Greetings, and welcome to Kura Oncology's fourth quarter 2022 earnings conference call. At this time, all participants are on a listen-only mode. A question-and-answer session will follow the formal presentation. If anyone should require operator assistance during the conference, please press star zero on your telephone keypad. As a reminder, this conference is being recorded. I would now like to turn the conference over to your host, Mr. Pete DeSpain. Thank you. You may begin. Thank you, Rob. Good afternoon, welcome to Kura Oncology's fourth quarter and full year 2022 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. Dr. Stephen Dale, our Chief Medical Officer, is also with us and available to answer questions. Before I turn the call over to Dr. Wilson, I'd like to remind you that today's call will include forward-looking statements based on current expectations. Such statements represent management's judgment as of today and may involve risks and uncertainties that could cause actual results to differ materially from expected results. Please refer to Kura's filings with the SEC, which are available from the SEC or on the Kura Oncology website for information concerning risk factors that could affect the company. With that, I'll now turn the call over to Troy. Thank you, Pete, and thank you all for joining us. Let's jump right in. In December, we were proud to report updated data from our phase I trial of ziftomenib at the American Society of Hematology annual meeting. Ziftomenib is our once daily oral drug candidate targeting the menin-KMT2A protein-protein interaction for treatment of genetically defined AML patients with high unmet need. The data at ASH highlighted the encouraging safety profile and clinical activity of ziftomenib in patients with relapsed refractory AML. Notably, the data included a 30% complete response rate with full count recovery among 20 patients with NPM1-mutant AML treated at the 600 milligram dose. To our knowledge, this represents one of the highest response rates reported to date for targeted therapies in a relapsed refractory setting. A median duration of response had not been reached as of the ASH data cutoff on October 24th. In addition to the strong observed clinical activity, ziftomenib demonstrated a favorable safety profile and encouraging tolerability, which resulted in designation of 600 mg once daily dosing as the recommended phase II dose and schedule following a positive Type C meeting with FDA. Building on the momentum of our phase I data and FDA interactions, we recently announced the first patients dosed in our phase II registration-directed trial of ziftomenib in NPM1-mutant relapsed or refractory AML. We expect to enroll a total of 85 patients in the United States and Europe. The primary endpoint is CR or CRH, and key secondary endpoints include duration of response, transfusion independence, safety, and tolerability. Dosing the first patients in our registration-directed trial of ziftomenib marks a significant milestone for our menin program and is a testament to the hard work and dedication of our team. The speed with which we've begun enrolling patients in the trial also speaks to the significant interest in ziftomenib among investigators. NPM1-mutant AML accounts for approximately 30% of new AML cases annually and represents a disease of significant unmet need for which no approved targeted therapy yet exists. Although untreated NPM1-mutant AML may pretend a more favorable prognosis upon initial diagnosis, the risk of relapse remains high and survival outcomes are poor after initial chemotherapy, particularly when other poor risk mutations such as IDH1 or 2 or FLT3 are also present. Notably, in our phase I trial for ziftomenib, two-thirds of NPM1 mutant AML patients who achieved a CR at 600 mg had either IDH and/or FLT3 co-mutations, all of whom had failed prior treatment with IDH and/or FLT3 inhibitors. An additional NPM1 mutant patient who entered the trial with multiple co-mutations, including DNMT3A following two prior stem cell transplants, also achieved a CR with no evidence of minimal residual disease and remains on ziftomenib for more than 31 cycles as of the October 24th data cutoff. In addition to impressive activity as a monotherapy in patients with NPM1 mutations, we believe ziftomenib is well-positioned for future combination strategies. Our conviction is supported by several key competitive advantages, including no evidence of drug-induced QTc prolongation, no predicted adverse drug-drug interactions, and oral daily dosing that should enable convenient administration with standards of care. Our team is working diligently to initiate the KOMET-007 and KOMET-008 trials to evaluate ziftomenib in combination with current standards of care in earlier lines and across multiple patient populations, including NPM1-mutant and KMT2A-rearranged AML. We've designed these phase I studies to assess the safety, tolerability, and