My name's Pete Lawson. I'm one of the biotech analysts at Barclays. I have the pleasure of covering Kura Oncology. Up on stage with me, I've got Troy Wilson, President and CEO, and also Mollie Leoni, the CMO. Questions we have been asking today have just been kind of some macro questions around, you know, whether you think there's any impact on the supply chain with tariffs and any worries or learnings from COVID as we think about the new environment that we're in. Sure. First of all, thank you, Peter and Barclays, for the invitation to participate in the conference. With respect to the macro, during COVID and actually during the, you know, the BIOSECURE debate, we actually took a long look at our supply chain and made some adjustments. We at Kura specifically are not experiencing or anticipating any kind of disruptions or slowdowns from either tariffs or, you know, any of the kind of macro features, as well as, you know, there are some questions just around, you know, federal headcount and the agency, the FDA. We are also not expecting anything there, but we are being vigilant and will be prepared, you know, in the event that that happens. Gotcha. Has there been any changes in the rate of communication and any levels of confusion there? No, not that we've seen. It's been pretty much just business as usual. We've not seen any difference at all. Gotcha. I know you're funding your own trials, but are there any kind of knock-on effects that we should be thinking around for NIH budgetary funding and if that trickles through to clinical trial sites? I think that's a longer-term issue. Most of the, I mean, the trial sites, back to your question around COVID, a lot of the trial sites are still recovering from the bolus of trials that went through during COVID. A lot of, unfortunately, a lot of those clinical sites have lost staff due to the sponsors, you know, recruiting good people out of the clinical sites. That is a constant kind of work in progress. We haven't, again, seen anything immediate from, you know, any of the NIH cuts. That will probably be a longer-term issue for the sector. Gotcha. Maybe before we dive into the Q&A around the various aspects, if there's kind of any kind of state of the union or any kind of initial lead-ins you want to prepare or talk through around some kind of catalyst that we should be thinking through over the next 6 to 12 months? Sure. Yeah. As we look out six to twelve months, we, you know, beginning with ziftomenib, we're expecting to submit an NDA next quarter. Hopefully that would lead to review this year and potentially commercialization either late this year or early next year. That's in the monotherapy setting. In the combination setting, we will initiate the two- phase III randomized trials in the fit and unfit segments later this year. We've guided to second half. That'll, you know, I think we'll talk a little bit about the timing there, but that's really a big push into the front line. You'll see us continue, Peter, to innovate in the AML space. You'll see us starting the trial in GIST with ziftomenib and imatinib. We're quite excited about that. You'll see us release data for the FTI program here in the second half, potentially at ESMO. That'll, I think, start to get, hopefully get people to pay attention to the FTI programs. If you look back, I mean, we are, particularly in these challenging times, you know, extremely well-capitalized, financially de-risked, I think scientifically and regulatory de-risked. At this point now, we're looking at how can we make a big difference for patients, whether it be in AML, in GIST, or in solid tumors. We're hoping to have clinical data at every major medical meeting this year and on into next year. It's going to be a good year. It's tough out there in the markets, but it, you know, we're in the enviable position of being able to keep our heads down and just execute. Gotcha. Thank you. Just specifically around Komet -001 and you've got the 2 top line data, kind of where do we see that data? Is that kind of an ASCO thing, abstract? How do we, how much do we see? Yeah, potentially at ASCO, that's where we've submitted. The abstract release, I think, is in late May. The titles come out a little earlier than that. We're hopeful. It is a positive pivotal trial, so we're hopeful that it gets a proper venue. What should we expect to be seeing in terms of CR/CRh rates and response rates in that data set? Yeah. So we've consistently guided, you know, the trial was designed to deliver between a 20%-30% CR/CRh rate. I think we've never once wavered from that. It is within that range, and I think we've said it's not on the boundary. In terms of the safety, tolerability, and clinical activity, we think it's going to be very competitive with what's already out there. We'll look forward to sharing that data initially in the abstract and then, you know, hopefully in an oral presentation, potentially, as I said, at ASCO. Gotcha. How should we think about, like, patients that are pretreated with venetoclax? Does that have any impact on the results and/or does that matter? I can't really speak to the second half of the question of does it matter. The first half of the question is the rate of venetoclax pretreatment is consistent with what we saw in the phase I- B. That'll be one of the things, you know, if we look at the forest plot, I think that'll be one of the things that we can talk about when we have the data. It's actually a really interesting data set, and we're looking forward to sharing it with you. Gotcha. Remind us the number of patients you expect to see. I guess on the side effect profile, is it differentiation syndrome that kind of we hone in on, or are there other components that we should be thinking about? Yeah. The number of patients, we over-enrolled in the pivotal registrational study. I think it's 92, something like that. Is that right? 