All right, good afternoon, everyone. My name is Frank Tang, and I'm with the Investment Banking Division at Morgan Stanley. Before we get started, I'd like to read a quick disclaimer. For important disclosures, please see the Morgan Stanley Research Disclosure website at www.morganstanley.com/research-disclosures. If you have any questions, please reach out to your Morgan Stanley sales representative. All right, with that, thank you all for joining us today for the Fireside Chat with Kura Oncology. I'm joined today by Chair and CEO Troy Wilson and Chief Commercial Officer Brian Powl. For those of you who are not familiar with Kura, for those of us who are not, can you, Troy, give us an overview of where Kura sits today, your pipeline, your priorities heading into 2026? Sure, and thank you to you and Morgan Stanley for the invitation, Frank. It's been a productive conference. As we look at Kura, we have sort of several drivers to the business. The focus is developing targeted therapies for treatment of cancer. We are working across a range of different cancers. Most of the work, which we'll probably talk about today, is focused on acute leukemia with our Ziftomenib program, where we're really looking to potentially transform the treatment of genetically defined acute leukemias. We're also working on other solid tumors, including GIST, gastrointestinal stromal tumors. Our pipeline programs with FTIs focus in renal cell, lung, colorectal, breast, neuroendocrine, and then we also have an effort in diabetes. We sort of go where the science goes. We're very well capitalized. We had $630.7 million in cash as of the end of the last quarter. If we receive the milestones that we expect to receive under our co-development, co-commercialization agreement with Kyowa Kirin Co., Ltd. for our partners on Ziftomenib in acute leukemia, that would take us into 2029, which should take us through commercialization in frontline AML. Just to put that in perspective, our view on the initial commercial opportunity in acute leukemia is $350 to $400 million. If the market unfolds, as we think it will, given the data we have, the frontline opportunity is $7 to $10 billion for the class. We think our program, Ziftomenib, could take up to $3 billion of that. We're really working toward building a precision oncology company with multiple products, multiple approvals that actually work to help make existing standards of care that much better. Great. You have a lot going on. Going on. If we start with the broad kind of AML space, it continues to be large and competitive. Can you give us an overview of where Ziftomenib sits today, the clinical data that's been generated, as well as how you'd see Ziftomenib differentiating from other therapeutics in development? Right. Maybe we can take those answers just in a slightly different order, if we will. Where we are versus where we're going. In order to realize the commercial value that I described, $7 to $10 billion in peak sales, what you need to do is you need to be able to provide clinical efficacy for patients, but also safety and tolerability that allows them to take the drug as a chronic therapy. What will drive the market opportunity is duration of treatment. Because the patient population is roughly 20,000 in the U.S., we think menin inhibitors can address about half of that. Now, to your earlier questions, there are multiple menin inhibitors in development. We currently have an NDA under review with FDA. Our PDUFA action date is November 30. That review, by all accounts, is going well. As Brian and I'm sure we'll speak to here in a few minutes, we're ready to go from a commercial standpoint. That's the beachhead to get into acute leukemia. We have data building on that initial approval, which is in the relapsed refractory setting for patients who have NPM1 mutations, building on that initial data set and now moving into the frontline. We have a study called 007, 007, that is evaluating Ziftomenib in frontline combinations with approved standards of care in the intensive setting and the non-intensive setting. That data is very encouraging. What it says is Zifto is safe, it's well tolerated, it's easy to combine, and it's driving really meaningful activity. We provided a data update at the European Society of Medical Oncology Meeting in June in Europe. We'll provide an update here at the American Society of Hematology Meeting, ASH in Orlando, likely in December. That is feeding into, I mentioned, 007. That's the phase 1 studies. We should be starting 017, 017, which are two phase 3 trials under a single protocol. It's really kind of a first of its kind clinical trial that will be open, Frank, essentially to any patient in the frontline setting. That's going to be a global study. That will be, again, two parallel phase 3s, one in intensive, one in non-intensive, for which we have alignment with FDA on pathways to both accelerated approval and full approval in each of those two settings. In terms of the competition, I'll just say when you look at clinical activity, you look at convenience, you look at simplicity of administration, you look at safety, Zifto is best in class. You know we were very much kind of in a show-me state. As we continue to generate clinical data and hopefully looking forward to commercial launch and sales, we think that best-in-class profile will continue to show itself. I mean, safety is often viewed as a key differentiator here, as you said. Are you able to elaborate a little bit on what you've seen with regards to a differentiation syndrome, QT prolongation, and other AE versus some of the competitors? Yeah, let's take those in turns. Differentiation syndrome