therapeutic activity of ziftomenib in combination with key regimens such as venetoclax and azacitidine, gilteritinib, and 7+3. Our approach is to establish a foundation where ziftomenib can be combined safely with various commonly used regimens and then prioritize those combinations that represent the largest populations and greatest potential commercial value, primarily venetoclax and FLT3-containing regimens. In particular, we believe ziftomenib has potential to combine more safely and effectively with FLT3 inhibitors relative to other menin inhibitors in development. Notably, up to half of NPM1-mutant AML patients also exhibit co-mutations in the FLT3 gene. We also believe that rational combination approaches will help to mitigate differentiation syndrome in the KMT2A rearranged population, as has previously been demonstrated in the development of IDH inhibitors in combination with azacitidine. We're very excited about the potential for our combination studies to further unlock the value of ziftomenib for patients with acute leukemias. We anticipate initiating the first of these studies, KOMET-007, in the first half of 2023. We continue to have strong conviction in ziftomenib and its potential to be the best-in-class Menin inhibitor, and we continue to prioritize investment in the program, including significant investments in NDA preparedness as well as combination studies. We look forward to sharing further updates on the program as the year progresses, including presentation of a more mature dataset from our phase I trial of ziftomenib in NPM1 mutant AML at a medical meeting in mid-2023. Let's turn our attention to our farnesyltransferase inhibitor programs. Over the past several years, we've pioneered the development of FTIs as combination agents to delay or prevent emergence of resistance to certain classes of targeted therapies in large solid tumor indications. Our preclinical data is supportive of FTIs in combination with a growing number of targeted therapies, including EGFR inhibitors and PI3 kinase alpha inhibitors, as well as tyrosine kinase inhibitors in renal cell carcinoma and KRASG12C inhibitors in lung cancer. Our next-generation farnesyltransferase inhibitor, KO-2806, was developed with these applications in mind. KO-2806 was designed to improve upon potency, pharmacokinetic, and physicochemical properties of earlier FTI drug candidates. Last month, we were pleased to announce FDA clearance of the investigational new drug application for KO-2806 for treatment of advanced solid tumors. We intend to evaluate safety, tolerability, and preliminary antitumor activity of KO-2806 in a phase I dose escalation trial, which we're calling FIT-001, as a monotherapy and in combination with other targeted therapies in adult patients with advanced solid tumors. Clearance of the IND for KO-2806 marks an important next step for this program, and we look forward to starting FIT-001 in the third quarter. Meanwhile, we continue to evaluate tipifarnib in combination with the PI3 kinase alpha inhibitor alpelisib to address larger genetic subsets of HNSCC patients. In October, we reported the first demonstration that the combination of tipifarnib and alpelisib can induce a durable clinical response in a PIK3CA-dependent HNSCC patient at the EORTC-NCI-AACR Molecular Targets and Cancer Therapeutics Symposium. Notably, a patient with stage three squamous cell carcinoma of the tonsil with a PIK3CA mutation has achieved a durable partial response in our KURRENT-HN trial and has continued on study for more than 27 weeks as of the September 14th data cutoff. Treatment-related adverse events in KURRENT-HN are consistent with the known safety profiles of each drug and are manageable, with no dose-limiting toxicities reported to date. Our team is now focusing its efforts on identifying a recommended phase II dose and schedule for the combination, with a goal of determining the optimal biologically active dose in mid-2023. In an ongoing effort to prioritize those programs with highest potential to create value for patients, healthcare providers, and shareholders, we've decided to close our current lung trial and discontinue further development of tipifarnib in combination with osimertinib. We believe taking this disciplined approach enables us to enhance our focus on those development programs with the highest potential value, namely ziftomenib and KO-2806, while maintaining a strong cash position. In support of our ongoing corporate development strategy, we were pleased to announce a $25 million equity investment from Bristol Myers Squibb in the fourth quarter. The equity investment from BMS strengthens the relationship between our organizations and provides us with key insights and expertise. We're pleased to have the confidence of the BMS team and excited to work with them to deliver innovative science with the potential to benefit patients. With that, I'll now turn the call over to