Good afternoon, ladies and gentlemen, welcome to the Q1 2023 Kura Oncology, Inc. earnings conference call. At this time, all lines are in a 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 Wednesday, May 10th, 2023. I would now like to turn the conference over Pete De Spain, Senior Vice President, Investor Relations and Corporate Communications. Please go ahead. Great. Thank you, Julie. Good morning. Welcome to Kura Oncology's first quarter 2023 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. I'll now turn the call over to Troy. Thank you, Pete. Thank you all for joining us. Our strong conviction in ziftomenib and its potential to be the best-in-class menin inhibitor continues to increase. This confidence is supported by one of the highest complete response rates reported for a targeted therapy in the setting of relapsed refractory leukemia and is reinforced by the rapid pace of enrollment in our registration-directed trial. More on that in just a moment. We're also encouraged by the durable remissions in our phase I trial, driven primarily by single-agent activity of ziftomenib, and we look forward to sharing an update at the European Hematology Association Congress next month. You got a glimpse of these data in our recently released abstract, which showed that ziftomenib continues to demonstrate significant clinical activity in patients with heavily pretreated and co-mutated relapsed or refractory NPM1 mutant AML. As of a January 31st data cutoff, 6 of the 20 NPM1 patients treated at the recommended phase II dose achieved complete responses with full count recovery. The abstract showed a median duration of response of 8.2 months, with a median follow-up of approximately eight months. Four patients were still ongoing at the time of data cutoff. Ziftomenib is well-tolerated, and the on-target effect of differentiation syndrome is manageable. We are excited by these evolving data, and we look forward to reporting updated data as of an early April data cutoff. Now, building on the momentum generated by our positive phase I data, we announced in February that the first patients were dosed in our phase II registration-directed trial of ziftomenib in NPM1 mutant relapsed or refractory AML. Site activation and enrollment in our registration-directed study are outperforming our projections, an indication of the continued enthusiasm surrounding ziftomenib among investigators and patients. As a reminder, 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 exists. Once the disease becomes relapsed or refractory, the prognosis for NPM1 mutant AML patients is particularly poor, with an overall survival of approximately six months after initial chemotherapy. NPM1 mutant AML is further compounded with co-mutations such as IDH or FLT3. Notably, in our phase I trial for ziftomenib, two-thirds of NPM1 mutant AML patients who achieved a CR at 600 milligrams had IDH and/or FLT3 co-mutations, all of whom had failed prior treatment with IDH and/or FLT3-targeted inhibitors. I'm sorry, a 30% complete response rate with full count recovery after prior failure of these targeted therapies makes the clinical activity of ziftomenib even more striking. We're also impressed with the potential for ziftomenib to drive durable remissions as a monotherapy. An additional NPM1 mutant patient who entered the trial with multiple co-mutations, including DNMT3A, following two prior stem cell transplants, achieved a CR with no evidence of minimal residual disease and remains on ziftomenib for more than 32 cycles as of our January 31st data cutoff. In parallel with our efforts to advance ziftomenib as a monotherapy, we're preparing to initiate a series of combination studies to significantly broaden the addressable patient population. We believe ziftomenib is uniquely positioned for these combination strategies. This belief is driven by several key competitive advantages, including no evidence of drug-induced QTc prolongation, no predicted adverse drug-drug interactions, and once-daily oral dosing that should enable convenient administration with current 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 of therapy and across multiple patient populations, including both NPM1 mutant and KMT2A rearranged AML. We've designed these phase I studies to assess safety, tolerability, and anti-leukemic activity of ziftomenib in combination with key regimens such as venetoclax and azacitidine, the FLT3 inhibitor gilteritinib, and a chemotherapy regimen of 7+3. Our approach to combinations is to establish ziftomenib as a foundational therapy that can be combined safely with various commonly used regimens and then prioritize those combinations that represent the largest unmet medical need and the greatest potential commercial value, namely venetoclax and FLT3 inhibitor-containing regimens. Notably, up to half of NPM1 mutant AML patients also exhibit co-mutations in the FLT3 gene. Given the safety profile of ziftomenib, we believe it may be the ideal menin inhibitor to combine with FLT3 inhibitors to address this population, a difficult-to-treat group that represents approximately 15% of AML. 