is something that gets talked a lot about. Differentiation syndrome is a phenomenon where when you're treating a patient with leukemia who has a lot of tumor burden and you begin that tumor differentiating, turning into normal cells, which is what you want, if you differentiate the entire tumor burden all at once, people have heard of tumor lysis syndrome, sort of a similar phenomenon. The body perceives that as shock and the patient can spiral out of control very quickly. The best way to treat it, and I'm now happy to say in all of our trials, it's well managed. We see a very low rate of even grade 3 differentiation syndrome. It's really education, it's usage of steroids. If necessary, you can give them a little bit of a cytoreductive agent to help manage it. I think for Ziftomenib, differentiation syndrome is in the past. It will be likely a black box warning for the class because it's the mechanism of action. Let's go to the other ones. There's really, Frank, three other things to think about relative to the competition. The first is I mentioned to you, we have no drug-drug interactions. That's important in this initial indication, NPM1-mutated AML. These are patients who are 60 to 75. They're typically on a number of concomitant medications, including azoles, which protect them from fungal infections. One of our competitors, in particular, has a very, very strong drug-drug interaction and QT prolongation, which can lead to sudden cardiac death as an associated dose-limiting toxicity. We have neither of that. We have no clinically meaningful drug-drug interactions. We have no clinically meaningful QT. We will not require regular cardiac monitoring for QT. In a setting, even in the relapsed refractory setting, that's going to be important. If physicians have a choice, our research tells us physicians will go with the drug that gives the best safety profile, the best simplicity, the best ability to not have to change or even monitor concomitant medications. I think we're well in sync. Yeah, that's great. Thank you. Shifting gears a little bit, Ziftomenib in NPM1-mutated AML has the PDUFA date, as you mentioned, in November. Can you give us an update on your commercial preparation plans as well as anything you can say about the anticipated approval? Sure, thanks. Thanks, Frank. Yeah, our team has been building our anticipation of this approval for the last couple of years. We are ready for a potential approval as that comes forward. We've been building out our organization to build the capabilities across, starting with the Medical Affairs team that we've had in place for a number of years, Market Access team, our Marketing team, Commercial Operations, and then our Sales team. We have a Sales team that we've hired and have been trained. They're a fantastic group of experienced sales reps, and they're out in the field already now doing some profiling, starting to engage with their customers, getting to know, getting to work with them, and understanding, kind of being ready in case as soon as an approval comes so they'd be able to engage. In addition to that, as Troy mentioned, our partnership with Kyowa Kirin Co., Ltd. Our partners in Kyowa Kirin Co., Ltd. also have a field force that's going to be working with our field force in tandem. We have the benefit of two organizations that will have a national field force that will help to reach these key physicians and potentially have a broader depth to see more physicians than we would with one company, but also see them more frequently. That gives us an opportunity to find the patients and get to those physicians as soon as we know there could be an opportunity for an NPM1 patient to be treated. We are, of course, waiting on our discussions that have been ongoing with FDA. We're waiting on that approval, but the team is ready to, if we get an approval, we'll be ready to get out very quickly upon that approval. Okay, that's great to hear. You mentioned the collaboration with Kyowa Kirin Co., Ltd. Perhaps we can just talk a little bit about that. Can you give an overview of that arrangement, that partnership, and understand a little bit more around how responsibilities are divided, especially as it relates to U.S. and U.S. commercialization development? Yeah, I'm happy to take that. It is a global co-development, co-commercialization relationship. Within that, though, Kura leads global development. Kura leads U.S. commercial strategy. Kura books all U.S. sales. We very much value our partners at Kyowa Kirin. For us, this program is live or die. We are the lead party here in the U.S. The trials that I mentioned to you, the Comet-017 trials, are global trials for full approvals in the frontline setting. We led the design of those trials. We're leading the operational aspects. I'll let Brian speak to how the organizations work together a bit more commercially. Another key component, Frank, is Kyowa Kirin provided a $330 million upfront payment. What we've said is $475 million, I believe, in near-term milestone payments. Sorry, $420 million in near-term milestone payments. We received $45 million when the NDA was submitted. We are in a position to receive the balance of that, which is, I think, $375 million here in the next couple of years. That's intended to fund the development in those frontline indications that I mentioned. We're in a position where, as we incur expenses, particularly in development, those expenses are offset by anticipated milestone payments. In that context, that's what gives us confidence that we should, we can have cash guidance out to 2029 because we have very good line of sight on those milestones. Brian, maybe you can speak any more to