Tom for a discussion of our financial results. Thank you, Troy, good afternoon, everyone. I'm happy to provide a brief overview of our financial results for the fourth quarter and full year 2022. I invite you to review our 10-K file today for a more detailed discussion. Research and development expenses for the fourth quarter of 2022 were $22.7 million compared to $21 million for the fourth quarter of 2021. R&D expenses for the full year of 2022 were $92.8 million compared to $84.7 million for the prior year. The increase in R&D expenses was primarily due to increases in clinical trial costs related to our ziftomenib program, offset by decreases in clinical trial costs related to our tipifarnib program. General and administrative expenses for the fourth quarter of 2022 were $12.5 million compared to $12.1 million for the fourth quarter of 2021. G&A expenses for the full year of 2022 were $47.1 million compared to $46.5 million for the prior year. Net loss for the fourth quarter of 2021 was $33.1 million compared to a net loss of $32.7 million for the fourth quarter of 2021. Net loss for the full year 2022 was $135.8 million compared to a net loss of $130.5 million for the prior year. Net loss for the fourth quarter and full year of 2022 included non-cash share-based compensation expense of $6.8 million and $26.3 million, respectively. This compares to $6.4 million and $23.6 million for the same periods in 2021. Our cash equivalents, and short-term investments were $438 million as of December 31, 2022, including the $25 million equity investment from Bristol Myers Squibb and a one-time $10 million draw from the Hercules loan facility. This compares to $518 million as of December 31, 2021. We believe that our cash equivalents, and short-term investments will be sufficient to fund our current operating plan into the fourth quarter of 2025, assuming no further draws on the debt facility. 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 milestones for this year. For ziftomenib, dose the first patients in the KOMET-007 combination trial in the first half of 2023. Present updated data from the phase I trial in NPM1-mutant AML at a medical meeting in mid-2023. Dose the first patients in the KOMET-008 combination trial in the second half of 2023. For tipifarnib, determine the optimal biologically active dose in the KURRENT-HN trial in combination with alpelisib in mid-2023. For KO-2806, dose the first patients in the FIT-001 dose-escalation trial in the third quarter of 2023. With that, Rob, we're now ready for questions. Thank you. At this time, we will be conducting a question-and-answer session. If you'd like to ask a question, please press star one on your telephone keypad. We ask that you please limit to one question and one follow-up. A confirmation tone will indicate your line is in the question queue. You may press star two if you'd like to remove your question from the queue. For participants using speaker equipment, it may be necessary to pick up your handset before pressing the star keys. One moment, please, while we poll for questions. Our first question comes from Jonathan Chang with SVB Securities. Please proceed with your question. Hi, guys. Thanks for taking my questions. First question on the mid-2023 phase I KOMET-001 update, can you help set expectations around what information you plan to share? Clarify whether this updates for NPM1 mutant patients only. The second question on the phase II portion of the KOMET-001 study in NPM1 mutant patients, how has the early experience shaped your thinking around timelines for the study? Thank you. Thanks, Jonathan, for the questions. Starting with the update that we anticipate in mid-2023, we do intend to focus that update on the patients with NPM1-mutant AML who were enrolled in the phase I study. The intent there is to provide an update on all the patients in the study. Obviously, one of the key questions at ASH was the durability of response, and we'll be in a position to provide a, you know, significantly more mature dataset. As is customary, we'll give, you know, a full clinical update on all the NPM1-mutant patients on the study. Recall, there were 20 patients, 20 NPM1-mutant patients dosed at the 600 milligram dose. In terms of the experience in the phase Ib and the timing for the phase II, I think that's your second question. It's still early. I mean, we've been very encouraged. We were deliberate to say that we had dosed multiple patients when we first put the press release out announcing the initiation of the study. Interest among and enthusiasm among the investigators has been robust. We're still in study startup. That'll take really, you know, the first fully through the first quarter here in the U.S. Every week that goes by, we have, you know, additional sites coming online. As you recall, all the sites were up and running in the phase Ib, we dosed 14 NPM1-mutant patients in three months. Here we've got to get