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've begun site activation in the first of these studies, KOMET-007, we're on track to dose first patients this quarter. We're very proud of our team's execution, grateful for the continued support of our study's investigators. Their enthusiasm, coupled with a growing body of clinical data and multiple emerging lines of evidence, reinforce our confidence in Ziftomenib as the best-in-class menin inhibitor. We look forward to sharing more at our upcoming presentation at EHA. Let's turn our attention to our farnesyl transferase inhibitor programs. Over the past several years, we've pioneered the development of FTIs as combination agents to prevent or delay emergence of resistance to certain classes of targeted therapy in large solid tumor indications. Targeted therapies have demonstrated meaningful clinical activity across a range of solid tumors, adaptive resistance almost invariably emerges over time, which limits the ability of targeted therapies to drive sustained clinical benefit. We have generated a growing body of preclinical and clinical data that support the combination of FTIs with multiple classes of targeted therapies, including EGFR inhibitors as well as PI3 kinase inhibitors. In April, we presented encouraging preclinical data at the American Association for Cancer Research Annual Meeting, which supports the potential use of FTIs in combination with two additional distinct classes of targeted therapy. The first of two posters revealed robust synergy between tipifarnib and the standard of care anti-angiogenic TKI, axitinib, in cell and patient-derived xenograft models of clear cell renal cell carcinoma. The second poster reported regression of multiple models of KRAS inhibitor-resistant non-small cell lung cancer through the addition of tipifarnib either to adagrasib or sotorasib therapy. These promising preclinical data illustrate the potential for FTIs to drive enhanced antitumor activity as well as address mechanisms of both innate and adaptive resistance to targeted therapies. We believe these data strongly support our rationale to combine our next-generation FTI, KO-2806, with TKIs in clear cell renal cell carcinoma as well as KRASG12C mutant inhibitors in non-small cell lung cancer. In January, we were pleased to announce FDA clearance of our investigational new drug application for KO-2806 for the treatment of advanced solid tumors, an important next step for this program. We intend to evaluate safety, tolerability, and preliminary antitumor activity of KO-2806 in a phase 1 dose escalation study, which we're calling FIT-001. We're now in study startup, and we look forward to dosing the first patients in FIT-001 later this year. Concurrent with the dose escalation as monotherapy, we also plan to evaluate KO-2806 in dose escalation combination cohorts in advanced solid tumors. Meanwhile, we continue to evaluate tipifarnib in combination with the PI3K alpha inhibitor alpelisib, a combination that has potential to address up to half of all patients with recurrent and metastatic HNSCC. We're encouraged by the preliminary activity observed in our ongoing current HN trial, including a durable partial response in a patient with PIK3CA-mutated squamous cell carcinoma of the tonsil. We're also very pleased by our ability to combine tipifarnib with another targeted therapy, in this case alpelisib, with no dose-limiting toxicities reported to date. We remain on track to determine the optimal biologically active dose in mid 2023. We continue to unlock the potential therapeutic and commercial value of farnesyl transferase inhibition, the challenging but we believe increasingly substantial opportunity that has potential to address large solid tumor indications such as renal cell carcinoma as well as cancers of the lung and colorectal system. As with our menin inhibitor program, we believe FTI programs have potential to create significant value for patients, healthcare providers, and our shareholders. We're confident we have the leadership, experience, and operational and financial resources to realize that value. With that, I'll now turn the call over to Tom Doyle 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 first quarter of 2023. Research and development expenses for the first quarter of 2023 were $25.2 million, compared to $20.9 million for the first quarter of 2022. The increase in R&D expenses was primarily due to increases in clinical trial costs related to our ziftomenib and KO-2806 programs, offset by decreases in clinical trial costs related to our tipifarnib program. General and administrative expenses for the first quarter of 2023 were $11.4 million compared to $11.9 million for the first quarter of 2022. Net loss for the first quarter of 2023 was $34.1 million compared to a net loss of $32.5 million for the first quarter of 2022. This included non-cash share-based compensation expense of $6.8 million compared to $6.7 million for the same period in 2022. As of March 31st, 2023, we have cash equivalents and short-term investments of $405.9 million compared to $438 million as of December 31st, 2022. 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. 