how the two organizations are working together in terms of decision-making and whatnot from a collaboration perspective. Sure. Yeah. We've had a very good relationship with our partners since the deal has been signed. As Troy said, we built the structure of this partnership to really help us support the fully integrated commercialization capabilities of Kura Oncology while also building on the partnership that we have with Kyowa Kirin Co., Ltd. As I said, our team has been built out to support the functions across medical, market access, marketing. We work with them on their teams on a number of these functions. Our team is kind of leading a lot of the elements of the commercialization aspect. They do partner with us as thought partners, thinking about the best ways to get to patients. They have some capabilities that we're learning from and working with them and relying on their capabilities around some of the patient finding capabilities, data mining, all of those types of things in order to get to patients. They've got really great experience in the rare disease space that we're capitalizing and working with them on. Our field teams are partnering together. They're going to be launching as one group out to engage with the teams. We've had a very strong collaboration with the teams, been working well with them. They recognize the AML expertise we've brought in, and they also have their experiences helped us as well. Great. Thank you. Troy, you had mentioned earlier that you guys are obviously pursuing frontline. You've initiated two phase 3 in the frontline AML populations. Can you walk us through those designs as well as the enrollment strategy? Sure. Yeah. Those two trials fall under a single protocol, which we've called Comet-017. Each of them are placebo-controlled, randomized phase 3 trials. You can think of them as triplets. In the intensive setting, these are patients who can tolerate intensive chemotherapy. We are evaluating the regimen of 7 plus 3 plus Ziftomenib versus 7 plus 3 versus placebo. The FDA has agreed to a novel design where there's the potential for accelerated approval based on an endpoint that is called MRD negative CR, rate of MRD negative CR, and then a survival-based endpoint of event-free survival. The significance of the MRD negative CR accelerated endpoint is the following. With 7 plus 3, we see relatively high response rates, CR rates, in excess of 70%. The issue that you're trying to address in frontline AML is, although you'd love to see higher response rates, what ultimately you're trying to solve for is even among patients who respond, more than half of them go on to relapse within three years. Once they relapse, they have a very difficult sort of treatment journey. If we can delay that recurrence, if we can drive deeper responses, that's the goal. MRD stands for measurable residual disease. You can have a CR in AML and still have 5% blast counts. What MRD negative means is that to the limit of detection of the assay, typically 10 to the minus fourth or 10 to the minus fifth, we can't detect any leukemic cells. There is now very strong data that associates MRD negativity with survival. The FDA is open and worked very closely with us to design a trial where we'll assess MRD negativity in both populations if that's clinically meaningful. The 7 plus 3 delivers about 40%, 40 to maybe 47% as assessed in bone marrow. We're looking to do clinically meaningfully better than that. We've guided, Frank, we could have that top line result in 2028. Shifting gears to the non-intensive trial, there the CR rate is lower. It's typically with venetoclax and azacitidine, which is the standard of care. It's typically 40 to 45%. You're looking to do clinically meaningful. You want a full CR, so disappearance of disease as well as full count recovery. The full endpoint will be overall survival. The best metric for how to think about that is a trial that's called VIALE-A, which is venetoclax and azacitidine. You talked about enrollment. As we were designing these trials, we went out to a number of sites and asked them. We said, "Listen, you know this is a competitive space. There's multiple sponsors. How do we win you over? How do we become your best partner?" What the sites told us was, "Put the two trials under one because for them, you know even the large sites, they can only take on one phase 3." What we've done is we've given them essentially one-stop shopping. With a single protocol, they can enroll nearly any patient who walks into their clinic in the frontline setting. They have only one protocol, one budget, one site initiation. We'll do 150 to probably 190 global sites. What it's allowed us to do is to get exclusivity with many of the leading sites, not only in the U.S. but worldwide. That was back to what was the rationale for the partnership with Kyowa Kirin Co., Ltd. We knew that as a small company, we needed to be able to out-execute the competition in the frontline setting. Whoever gets to the frontline first has a tremendous advantage. This innovative trial design of two phase 3s is different than what any of our competitors are doing. What we've heard from the sites is it should really pay dividends in terms of enrollment. We're seeing that with 007. 