to steady state in the phase II, we'll have more sites from which to draw, and we expect to see robust enrollment. Got it. Thanks for taking my questions. Thank you. Our next question is from Roger Song with Jefferies. Please proceed with your question. Great. Thank you for taking the question. Maybe just quick two questions for ziftomenib. One is, given the very strong data from the phase Ib, have you started a conversation with the FDA regarding the BTD potential? The second question is around the phase II statistical assumption. Given you're enrolling 85 patients, what is the null hypothesis you try to clear for enroll this 85 patients? Thank you, Troy. Yeah. Thanks, Roger, for both of those questions. On the question of BTD, maybe stepping back for a second. You know, we intend to take advantage of every development and regulatory strategy we can to accelerate the development, accelerate time to market, and overtake our competition. And I, you know, I don't wanna be specific on our interactions with the agency. As everyone recalls, we were very measured in giving guidance around our FDA interactions around the Type C meeting. I'll just tell you that, again, I'll reiterate anything that we can do to accelerate the timelines we intend to do. We certainly feel like we have a very strong data set with a 30% CR rate with full count recovery, and NPM1-mutant relapse refractory AML is clearly a high unmet medical need. In terms of the second part of your question, Roger, around the phase II design, the 85 patients is really driven by safety. That's, you know, that's our view on what's needed to support a marketing application. Again, in the NPM1 mutant, relapsed refractory population, we haven't disclosed the specifics of the statistical design, nor do we intend to. Again, I'll reiterate to you that we intend, and we've built into our development strategy and our protocol, every opportunity to go more quickly if the data permits. I'll just leave it at that. You know, don't wanna get too much more into the details, but we're quite enthusiastic at the rate of enrollment, the rate of interest, and very much look to continue the, you know, the trend that was becoming clear in the phase Ib. Great. Thanks for the comment. Appreciate it. Sure. Our next question is from Peter Lawson with Barclays. Please proceed with your question. Thanks, Troy. I guess on ziftomenib, two questions. When could we see the combination data? Like, could we see that by year end? Just as we think about EU, kind of how's the strategy panning out there, and just do you think those sites would be comfortable with DS? Thank you. Peter, forgive me. Could you repeat the second part of the question? I wanna make sure I understood it. The first part I think was clear. Yeah. As you think about kind of a global study and EU, trials in the EU... Oh, EU. Got it. How you think about adding European sites and if they're comfortable with DS. Yeah. Yeah. Let's take that question first. As we alluded to in the prepared remarks, there's, you know, strong precedent that of the ability to manage differentiation syndrome in combination with standards of care. That's what was seen with the IDH inhibitors. If you look at the data, you know, the DS was certainly mitigated. I think in the discussions we've had with investigators, they're very much of the mind that that should both allow us to mitigate the DS that was seen in the phase I and really unlock the full therapeutic value of ziftomenib. There isn't any real concern. The European sites, as you know, they just take longer to get up and running. It's, you know, not unusual for some of the European sites to take 9-12 months. Now going to kind of the first part of your question, we expect that we're very much working toward initiation of the KOMET-007 trial here in the second quarter. I'll just remind everybody that in the phase I, we observed, you know, responses as a monotherapy at both the 100 mg and 200 mg doses, where the starting dose in combination is at 200 mg. I think we're well within the window in terms of potential activity. I don't wanna guide Peter yet to disclosure to sort of timing of disclosure of data. I will say we appreciate it's a question on people's minds. We're confident in our ability to mitigate any DS through combination, and we'll look for an opportunity, if possible, to share that data later this year. I think it's premature to be more specific on venue or timing, but it's something we definitely are, you know, it's one of our goals. Great. Thank you so much. Pleasure. Our next question is from Li Watsek with Cantor Fitzgerald. Please proceed with your question. Hey, thanks for taking my questions. I got a couple of questions on, you know, the combo study. I guess you initiate the 007 study in, I guess, second quarter. Just wondering, you know, what are the gating steps here, and how should we think about, you know, the enrollments, the in these two