92. Yep. In terms of the safety and tolerability profile, yeah, I mean, the big questions for the class are, you know, presence or absence of drug-drug interactions, QT prolongation, myelosuppression, and differentiation syndrome. Those are the four things you watch, right? Because that's what's going to impact your ability to combine with other agents. I think you'll see we score very highly on all four of those metrics, I think. You can, and Mollie's going to speak to it, I know, in your next set of questions, but I think the safety and tolerability of ziftomenib on a once daily schedule is part of what allows us, has allowed us to combine so effectively with the standards of care, and is what is driving enrollment to be so robust. It's just, it's very, very easy to work with. Differentiation syndrome, Peter, as you know, really wasn't much of an issue in the NPM1 segment as a monotherapy, and it really becomes well-managed, well-mitigated in combination. Okay. Perfect. You're on track for the BLA submission? We are, yeah, for the NDA submission. NDA, sorry. What are the gating factors that we should be thinking about? The team just has to, you know, the team to think we're like whipping them. It's really down to the team doing the work to put the application together. It's in its, you know, it's 90+% of the way there. You're just finishing it off. There's a lot of QA and QC that goes into it, but, you know, it's in very good shape. We're on track to hit that second quarter, and the team will hit it. It's not kind of last- minute 2Q, you're thinking, or? No, I don't think it's last- minute. We've given our, we try now to give ourselves, you know, some room, some room to breathe, some room to maneuver. We're in good shape. The team's done a phenomenal job. Komet-0 07, so the fit population, seven plus three, and for that data set, kind of when should we expect that? It's 2Q, and kind of what do you want us to hone in on that data set? You want to expect? Sure. Yeah, Q2, as Troy said, we're submitting to as many major conferences as we can with our data. You're going to want to hone in again on the safety, tolerability, and combinability. That's the biggest thing. That's where drugs win or lose is combinability. Of course, just to continue to see the positive trends we set in the data we've already shared previously at ASH, continuation of really good efficacy and safety in these patients. Gotcha. For that combinability and what we should hone in on, are there particular segments of that safety profile that we should be focused on around? You know, for the 7+3, the patients continue on with our drug as a monotherapy for significant periods of time, in addition to using it in combination with the backbone therapies. However, you'll notice that patients don't require dose reductions or dose interruptions, et cetera, to handle adverse events when they continue on as a monotherapy. That'll be a very important piece to hone in on. Gotcha. Okay. For the 7+3 alone, what's the best bar that we should be thinking about? You know, I was thinking about this. It's a 70-year-old treatment, so there's so many references out there, but usually the ranges are between 50-80% for a complete response rate in these patients. NPM1 probably higher, probably closer to that 80%, and KMT2A a little bit lower just because they have a harder time with all treatments in general. How do, what's a good bar for success when you add on top of something that's already getting kind of 80%, or do we think about it in terms of durability, et cetera? Yeah, that's exactly right. At this point, with adding targeted therapies on top of these really good backbones, it's like, for instance, with the quizartinib trial, they didn't see a significant increase in the complete response rate. They saw a significant increase in the durability and the overall survival. It is looking for markers of that increase in the durability and the overall survival that are extremely important because it is hard to make an improvement upon an enormous CR rate in the backbone. That's why this MRD-negative CR endpoint becomes so important because it likely is one of the best markers to be looking at for that increase in durability and increase in overall survival. Gotcha. Thank you. I guess moving on to the unfit population, so the Ven/Az a, kind of what should we be thinking about for the Ven/Aza arm and what's the appropriate bar for Ven/Aza and kind of where do you want that to go? Again, around durability, how should we be thinking about that? Yeah. The VIALE-A study, which is still, you know, the premier source of information on that, puts the CR rate at about 38% for these patients. Obviously, people are used to seeing the mixed CRc rate where it gets you closer to 60%, but FDA is only focused on CR. You'd want to see about 40% with the Ven/Aza