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 the remainder of this year. For ziftomenib, dose the first patients in the KOMET-007 combination trial in the first half, present updated data from our phase I trial in NPM1 mutant AML at EHA in June, and dose first patients in the KOMET-008 combination trial in the second half. For tipifarnib, determine the optimal biologically active dose in the current HN trial in combination with alpelisib in mid-2023. For KO-2806, dose first patients in the FIT-001 dose-escalation trial in the second half of 2023. With that operator, we're now ready for questions. Thank you. Ladies and gentlemen, should you have a question, please press the star followed by the one on your touchtone phone. If you'd like to withdraw your question, please press the star followed by the two. One moment please for your first question. Your first question comes from Jonathan Chang from SVB Securities. Please go ahead. Hi, guys. Thanks for taking my questions. First question, can you help set expectations for the upcoming EHA ziftomenib update and discuss the importance of achieving a good duration of response? Sure, Jonathan, thanks for the questions. As you saw from the abstract, which was released, the abstract is focused on the NPM1 mutant AML patients treated at 600 mg, which of course is the FDA's accepted recommended Phase II dose. The abstract, Jonathan, was as of, as I said, a January 31st data cutoff. We're going to bring forward all of the clinical data on those patients, and report it as of an early April cutoff at EHA. As we said in the prepared remarks, you know, we're seeing now multiple converging lines of evidence that suggest to us that ziftomenib is potentially the best menin inhibitor in acute leukemias. We very much look forward to sharing that data with you and others at EHA. Importance of duration. In terms of your question, Jonathan, on-- Yeah, let me follow up on your second question. Sorry, I didn't mean to neglect it. In terms of duration of response, there's two things to think about here. The first is what's the bar for registration? The second is what's clinically meaningful and how do you think about that, right? First things first, as we've said consistently, what we understand is that for, you know, FDA approval as a monotherapy, you're looking at a 20%-30% CR/CRh rate, as well as a median duration of response of 4-6 months. I don't think we've ever deviated from that. The reason that those are meaningful numbers, of course, is you're talking about patients who failed all other options, and the overall survival for NPM1 patients in the relapsed refractory setting is about six months. If you're driving a duration of response that's in that same, you know, that same timeframe, that's clinically meaningful. Nothing has changed in our understanding of that, those being, you know, the registrational bars. In terms of what's important clinically, I would draw your attention to a couple of things. The first is that we are driving CRs with full count recovery. This, you know, again, not CRIs or even CRHs, but really the full complement of the immune system and the hematopoietic system back. Why is that important? The patients are healthier, right? These patients are at tremendous risk of infection, and all of the docs that we talk to tell us the more you can take patients to full CR, the better off you are. The second, of course, Jonathan, is your question around duration. I don't wanna get in front of the abstract or kind of under the four corners. I'll tell you this. We have been very pleasantly surprised by the ability of Ziftomenib to drive durable responses as a monotherapy, i.e., without needing to go to either to transplant or to other therapies. We see quite a different sort of mutational profile from what has been reported for other agents, and I think that's going to be important not only in the relapsed refractory setting, but it will become even more important as we roll forward into combinations. We'll look forward, as I said, to sharing all of this both at EHA, Jonathan, and very likely at an associated investor event alongside. Understood. Second question, can you provide any more granularity on what you mean by the phase II NPM1 study enrollment outperforming projections? Yeah. I'm happy to. I'll just remind everyone that last year we reported that we had enrolled 14 patients in our phase Ib study in approximately three months. Here's where we are today. Our total goal for this trial is 62 clinical sites in the US and Europe. We're now open, Jonathan, in a majority of those sites. We've seen site activation in both the U.S. and Europe that has exceeded our expectations. The only thing we can attribute that to is excitement of the investigators, the sites, the patients for getting their hands on Ziftomenib. What, you know what? As you know, and an obvious competitor of ours has extended its timelines for recruitment of NPM1. We're not ready yet, Jonathan, to pull timelines in. What I can tell you is the investigators on the phase Ib study, as well as the new investigators, have picked up exactly where they left off. And site activation is always a leading indicator, but we've seen both site activation and now enrollment that it's exceeded our