Good day everyone. My name is Jenny, and I will be your conference operator today. At this time, I would like to welcome you to Kura Oncology's 2026 IKCS investor event. All lines have been placed on mute to prevent any background noise. After the speaker's remarks, there'll be a question- and- answer session. If you would like to ask a question during this time, and if you have joined via the webinar, please use the raise hand icon, which can be found at the bottom of your webinar application. To allow everyone the opportunity to participate, we ask that you please limit yourself to one question and then re-enter the queue for any follow-ups. At this time, I'd like to turn the call over to Troy Wilson, President and Chief Executive Officer of Kura Oncology. Please go ahead, Dr. Wilson. Thank you, Jenny. Hello everyone. Today we're delighted to share with you some updates that were presented at the International Kidney Cancer Symposium that's being held over the next couple of days in Paris, France. This relates to the ongoing study evaluating darlifarnib and cabozantinib in patients with kidney cancer. If we can go to the next slide, please. In today's presentation, we're going to be making forward-looking statements. I would refer you both to our filings and our website, our SEC filings and our website for more information about Kura Oncology and the risks and uncertainties of an investment at this time. I'm joined on today's call by two participants. Dr. Ayana Buckham is Assistant Professor of Hematology Oncology and Medical Director of the Genitourinary Medical Oncology Research at Oklahoma Health Sciences Center. Also joining us today is Dr. Mollie Leoni, Kura's Chief Medical Officer. Both of them are going to be presenting slides through this presentation. This is an incredibly exciting and dynamic time at Kura. We are squarely focused on the launch of our first commercial product, KOMZIFTI, which was approved just last year in relapsed refractory NPM1 mutant AML. We're looking forward to giving an update on how the launch is going at our earnings call next month. We're also broadening out the opportunity with ziftomenib, or KOMZIFTI as it's known commercially, to be able to treat up to 50% of AML patients. What we're here to talk about today is one of our pipeline programs, and we have a thesis at Kura that cancer is best treated in combination. We'll talk more about that today, but as you'll see, with both our MENIN inhibitors and our farnesyltransferase inhibitors, we're advancing innovative therapies that I think have the potential to combine with other agents to really drive better outcomes for people with cancer. If we can please go to the next slide. We call these precision combinations, and if we can go to the next slide. On the left-hand side, you can see the combinations that we're undertaking with ziftomenib. Many of these are familiar to you. We're of course evaluating ziftomenib in acute myeloid leukemia, both in the relapsed refractory and in the newly diagnosed setting. Importantly, we'll be giving an update on the intensive chemotherapy combination in newly diagnosed patients, middle of this year. We're looking toward a publication, with the non-intensive chemotherapy combination, to be published a little bit later this year. Then finally, we'll give an update on the FLT3 combination, specifically with gilteritinib in the relapsed refractory setting. Our view is and always has been, while MENIN inhibitors offer tremendous promise, we want to move them forward and move them into combination as quickly as we can. Continuing that theme, we've got ziftomenib in GIST, and we're looking forward potentially to an update next year for that program. On the right-hand side, if we can go to the next slide, we're going to focus today on our pipeline program, darlifarnib, which is just now beginning to come into its own. Specifically, as you know, we're evaluating darlifarnib in two contexts. Today, we're going to talk about the data combining darlifarnib with cabozantinib, which of course is an anti-VEGF receptor inhibitor. A little bit later this year, we're looking forward to sharing with you the darlifarnib data in combination with adagrasib, which of course is a KRAS G12C mutant-specific inhibitor, and there we'll be showing you data in lung, colorectal, and pancreatic cancer. This idea of precision combinations is not new, but we think it's really the right way to go. Cancers use a number of different mechanisms to be able to grow and evade and metastasize everything from genomic instability, inducing angiogenesis, avoiding immune destruction, and our view is, and our focus is to develop therapeutic agents that can combine with other therapies. If we go to the next slide. That's in fact what we've seen in renal cell carcinoma, the evolution of treatments in kidney cancer, and Dr. A is going to speak to this as he goes through the data slides. Initially, the first approvals were with classical immunotherapy, then we saw a wave of tyrosine kinase inhibitors, as well as mTOR inhibitors. Now, increasingly, we're seeing doublets and triplets. That's in fact where we anticipate darlifarnib will go, ultimately is in combination. We