backbone alone. We do look to improve upon that 40% in the front line. Gotcha. Did we get any other doses with the updates? Like, did we get higher dose levels with the updates? When we share this data, you're going to be seeing for the first time the front-line Ven/Aza data because we did our dose escalation in the relapse refractory setting. You'll be seeing the Ven/Aza at the 600 mg dose level. Again, the safety and combinability is the first, second, and third thing you should be looking at because if you can't combine it well, if you have to keep reducing the venetoclax or interrupting the ziftomenib, it would be a problem. Luckily, these are not things we're seeing because it is so easily combined. Gotcha. There is no worry that, you know, physicians in the real world setting will end up dose reducing one of these components, whether it's. I think that's actually the goal. I think physicians would love to be able to back off on the venetoclax dosing, at least the amount of dosing per month, because we see that in the real world. It is very toxic, and these patients have a hard time with that and with infections and with bleeds and everything else. If we have a drug that can help get these patients into a response, help maintain them in their response, and you can lessen that backbone therapy, you're actually making a huge improvement for these patients. As we shared at a previous update, we got agreement with FDA to formalize a dose reduction for the venetoclax backbone in our pivotal trial so that we do not have to be adhering to labeled dosing and can go to a lower dosing over the course of the trial. Gotcha. How's enrollment proceeding as you kind of think about the Ven/Aza versus the 7+3 combination? Is there any kind of delta between the two? Is there anything to read between the lines? They are both keeping the team extraordinarily busy. It is, the enrollment rate is extraordinarily robust. It does appear that 7+3 is still the treatment of choice for the majority of these patients, but still the enrollment is incredibly quick for both patient populations, the Ven/Aza and the 7+3. Okay. Is there any reason to believe menin is going to combine better or generate better results with 7+3 versus Ven/Aza, or? Certainly not combine better. There's theoretically always been that assumption that maybe there's some synergy with venetoclax, but the populations are so different that you're not going to be able to compare head to head the 7+3 of the venetoclax patient populations, but they both do very, very well on treatment, and it's a very robust effect. What's the read-through from these studies to the front- line study? I mean, you mentioned the front- line data with Ven/Aza and 600 milligrams, but are there other read-throughs we should be thinking about triangulating between this data set and future data sets? It's really taught us a lot. I think, as you've seen with others developing in this space, it was the belief that it was venetoclax and azacitidine that was the preferred combination partner. Our data, our experience, and our investigators and KOLs have showed us that that is not necessarily true, that it really is both the 7+3 and the Ven/Aza that are extremely important to developing this molecule. That's one of the biggest read-throughs we've had from our trial in general. Secondly, it's the ability to get these patients on, get them into a response, and maintain them, at least for the NPM1s, in that response without necessarily having to go to transplant. These patients are doing overall, especially the NPM1s, extremely well not having to go to transplant. If you can avoid that toxicity, it's huge for this population as a whole. Gotcha. And then thinking about 17 or 017, kind of what are the timelines for initiation for that pivotal study? As we shared, we've obviously already had our regulatory interactions, and we hope to be fully operationalized and enrolling by the end of the year. Okay. What are the gating factors there? I was saying to Troy at one point, my team is going to kill me if we do not stop pressing them to do everything very quickly, all at once. It is really just operationalizing. It takes time to get the sites up. It takes time to get the contracting done. That is where we are now. We are in those bureaucratic hangups rather than any scientific jiggering or, you know, anything from our end. It is really just actually getting through the red tape. We're in the process of study startup. For big global trials like this, that can take a while. The contracting, the budgeting, just the, you know, the blocking and tackling that has to happen for a study to, for sites to open and a study to begin. That is why we did it as two studies in one, because now we only have to do it once rather than twice for Ven/Aza and 7+3. Yeah. No, it's a clever design. And just the rationale for the partner, so Kyowa Kirin, kind of how, what do they add to that process? Do they slow it down? Do they speed it up? Yeah, they definitely, they've been very additive. They definitely don't slow it down in any way. I mean, the first, I think, is obviously financial. You commented the trials, it's a clever design, right? You're doing two phase III studies under a single protocol. There's a significant, some significant operational synergies that I don't know we could have done alone with just the capital