already, you know, pretty aggressive, pretty aggressive goals. I think we're seeing a continuation of the excitement, the enthusiasm from the phase Ib, and I think it positions us very well, not only to come forward with potentially best-in-class data, but to be very competitive on timelines in the NPM1 setting. Got it. Thank you for taking my questions. Thank you, Jonathan. Your next question comes from Roger Song from Jefferies. Please go ahead. Great. Thanks for the update and taking our question. Maybe just a follow-up on your earlier, Troy, your earlier comment related to the best-in-class, profile, particularly in the emerging, resistant, data, on the menin inhibitor. Maybe just tell us a little bit more about this, how ziftomenib will differentiate it in this kind of- Yeah. -resistant mechanism, and why- Yeah. You think it's better suited. Thank you. Sure, Roger. Thank you for those two questions. Let's start with kind of what we see, and then we can talk about the implications for what it means. First, what we see. One of our competitors, you know, it was reported that they're seeing the emergence of resistance mutations at roughly 30%-40% of patients, and they're seeing it very early on. You know, cycle one, cycle two. It's not. You know, we've known for a long time about the potential for resistance mutations. What have we seen? By comparison, and we're still analyzing our data, Roger, but to this point, having analyzed quite a number of patient samples, I can tell you we've seen three examples of resistance mutations. Two of them were patients who presented with the threonine 327 methionine mutation as soon as they presented to the study, having failed revumenib. You know, do we see them? Yes, we do. What's interesting is we don't seem to see them, you know, nearly at the same frequency as perhaps our competitors do. What's the implication of that? As we know from, you know, pick EGFR, pick any other small molecule oncology target, right? The emergence of resistance mutations typically means, you know, the therapy is becoming less effective. What I think this is going to mean, Roger, I should say what we think is, it'll be important as a monotherapy. Again, I'll stress to you, we're seeing durable responses just in the presence of Ziftomenib. As you now go forward into combinations, that's going to become incredibly important because if those menin clones can get away with resistance mutations, now you've lost that therapeutic activity. I think it sets up very nicely. There are a number of both, you know, biochemical and drug-like properties that we think are contributing. It's very clear, Roger, that these compounds have very different profiles. Again, as I said to Jonathan, look forward to sharing much more of this data at and around EHA. Excellent. Thank you. Yeah. Moving on to the tipifarnib or your FTI franchise, since you're planning to announce the biologically optimized date, dose for alpelisib combo midyear. What would be the next step for that program, and also how that will play into your KO-2806 overall FTI franchise? Thank you. Yeah. Thank you, Roger, for that question as well. Stepping back, just for a second, you know, a number of our analysts and shareholders have been with us for a number of years, and they know, you know, this is a program that we've been very passionate about. I don't think, Roger, that it's an overstatement to say that FTIs may turn out to be one of the ideal combination agents for targeted therapy. People have looked at SHP2, they've looked at SOS. You know, people have been trying to drug both the MAP kinase and the PI3 kinase pathway for at least the past couple of decades. You might ask, why did nobody discover this sooner? By the time most of the FTI programs were discontinued, that was right at the dawn when a lot of these targeted therapies were discovered. It wasn't until really until our team began doing first preclinical and then clinical work on the combinations that we really began to see the opportunity. When we started, we naively said, "You know, we need to go after farnesylated oncoproteins," the HRAS being the most, you know, the most obvious and perhaps the only. What we've learned is actually when you stress the cell with EGFR inhibitors, KRAS inhibitors, TKIs, the cell responds in a very organized, highly choreographed way, and it exposes farnesylated proteins such as RHEB, and those become ideal targets for drug synergy. I think it's that, Roger, that's driving what the biology that you see in the two posters at AACR. Just incredible synergy, both in the context of RCC and KRAS mutant inhibitors. To your question now, ’cause I think that's important background. We, I think the most immediate takeaway from our alpelisib combo is we can actually take these two drugs I think to their full dose with no dose-limiting toxicities. I think most investors, and in fact, even many people at Kura, would not have expected that would have been the case. That bodes extremely well for combining twenty-eight oh six with these various targeted therapies. If you can combine with alpelisib, that sets a pretty high bar. For that program, specifically, Roger, we're gonna do two things. The