cohorts? Any chance that we can see the combo data in KMT2A cohort this year? Li, so sort of a follow on from... Thank you for the two questions. Bit of a follow up from Peter's question. What we're waiting for is the site activation and study startup. Over the last several years, it's just taken longer to get sites up and running. You know, I think not only in oncology but in a number of disease areas. That's just, you know, they're overloaded. They're, you know, they don't have enough staffing. I mean, we all sort of know what's going on. Our sites are very motivated. They are very engaged. We have, we've had no challenges at all in getting sites interested to participate now in 3 potential studies, the registrational study O01, the O07, and the O08. I should have commented in response to Peter's question, we actually will have European sites on the O01 study. They're just gonna come online a little bit later than the U.S. sites. Lee, as you know, What we've tried to do with the strategy with O07 and O08 is to make the funnel as large as possible so that any potential patient with KMT2A or NPM1 on any regimen is eligible to come into one of those two trials. That's one of the ways we're looking to really maximize the value of ziftomenib in AML, and that's really resonated with investigators. It's likely, of course, that the venetoclax containing regimens will probably go more quickly because that's, you know, those are the largest number of patients. You know, we're gonna open the cohorts as quickly as we can. With regard to your question around timing, I'll just repeat what I said to Peter. You know, the focus is very much gonna be on a mid-year clinical update in the NPM1 population. As soon as it's appropriate to provide an update on the combo in either the KMT2A or the NPM1, we'll look to do that in some form and fashion. I just can't be any more specific because, again, the team is just cranking on getting the trial sites open and the first patients on the study. Great. Thank you. Sorry, and one other, one other additional point that I'm just reminded of, just for everybody's benefit, we can, of course, combine data on KMT2A regardless of the combination regimen to show the mitigation of differentiation syndrome. It's not as though we have to wait for any one of those cohorts to enroll. Certainly, the expectation is the combination will mitigate the signs and symptoms of differentiation syndrome, and we'll look to show that. It's just with us not yet having patients on study, it's a little hard to... You know, the crystal ball isn't as clear as I'd like it to be. Our next question is from Brad Canino with Stifel. Please proceed with your question. Great. Thanks for the question. And Troy, this will really be a follow-up to what you just said 'cause I wanna get your working thoughts on the ziftomenib combination data and how quickly you think they can be used to serve as evidence that DS can be mitigated. Really it's a question of sample size. Do you think it would only take a handful of KMT2A patients to show that DS is lower and that you can drive those patients towards a response? I think the corollary there is on efficacy, how do you then think about parsing the contribution of efficacy from the components with a small N in that scenario? Brad. Two good questions there. On the, you know, what does it take, it's probably a little larger than a handful, you know, just to be colloquial, maybe a couple of handfuls. If you've got, you know, if you're not seeing or if you're seeing sort of mitigated DS, i.e. grade one, grade two, you're not seeing the more severe forms of DS, you can calculate the posterior probabilities and figure out, you know, what's needed. The more patients you have, the more confidence you have. You know, we were seeing a 30%+ rate of DS, it won't take too long. In terms of the contributions of efficacy, that's, you know, that obviously will require more patients to parse them out. I'll just remind folks, neither 7+3 nor venetoclax are particularly effective at driving durable responses in these patients, particularly in the KMT2A patients, so you should get a signal fairly early on. I'll just remind you, Brad, we were seeing many of the other correlates of disease control, blast count reduction, you know, symptomatic improvement and so forth. We're pretty confident that this is gonna solve the problem. As far as the NPM1 is concerned, we're in good shape there. We don't, we don't really have to take anything beyond the traditional measures to manage the DS. This is really just a question now about KMT2A. I appreciate that. If I can sneak in one on the FTI decision to deprioritize the EGFR combination. Sure. How should we read that to the potential KO-2806 combination partners? 