007 is the phase 1 version of what I just described. We've enrolled more than 100 patients in just a handful of sites in both the intensive and non-intensive setting. You should see us. We've guided that we'll start 017 in Q4. We're on track. Everything's going well. As I've said to people, it doesn't matter when you start. It matters when you finish. It matters the quality of your data. I think we're very well positioned. That's good to hear. We talked a lot about combination approach here, but how do you expect these trials to complement a monotherapy approach? How do you think about monotherapy fitting in? Yeah, so the monotherapy obviously is our first foray into the commercialization space. It's really the entry point for any therapy really in the AML space to get a foot in the door. We know that this is going to be a competitive space given that there will be other competitors likely that are menin targets that are approved in this space, probably very closely to us. There are also other therapies that these patients have opportunity to receive. Some of these patients are co-mutated with either a FLT3 mutation or IDH mutation. They may have opportunity to receive venetoclax in the relapsed refractory space as well. We know it's going to be a very competitive space. We think that the profile that the venetoclax offers, that Troy mentioned, around having good, strong efficacy, delivering durable responses with good safety, being able to combine and not dose reduce a lot of, you know, for a lot of patients, as well as a simple, single once daily oral opportunity. That really helps to position it as a potential differentiator and a potentially, we think, best-in-class therapy for here. The data generation strategy that a lot of our teams have been building around other combinations, Troy mentioned KOMET-007. We also have another study, KOMET-008, which is looking at a couple other combination approaches, including FLT3 inhibitors like gilteritinib. As those data come forward, we think that also will help physicians to be educated around the potential to combine with other therapies. That will, of course, not be a focus of our commercial promotional team, but we will make sure that the data are available for physicians because of the physicians we've been speaking to over, particularly since we presented the 01 data at ASCO. They're very enthusiastic about the role of menin in this NPM1 space. A lot of the physicians are very excited to be able to have that take use their discretion to use it in combination with other agents as well. Our goal will be able to educate them on that. We think that the entrance in the monotherapy space is our first step where we'll be able to engage and really start to build that strong reputation in this space while also enrolling these studies that will help us to supplement and hopefully get to where that real opportunity of having the biggest impact on patients is in the frontline. Absolutely. Thank you. Beyond Ziftomenib, you have a lot going on in terms of your FTI programs. Can you give us an overview there and what near-term data readouts investors should watch out for? Yeah. We'll actually be hosting an investor analyst event, a virtual event. I believe it's next week. It's available on our website to help share the scientific rationale, the preclinical data, and set expectations for a clinical update at the European Society of Medical Oncology in Berlin in October. That clinical update at ESMO will be meaningful. If we step back, you know, what problem are we trying to solve? We have been working for a number of years on a target called farnesyltransferase. Farnesyltransferase is one of the very first targets ever explored in oncology. It predated EGFR. It was developed before there were any targeted therapies. It was developed before next-generation sequencing existed. I would tell you it was the right target at the wrong time. If you bring it now fully forward, I think it will end up being an ideal combination agent with three big classes of targeted therapies: tyrosine kinase inhibitors, PI3 kinase alpha inhibitors, and KRAS inhibitors. Each of those classes of targeted therapies, you know, they work. They drive responses in patients. However, some fraction of patients don't respond. Even among the responders, many, unfortunately, develop resistance and go along to progress from their metastatic disease. Why is that? Resistance, innate and adaptive resistance. Tumors are very, very good at developing resistance to targeted therapies. It so happens that farnesyltransferase targets a protein called Rheb. Rheb controls something called TORC1 in the target of rapamycin complex. Within TKIs, PI3 kinase alpha and KRAS inhibitors, they all have a common mechanism of resistance, and FTIs address that mechanism. The total addressable market opportunity, when you look across renal cell carcinoma, neuroendocrine tumors, breast cancer, endometrial, urothelial, cervical, colorectal, lung, you're talking about a TAM greater than 200,000 patients in the U.S. just for the FTI program. What we're looking to show you in our two virtual events is the preclinical data that supports what I've said, right? Do you actually, are you able to overcome innate and adaptive resistance? From the clinical data, we're going to show you three of the four phase 1 trials ongoing are new FTI, KO-2806 as monotherapy. That will show you it's safe, it's well tolerated, we have the right dose, is it active in particular HRAS mutant patients, which is where one of the few places you would expect an FTI to be active as a monotherapy. We're then going to show you two combination trials, KO-2806, our new FTI plus cabozantinib in renal cell carcinoma, and our first generation FTI called tipifarnib with a drug, Novartis's alpelisib or Piqray, in PI3CA mutant head and neck. Within RCC, we know cabozantinib delivers 25% to 28% response rate in a cabo-naive population. We've seen now with the HIF2 alpha inhibitors in combination, we'll see response rates of 31% for belzutifan, 46% for casdotanib. You want to see that you're in