markets as our partner. That would have been challenging, particularly given we haven't shown front-line Ven/Aza data yet, right? We're starting a phase III when you and the market haven't yet seen the Ven/Aza data. Obviously, Kyowa Kirin has, the FDA has. That's part of it. In terms of operationalizing it, Kyowa Kirin has people on the ground in territories where we just have no hope. Europe, Asia, these are going to be global studies. Sometimes it's helpful to have someone there who can go and just physically walk around the site and help keep things lubricated and keep things moving along. We are, of course, driving global development. We're driving commercial strategy. Kyowa Kirin is, we're being very thoughtful with them about, you know, how can we work together to help move things forward. The final thing, Peter, is there's two additional opportunities that are under the collaboration in AML. One is in the front line FLT3 population. One is in the post-transplant maintenance population. Remember that those are also included under the collaboration. You'll see us take those on in due course. It really gives us the ability to compete effectively in all of the relevant segments of the front- line population. Gotcha. MRD-negative CR, that's changed the field and kind of, I guess, what drove that or all the new trials in front line, do you think going to be MRD-negative CRs? Yeah. You have to realize we've been thinking about this for, you know, four years and preparing for the idea of this for four years. The fact that it's actually come to fruition is, you know, a testament to the team and its preparation. Yeah, I think it will help change the field. I think it will help get these poor patients treatments more quickly. It's something that our KOLs are extremely excited about. I get texts regularly congratulating us and thanking us for helping to pioneer this. Gotcha. Okay. How should we think about interim analysis? When would you want, if there is that built in? We had previously shared that we will be doing, that we expect the data for the accelerated approval, that would be the MRD-negative CR in 2028. Okay. Perfect. And kind of the expectations of the control arms, whether it's for the MRD-negative CR rates or event-free survivals? Sure. Again, we're looking in the bone marrow for the MRD negativity. In the bone marrow with KMT2As, you're seeing in the 30%-ish area in terms of MRD negativity. And in the NPM1s, a little higher in the 40s. Depending on the mixture of patients we see, we expect to see about, for that control arm, you know, a 40% MRD negativity rate. Gotcha. This is like three minutes or so on the clock. I'd love to kind of pivot a bit to the diabetes program and kind of what we should expect to see over the next 6 to 12 months. Yeah. Our next goal is to nominate a development candidate for clinical development in diabetes. We have a range of potential candidates that we can choose. It's, you know, one has to kind of ask like what exposure do you want? Do you want it to be a menin degrader or just a menin inhibitor? We have all of it. We have all of the various flavors. I would look for us to nominate that candidate. We are currently evaluating different options of moving it forward into the clinic. We want to be mindful that we keep the company in a strong cash position and we maximize the value for patients and shareholders. We are running multiple options in parallel and we'll have kind of more to say about where we go beyond the development candidate in due time. Because the assumption would be it's probably not just your own spend as you go into something like that. Yeah, certainly. I mean, you could do some modest early clinical development, but I think it probably isn't appropriate for an oncology company to be considering doing mid to late stage diabetes trials, right? That's big pharma stuff. There is certainly an appetite for novel therapies in diabetes, as you know. Gotcha. Does the competitor menin drug, does that kind of help inform that process or are you looking more broadly? You take all the data into account. At the moment, I would say our, and we really only have preclinical data. Our preclinical data would not have us limit the utility of a next gen menin inhibitor to what they're doing. I'm not entirely sure why they're making those decisions. We think there's an opportunity in both type two and type one. That's part of thinking about, Peter, how you develop it clinically and commercially, you want to maximize the value. We'd also ideally be in a position where maybe you could take more than one menin inhibitor forward because for these big, you know, when you're talking about millions of patients, I think you really want to have the very best compounds move forward. We certainly have the chemical material. We have the, our chemical chemistry group is phenomenal. Now we just have to find the right way to translate it into the clinic. Gotcha. Degrader versus inhibitor, is that where are you in the? That's just, yeah, and that's just one example. I can tell you ziftomenib hits menin about as hard as it can be hit. It's not obvious to us you need to hit it quite that hard in diabetes. You may be able to dial it back. You may actually want to do that. Okay. That's perfect. Thank you so much. Our pleasure. Thank you. All right. Thanks, Troy. All right. Thanks, Troy.