'Cause you previously mentioned you'd be using new targeted therapy combo partners for that drug early on. Will those combo partners be the types where you're trying to enhance ORR, and we can see that earlier or versus delaying response like an EGFR combo or delaying- Sorry to step on your question there. I appreciate the way you asked the question because you've already, with your question, anticipated the answer. What we're seeing pre-clinically, you know, the potential to combine FTIs, and most notably 2806, with a number of different targeted therapies. I listed EGFR inhibitors, PI3 kinase alpha inhibitors. You've now heard us reference TKIs, specifically in renal cell carcinoma and KRAS inhibitors. To your specific question, one of the things, you know, that we're always doing is taking in data, Scientific data, clinical data, business data, you know, find macroeconomic data. We realized that we wanna get to clinical data sets that will show the ability for FTIs to realize the promise of, you know, the potential for additive or synergistic activity. We think there may be opportunities, Brad, to do that more quickly than was the case with osimertinib. It was not in any way a lack of interest or enthusiasm on our part, but really a recognition that we need... You know, we operate in a world where we have to show data as quickly as possible. The amount of value that we can create per dollar and per unit time is a measurement of our success. You know, we want our shareholders to understand, we think we've got a winner with ziftomenib. We think that KO-2806 is looking very strong and coming on more quickly than we expected. I think it's appropriate, particularly in these times, to look at the portfolio and say, "Where can you create the greatest amount of value in the shortest amount of time and the fewest dollars?" That's exactly what we did. Thanks again. Sure. Our next question is from Tiago Fauth with Credit Suisse. Please proceed with your question. Hey, this is Jeffrey Weiner on the line for Tiago. Thanks for taking our questions. We've heard a lot about discussion about the relative value of an MRD positive CR versus an MRD negative CRH in the relapse refractory setting. What's your perspective on that? Are there any data that really address that question? Is there any read-through to durability? Yeah. Let me parse that for you, 'cause, because there's a couple of things that are mixed in there. The value of a CR versus a CRH is that you have full reconstitution of platelets and neutrophils. If patients have incomplete responses, they're at risk either of infection or bleeding. You know, that's why we keep underlining. We observed a 30% CR rate, not CRH, not CRI. That's meaningful from the standpoint of putting the patients in the best possible position. The second part of your question is MRD negativity. There's pretty good evidence that MRD negativity is a useful surrogate in terms of thinking about survival. It's not yet at the point where it's acceptable as a surrogate endpoint, but. You know, there's definitely a, an effort underway, there's even a consortium to do that. You wanna be able, if possible, to drive patients to MRD negativity. You can have MRD negativity with various, if you will, grades of complete response. You'd like to get as many patients as possible to MRD negativity. The question becomes, though, you know, what are you using to measure it? Are you using flow? Are you using, you know, something more sensitive like PCR? That's where the, you know, the devil's in the details. I think we've been very impressed by the rate of MRD negativity that we've seen. We'll look forward to giving that as one of the elements of the update midyear. Really, you know, that's gonna serve as a comprehensive update on the entire NPM1 experience in the phase I trial, and MRD negativity will be part of that. Great. Thanks for taking the question. Sure. Our next question comes from Eva Privitera with Cowen. Please proceed with your question. Hi. Congrats on the quarter. Thanks for taking our questions. A clarification for the midyear update for the phase I. Do you expect to present data on patients who have gone on to transplant? Eva, yeah. Thanks for the question. We will provide an update of every NPM1 mutant patient in the phase I. The short answer to your question is yes. For a patient who's gone on to transplant, we'll, you know, to the best of our ability to extend the data in the database, we'll give you an update on all of the patient experience that we've seen. We've been very impressed with not only the depth of response, but the durability of response, and look forward to providing that update, you know, at the time. Great. I have a follow-up on the further work on KMT2A disease. What are the plans for pursuing additional monotherapy work? Will this happen prior to going into combos or happen concurrently? I'm glad you asked the question. Eva, we're not at this point intending on pursuing monotherapy further for the primary reason that we believe in order to maximize the benefit to patients, we need to pursue. In the case of KMT2A, we need