first thing is, I mean, we know we have adequate safety and tolerability. The question is the clinical activity sufficient to support continued development of tipifarnib and alpelisib, or do we perhaps prioritize KRAS-driven tumors RCC as potential next steps, next investments? The good news is I think we're gonna have options, we're gonna have choices. The team is doing a lot of work to get twenty-eight oh six into those targeted combinations as quickly as possible, where it's really not about the monotherapy, it's how quickly can you get into the combos, how quickly can we see if we can replicate that preclinical data. That's the data that we're expecting, Roger, and the way that we're gonna... the lenses that we're gonna use to look through it, as we say, is the next investment, one in head and neck, perhaps lung cancer with KRAS or perhaps RCC, or, you know, in a perfect world, more than one. Perfect. Thank you. Thank you, Troy. Sure. Your next question comes from Peter Lawson from Barclays. Please go ahead. Hey, good afternoon. This is Alex on for Peter. Thanks for taking our questions. Just given the comments on the pace of site activation and enrollment in the pivotal study, any color you could provide around, you know, when enrollment could complete in that study? Yes, Alex, thanks for the question. We've guided that. Maybe taking a step back. The phase II study is designed to enroll a total of 85 relapsed refractory NPM1 mutant patients. The reason it's 85 is we felt that that was an appropriate safety database to support a best-in-class menin inhibitor. Typically, the FDA wants to see about 100 patients at your recommended phase II dose just from a safety perspective. Obviously, from an efficacy perspective, you probably don't need 85 patients. And within the context of those numbers and that trial design, Alex, we've guided that full enrollment of the 85 is probably middle of next year. Given that we are, given that our initial site activation and enrollment is exceeding our expectations, although we're not yet ready, Alex, to pull the timelines in, I can tell you we're going to take advantage of every possible opportunity to be competitive. I think we'll have best-in-class data. The question is really gonna be, where are we in terms of timing? At this point, I think we're neck and neck, potential to even pull ahead of that. We've just been really pleasantly surprised by what we're seeing in the ongoing COMET registrational trial. Great. Thanks. That's very helpful. Then just a second question on EHA. I know the focus is on NPM1, but should we expect any updated data from the MLL-r patients you've treated so far? Thank you. Yeah, Alex, thanks for the question. At this point, I'll just refer you back to the abstract. Again, I don't wanna get ahead of the abstract or sort of get under the four corners. We'll focus at this point on giving you an update on what's laid out in the abstract. As I mentioned, we're intending to provide an investor event in connection with EHA. As I've said, we're seeing multiple lines of evidence really that are supporting ziftomenib as being a best-in-class inhibitor in acute leukemias. We'll look forward to sharing that data with you and the rest of the folks on this call at that time. Thank you. Sure. Your next question is from Brad Canino from Stifel. Please go ahead. Hi, thanks. Strategic ziftomenib question from me, Troy. You've been open in the past about the requirement for a global pharma partner to capitalize in the valuable frontline AML setting. As I look at it now, you're in a position where you have NPM1 data evolving positively. You've got this pivotal trial progress that's ahead of schedule, as you stated, and you're moving to dose optimize the combos as quickly as possible. Ahead of you've got competitor pivotal data and combo safety data in second half 2023. You know, I look at your cash burn guide. That would suggest, even with all the planned trial additions that you have laid out in your press release, you expect the cash burn to cap at about a 50% increase from the current levels this past quarter as I look through 2025. As you think about the evolution of all of these pieces, how are you currently weighing the ideal time for such a transaction? Thank you. Yeah. Brad, I appreciate the thoughtfulness with which you laid out the question. I can tell you that the discussions that we've had with sophisticated parties, you know, that do research, development, and commercialization of products in heme, have reinforced the idea that we have a best-in-class compound. Not only are they drawn to the clinical activity, but very much some of the other properties that we've continued to highlight, the lack of QT, the lack of drug-drug interactions, you know, the oral once-a-day dosing, the ability to not have to vary dose, as you're changing SIP regimen, you know, azole regimens or others, is very appealing. In particular, you'll hear us in our prepared remarks stressing the opportunity with the FLT3 inhibitors. That's fully half of NPM1, and you wanna hit that head on, as early as you possibly can because you have a real potential, you know, to drive durable responses in those