. Troy, just with KO-001 enrollment completion coming up here, any thoughts on when we could see data from that study? Could that be a 2024 event or in 2025? Yeah, Justin, let us let I know this is gonna be a bit unsatisfying. Let us complete enrollment. You know, we've said we're very close. Let us complete that, and then we can give you guidance on kind of what to expect. I wanna make sure we do this in the right time and the right place. We obviously wanna give the, you know, the trial per protocol needs six months plus the time to clean the data. I think we'll be able to answer that question better, coming on the back of full enrollment. Great, that makes sense to me. And just on KO-2806, could we expect additional studies with other combination agents in the future, or are you pretty comfortable with what you have right now? Thanks. Yeah. There's certainly a rationale, Justin, to combine with other, with other drug candidates. I think what we want to do is, and I'm gonna, just for 30 seconds, just go a level deeper. The big takeaway from the KURRENT study is that you're driving activity in that setting, both by blocking wild-type HRAS and we think by blocking farnesylation of RHEB. RHEB stands for RAS homolog expressed in brain. Why do I call that out? I call that out because that, if you look at the posters that we've presented, RHEB, de-farnesylation or, you know, removal of the farnesyl group from RHEB, is critical to blunting the innate and adaptive resistance that arises to KRAS inhibitors. As I said, if you inhibit KRAS, the tumor is gonna do a number of different things to try to escape. One of them is to upregulate PI3 kinase signaling through that pathway. Blocking RHEB farnesylation is critical to blunting that effect. So if we can block RHEB in KURRENT with one combination, it gives us confidence that we're gonna be able to block it in a different context with a KRAS inhibitor. If that's true and we see activity, I will tell you, initially, Mirati, now Bristol, have been great clinical collaborators on this study. They've been very supportive. They've given us great input. You could imagine, Justin, using an FTI in combination with almost any KRAS inhibitor. That's how fundamental that biology is. It's on par with SH2, with SOS1. That's how you think about it. It's taken us a number of years to get there, but that's the highest, probably the highest, best use, most valuable application of an FTI. Great. Thanks for taking my questions. Thank you. Your next question comes from George Farmer, Scotiabank. George, please go ahead. Hi, thanks for taking my question. I have two. Troy, could you address what you think the hurdles are for ziftomenib approval in NPM1 in relapsed refractory setting? It's first question. The second question is, how you think about resource allocation when developing ziftomenib in earlier lines of therapy, combining with 7+3 or venetoclax. Yeah. Can you ask the first part of the question again? I just wanna make sure I've got... The second part is resource allocation. The first part was the hurdle rate, or is that right? But, yeah. Yeah, what do you think the hurdles are for FDA approval of? Yeah. Zifto refractory? Sure. Yeah, so I think we think that the hurdle rate for the NPM1 cohort, the same is true for KMT2A, by the way. You know, we've consistently said for approval, our view is you need 20%-30% CR/CRh, 4-6 months median duration of response. Would you like to do better? Yes, but we know, and I think our competitors, have consistently said, in our view, that's the bar for approval in the relapsed refractory population. It's going to be different in combination. And, you know, one of the things that we expect in combination is that we expect the duration for both populations, particularly the KMT2A, to improve as we go to higher doses. But, you know, when we talk about the combinations, we're gonna set the bar a little bit differently. But the, you know, the fact that we had a 35% CR/CRh rate in the Phase 1b, again, don't get emotionally attached to 35%. That's great. You need to be 20%-30%. But that Phase 1b data, coupled with the BTD, you know, award, I think gives you confidence that we're in the right zip code for, you know, for being able to secure an approval for monotherapy. In terms of your question around resource allocation, you know, we can do. We, Kura, on a go-it-alone basis, can probably, you know, pretty readily do one global pivotal trial. Now, if we wanna really blow out zifto and maximize the value, you're talking about potentially multiple pivotal trials, including frontline, including maintenance, potentially solid tumors. We've said all along, there very likely will come a time when we need the resources, both financial and operational, of a party larger than we are. You know, running global pivotal trials is facilitated if you have people on the ground in all those different countries. But at the moment, we think we can drive really meaningful value for shareholders by just continuing to execute as we have. One of the things you wanna understand is, what's the safety, tolerability, activity, and some view into durability, both for NPM1 and KMT2A, as you go to frontline? Because the longer that is, both, you know, whether patients go to transplant or not, that's gonna help inform the commercial models, and really, we think, drive the value. So you'll see us, we're already actively evaluating what are different... You know, how can we be clever? How can we take advantage of everything the health authorities have to offer, be efficient about, you know, the first combination pivotal trial? I think we're providing a really good foundation that will inspire physicians to have confidence that ziftomenib can be used readily with these different combinations, right? And that's the starting point, is you give them comfort that they can use it safely, it can be given orally once a day, there's no other complications, and then you just let the efficacy and the clinical activity speak for itself. Mm-hmm. Okay, thank you. Thank you. There are no further questions at this time. I will now turn it back to Troy Wilson for closing remarks. Great. Thank you. Thank you all once again for joining the call today. We'll be participating in the Bank of America Healthcare Conference in a couple of weeks, 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, and have a good evening, everyone. Thank you. Ladies and gentlemen, this concludes your conference call for today. We thank you for participating and ask that you please disconnect your lines.