to pursue ziftomenib in combination. It will allow us to drive, you know, we believe deeper and more durable responses. It'll mitigate the DS. It's also probably obvious to folks, it will also support a global marketing application. Although it's not off the table that you can do a single arm study, for example, in Europe, it's highly unusual. These combination studies set the table for ultimately a global development, a global, you know, a global filing, both in the KMT2A and the NPM1. We'll get there, you know, just as quickly as we can, but all of our effort going forward with KMT2A will be in combination. Perfect. Thank you. Sure. Our next question comes from Reni Benjamin with JMP Securities. Please proceed with your question. Hey, thanks for taking the questions, squeezing me in. I guess starting off, Troy, you know, can you talk a little bit about a clinically meaningful median duration of response? I think in the phase I, we had seen somewhere around 4- 5 months or so and, you know, but we're looking at different doses, we had different genetic types. I guess within the NPM1 population, you know, what do you feel really drives kind of, you know, uptake and will give you know, kind of the go ahead, you know, that you, that you want? Yeah. Also, I guess as my second question, as you know, just building on Brad's kind of benchmarking of efficacy in the combination studies, as you think about prioritizing these studies, you know, just within KOMET-007, there's like eight cohorts, right? How do you go about doing that if, you know, the efficacy is meeting your benchmarks? Do you focus on frontline? Do you just, you know, spend everything you can on both frontline and relapse refractory? Any sort of thoughts as to how, you know, you start to funnel these studies into registrational combination studies? Yeah. Two good questions, Reni, and let's take them in turn. As far as we know, and the kind of the guidance that we're using, 4-6 months, you know, duration of response in the relapsed refractory population is approvable. Now, obviously, you wanna do as good as you can. You wanna give these patients the longest duration possible, but the bar to approval is probably 4-6 months. And you were right, kind of in, you know, the data was immature, but we were getting into the right zip code at the time of the ASH presentation. Look forward to providing an update sort of mid-year here this year. Consider that the NPM1 overall survival is a, is a median of about 6 months without menin inhibitors. If you're talking about 4-6 months duration of response, that's a good improvement. That's where that number comes from. The second piece of your question is kind of how do you know, a prioritization. I would say the following, in your scenario where, you know, multiple regimens look good, I like to say, several of you have heard me say, "Let's put that in our bucket of extremely high-class problems." Right? If we've got multiple regimens that look good, you don't have to register all of them. We will continue to be good fiduciaries and prioritize those combinations that we believe are gonna drive the greatest commercial value. You already know what they are. They've, you know... It's clear. Venetoclax containing regimen with or without azacitidine, let's see, you know, how that plays out. Do you need the triplet or the doublet? Of course, the FLT3-containing regimens because at least in the relapse population, a significant number of the NPM1 mutants are also FLT3 mutant, co-mutant. Those are probably ran the two greatest populations. If we've got a handful of 10-20 patients worth of safety and activity data to support other regimens, that just helps broaden the utility, broaden the knowledge base and the comfort among the hematologist oncologists who ultimately, you know, are out in the community using ziftomenib. We're gonna, you know, do just enough that we give everybody comfort that ziftomenib is almost a you know, it's an amazing drug, right? It's highly mutant selective, extremely efficacious, and yet it's also extremely tolerable. The patients say to us, "The only reason I know I'm on the drug is I take a pill once a day in the morning." If we can couple that up with the commonly used regimens, we think we're in great shape. Terrific. Thanks for taking the questions. Our pleasure. Our pleasure. We have reached the end of the question and answer session. I would now like to turn the call back to Dr. Troy Wilson for closing comments. Thank you, Rob. Thank you all once again for joining our call today. We'll be participating in both the Cowen and the Barclays Healthcare Conferences over the next several weeks, and we hope to see many of you there. In the meantime, if you have additional questions, please feel free to contact Pete, Tom, or me. Thank you all once again, and have a good evening. This concludes today's conference. You may disconnect your lines at this time, and we thank you.