that same zip code in combination. You also want to see, Frank, that you can overcome resistance. Can we take a patient who has failed cabo or maybe best response of stable disease and actually drive a response, right? That'll be meaningful. In the head and neck context, think of PI3CA mutant head and neck as a proxy for those other tumor types. PI3CA is the second most frequently mutated oncoprotein in human cancer. Alpelisib generates really only stable disease. Tipifarnib is inactive. If you put them together, the question is, does one plus one equal three? Are we seeing deep, durable responses? If so, now we step back. We have, I think, a very strong case for a go-it-alone strategy with TKIs. We can build on cabozantinib is continuing to gain market share in RCC and has opened up neuroendocrine. There are many companies pursuing both PI3 kinase and KRAS, all of whom have the same problem, right? They all have resistance. We'd like to work with more than one of them, if possible, to take their very good targeted therapies and make them that much better. The hope of the ESMO update is people look at this and say, it's been worth the wait. You have a separate, second, independent program with a very large addressable patient population, and we're excited to see what comes in 2026. That's great. We'll be looking forward to that. You've also discussed next-generation menin inhibitors for diabetes. Can you discuss that program and your development strategy with respect to cardiometabolic diseases? Sure. Menin is the gift that keeps on giving. Brian and I talked about what we're doing with Ziftomenib in acute leukemia. We have Ziftomenib in a trial with imatinib in gastrointestinal stromal tumors. That trial is in dose escalation. Again, you see variations on a theme here. It turns out that menin controls KIT overexpression in GIST. The challenge with GIST is you go from one KIT inhibitor to the next to the next to the next with ever lower response rates. It turns out by shutting down KIT overexpression in preclinical models with a menin inhibitor, it's highly synergistic with any KIT inhibitor. Hopefully we'll be in a position to share clinical data with you on GIST in 2026. That alone is a blockbuster opportunity on its own. Now jumping to what you asked about, which is diabetes, menin also, it was observed that in pregnant women who develop gestational diabetes, the way their bodies respond to that, or one of the ways, is they downregulate menin. Menin actually controls the growth and proliferation of pancreatic beta islet cells. By blocking menin in preclinical models of diabetes, by inhibiting menin, and we've done it with a whole range of different menin inhibitors, one can lower blood glucose, one can increase insulin production, restore insulin sensitivity, and importantly, selectively expand pancreatic beta islet cells. Where I think you'll see us go, Frank, is type 1. Type 1 is a very significant opportunity. One is going to have to contend with the autoimmune component of that, but we've got very strong preclinical data. You're going to see us do something creative, not tap Kura's, although we have a strong cash position. It is still finite. You're going to see us, I think, hopefully do a creative way of advancing one or two menin inhibitors in diabetes and cardiometabolic disorders. That's a whole, you know, very unique kind of completely new take on type 1 and potentially type 2. Let's start with type 1. If you can show that you can increase C-peptide in type 1 diabetics and really expand pancreatic beta islet cells, now you're on to something. Potentially there's a play in cardiometabolic, sorry, in type 2, as well as other cardiometabolic, but one step at a time. We've taken the last several years to optimize a development candidate, which we announced we had nominated last quarter. It is actually quite different than Ziftomenib, and it's tailor-made for these diabetic indications. That's great. Thank you. Sure. To close out, could you summarize and leave us with the most important milestones and updates that investors should be focused on for the remainder of the year into 2026? Yeah. Maybe in order of importance rather than chronological order, obviously the NDA. Hopefully, we have a positive decision from FDA. We get approval. We go to commercial launch. We become a fully integrated research, development, and commercial company. You will see us present data for Ziftomenib in AML at ASH, both in the frontline setting with venetoclax as well as in the relapsed refractory setting with venetoclax, and presuming we're accepted at ASH. You will see us, as I mentioned, present data from multiple phase 1 trials in October at ESMO. You'll see hopefully data now rolling forward. We're going to be out in the market. You will see us start—sorry, I skipped over. We're going to start the phase 3 studies. Let's not forget that, the frontline studies. You're going to see us selling into the market. Hopefully, you'll see data with gilteritinib next year. You'll see the KRAS data next year with our FTIs. You'll see potentially GIST data next year. You'll see more that this diabetes opportunity come to pass. There's a lot of ways in which we can create value, and we're in a strong cash position. I think at some point, we will be potentially open to raising additional capital to further build our pipeline, but for the foreseeable future, we have what we need. We are purely in execution mode. It's going to be an exciting 12 to 24 months. Absolutely. That's all the questions I had. I'd like to thank everyone for joining us today and look forward to our next conversation. Thank you so much for the opportunity.