NPM1 FLT3 patients. All of that, Brad, is saying, you know, the team is doing everything you've said and even more behind the scenes. I think there comes a point where we currently will need additional operational resources to fully maximize the value of zifto. What we see is zifto to be the preferred combination agent across the continuum of care, from frontline to maintenance, combination with every other approved agent as well as emerging agents. Clearly, you know, at some point you need global scale to be able to do that. We also very much, you know. We prioritize patients, we also prioritize our shareholders. We wanna make sure that anything we do, it ensures that our shareholders are appropriately rewarded. I can't be a lot more specific than that, obviously, I can tell you know, those of you who know me know, you know, I have a history of, on both the business side and the science side. I would say there's a lot of excitement about zifto-MENET kind of across the continuum. As we have more to say, we'll, you know, we'll give updates throughout the year. Great. Thanks, Fred. Thank you, Brad. Your next question comes from Li Watsek from Cantor Fitzgerald. Please... Fitzgerald. I'm sorry. Please go ahead. Hey, thank you for taking our questions. I guess for the deal that you just shared with us, just wondering if you could put this into perspective for us, you know, relative to your competitor. The second, you know, in terms of the combinations, you mentioned that you will dose the first patients this quarter. I guess just based on the fast enrollment you've seen so far for your NPM1 patients, do you think, you know, that's gonna translate into your combo studies as well? Yeah, in terms of excitement. Yeah, very good question. Your first question is, Li, I'm sorry. Can you tell me your first question again? Yeah. You, I know you have three of them. Yeah, duration of response. Maybe just, you know, share your perspective. Yeah. you know, relative to your competitor. Yeah. Okay, thank you. I wanted to make sure I answer the question you're asking. If you'll indulge me, if you look at the Phase Ib study, right? This is what we're updating. I just wanna underscore something for everyone. We're reporting data on 20 patients, 20 NPM1 mutant patients at our recommended Phase II dose. That's nearly, you know, between 25% and a third of the way to a registrational study, just in terms of pure patient numbers. Both you and the analysts, the other analysts and investors on the call are getting a very good look into potentially what a pivotal data set might look like, you know, if things continue on the current trajectory. I wanna just underscore that because you wanna make sure you're comparing apples to apples. The competitor is three patients, right? two of whom went to transplant almost immediately. I'll highlight that to you, Li. I'm not gonna give you an exact number. I'm gonna wait for EHA to do that. What you'll see is the duration of response being driven by zifto-MENET. As you saw from the abstract, we have had a couple of patients who've luckily for them, gone on to transplant with good results. It's clear both the efficacy, the potency of zifto, the ability to drive full count recovery, and the ability to avoid these resistance mutations were driving very good durability. I think, Lee, it's that entire package that is what is driving the excitement among investigators. To your, to your other question of, is that do we think that's gonna pull through to the combos? Yeah, very much. Again, You know, our combo strategy is we believe ziftomenib has the potential to be a cornerstone of therapy for acute leukemia. You know, our goal is to transform AML the way, for example, I think it might sound cliché, but the way Gleevec transformed CML, right? Turned it from a devastating disease into kind of a chronic condition. Menin inhibitors may be the first thing to come along in AML that have the potential to do that. We've seen similar levels of excitement and enthusiasm among investigators who are jostling to either get into the 007, the 008 study or both. Our goal, though, Lee, is to try to give as many sites around, you know, in both the U.S. and Europe, the opportunity to work with ziftomenib so that that enthusiasm where people actually, you know, use it with their own patients, that that continues to build. That's what's, I think, driving those exceeded expectations, and we fully expect that to pull through into the combos. Great. Thanks. Ladies and gentlemen, as a reminder, should you have a question, please press the star followed by the one. Your next question comes from Phil Nadeau from TD Cowen. Please go ahead. Good afternoon. Congrats on the progress, and thanks for taking our questions. A follow-up, perhaps on the last question. In terms of those earlier lines of therapy and the combination regimens, when we've discussed the opportunity for menin inhibitors with our consultants, in the earlier lines, some have questioned what trial design would be necessary to support approval and use. Do you have any thoughts on what a registration trial would look like, for an early line combo regimen? What in particular, what endpoints do you think would be meaningful and likely to be hit? Yeah, Phil, it's a good question. I don't wanna get ahead of the team on this. It is very much an active topic of discussion. I don't think we've said much publicly about what registrational studies would look like in the front line. You know, clearly you're gonna need to have. I think it's unlikely you can rely on MRD negativity. You may be able to go on the basis of response rate with survival. As for specific parameters, it's obviously gonna, you know, depend on the specific combination and the line of therapy. I will tell you know, we're, we've highlighted trying to do two things simultaneously: provide a data set so that physicians can use ziftomenib with whatever regimen they want to use, whether it be venetoclax, chemotherapy, other targeted therapies. That's our first goal. Our second goal is to go where there's the greatest unmet need and the greatest commercial opportunity. That's gonna be venetoclax. I think, Phil, we'll learn as we begin to get experience on those patients. You know, for example, is there the potential for either synergy or resensitization? I think we're cautiously optimistic, but it's just a bit early to speak to specific registrational designs at this point. Let us get a little bit more experience in phase, and build up that data set and then as we've started to lock it down with the investigators and the KOLs, we can communicate it. It's very much, very topical for our, for our team internally. Got it. That's, that's fair enough. Second question is, we're wondering whether you have any new visibility on the potential competitors, obviously not the competitors that are coming from the public companies, but investors have an eye out for those potential competitors, the menin inhibitors, either at big pharma or foreign pharma. Any visibility on when the first data from any of those programs could be announced, or are you running into any of them as you enroll your studies? I'll tell you, we're not running into them. No. I think, you know, there are three, right? There's Janssen, Daiichi, and Dai Nippon Sumitomo. We don't, we don't hear a lot about them. We don't, we don't bump into them, as you would say. We're not, we're not, you know... We're careful not to put our investigators in a position where we ask them for data because for obvious reasons, we wouldn't want them to share data on our programs. We've been impressed, Phil, to this point, as I said, by the pace of site activation and the pace of enrollment in the NPM1 setting. I think that, you know, that's as much of a biomarker as we probably have. I'll go even a step further and say my prediction as we go into KMT2A, you're gonna see the activity pick up significantly based on what we've seen with NPM1, and I'm cautiously optimistic we'll be best in class there as well. The ability to drive durable responses without necessarily needing to go to transplant so quickly. Obviously the proof is in the pudding on that one. That's what we're hearing back as we go out and we talk to investigators, our investigators both in the U.S. and Europe. Great. Last question from us, one that we get from investors. We're curious to hear your thoughts on it. Does Kura have any desire to go into diabetes? Yeah, it's a good question. I would say the following. We are doing work, we're doing preclinical work with not only Ziftomenib, but next generation menin inhibitors that are reversible. And we're doing them in diabetes models. And we're doing that to try to feel sort of be very data-driven. I think the data that you're referring to, it's provocative, but it, you know, it's just, it's very incomplete. I can tell you this. If there's a connection there, and there's a biological rationale for why one would use a menin inhibitor in diabetes, the question is really, you know, the effect size, the safety, etcetera. I would tell you this. We believe Ziftomenib is the best in class menin inhibitor in acute leukemia. If you want to go into whether it's diabetes or solid tumor indications, both from a safety perspective and from the perspective of the IRA, you wanna take a different chemotype. You wanna take a different compound forward. I believe based on the work that our chemistry group has done, we'll have a best in class reversible inhibitor to take into diabetes. Let us do the work and really validate that as a, as a meaningful opportunity, 'cause as you know, it's a completely different development paradigm. Yep, that makes a lot of sense to us. Thanks again for taking our questions. Our pleasure. There are no further questions at this time. I will turn the call over to Troy Wilson, President and CEO, for closing remarks. Thank you, Julie, and thank you all once again for joining our call today. We'll be participating in the JMP Life Sciences conference next week in New York and look forward to seeing a number of you there. In the meantime, if you have any additional questions, of course, please feel free to contact Pete, Tom, or myself. Thank you again, and have a good evening, everyone. Ladies and gentlemen, this concludes your conference call for today. We thank you for joining, and you may now disconnect.