think it's important to demonstrate the mechanism of action and validate that, as well as to get a sense of what is the safety, tolerability, and activity as we think forward. Mollie will be able to speak to this as she goes through our strategy, building on this initial data. If we go to the next slide. Darlifarnib, as all of you know, is our next-generation farnesyltransferase inhibitor. We've been working on farnesyltransferase really since the inception of the company. Darlifarnib is as good as it gets as far as a farnesyltransferase inhibitor is concerned. Extremely potent, has great safety and tolerability. We took everything we knew about Tipifarnib, and we optimized it. We're really delighted. We did share some data, some early data from the Phase 1a study late last year. This is now an update of that data, and ideally, we'll provide yet another update here in kidney cancer a bit later this year. If we go to the next slide. These are the last couple of slides before I turn it over to Dr. A. What's the rationale here? Well, we know that cabozantinib and other tyrosine kinase inhibitor therapies block various signaling pathways. In particular, they block VEGF receptor, but they also block PDGFR, they block other targets as well. TKIs have become a mainstay of treatment in kidney cancer. They're used throughout the treatment continuum. The challenge is, once TKI therapy fails a patient, the treatment, either with the same TKI or another TKI, or really any subsequent treatment, is reduced. There's a significant need to be able to either drive deeper, better responses, or ideally to resensitize patients to treatment with these TKIs. If we go to the next slide. That's really where darlifarnib comes in. Darlifarnib acts in this context, in renal cell carcinoma, by blocking a protein called Rheb. Rheb is Ras homologue expressed in brain. The significance of Rheb is that Rheb controls the transport of mTORC1. mTORC1 is one of the two mTOR complexes that sit at the bottom of the MAP kinase pathway. When you defarnesylate Rheb can no longer get mTORC1 to where it needs to be. What that does effectively is it provides a second complementary block on the signaling pathway. Each of the targets that these TKIs are targeting are signaling through these signal pathways. One has the ability. If we can go to the next slide. Once we introduce the combination, for example, of cabozantinib and darlifarnib, one can see you're blocking at the receptor level, you're also blocking down much further in the pathway. The consequence, as we've seen both pre-clinically and clinically, is you get less angiogenesis and tumor death. We've validated this. We have presentations available on our website, and that have been put in the published literature on the mechanism of action and preclinical data with various combinations. I think it's important to generalize these results. What we're going to show you today is the specific combination of cabozantinib and darlifarnib, but what we've seen, at least pre-clinically, is that these results are generalizable to any tyrosine kinase inhibitor. As we talk about, we've been quite encouraged by the safety, the tolerability, and the clinical activity that you're about to see. If we go to the next slide, I'm going to turn it over to Dr. A. to walk us through the slides. These slides were presented by Dr. Zakharia in a poster presentation at IKCS. Dr. A. is kind enough to present the slides and put them in the appropriate context. Dr. A., I'll turn it over to you. Thank you. Good morning, everyone. My name is Adeyemi Onabanjo. I'm a GU Medical Oncologist at the University of Oklahoma. On behalf of the FIT-01 team, I'm happy to present the data and give you a perspective on how things are moving along in this trial. Next slide, please. Briefly, disclosures all pertaining to research or consulting and advisory roles. Next slide, please. The FIT-01 trial is a Phase 1a/1b dose escalation, dose expansion study, and that evaluated both darlifarnib monotherapy and darlifarnib monotherapy plus cabozantinib. Now, the darlifarnib monotherapy, the dose escalation cohort was not in renal cell carcinoma. It was in predominantly RAS-mutated tumors. What we found was that it was an efficacious drug and also safe, and the recommended dose for expansion was around 8 mg-10 mg. We moved on to the dose escalation trial, and then this was when we combined it with cabozantinib and evaluated renal cell carcinoma patients. This is the portion of the study that we're talking about today. In order to evaluate the safety, we started off at a lower dose of cabozantinib at 40 mg, which is a lot more tolerable but not as efficacious as the recommended dose, which is cabozantinib at 60 mg. The study started at darlifarnib at 3 mg, escalated to 5 mg, 8 mg, in addition to cabozantinib 40 mg. When that was considered safe and we did not meet our DLTs, we moved ahead to the second part of the study, which looked at the ideal dose of cabozantinib, which is 60 mg, in combination, again, with escalating doses of darlifarnib to 3 mg, 5 mg, and 8 mg. Currently, the study has moved on to the expansion phase, where cabozantinib at 60 mg is being evaluated with darlifarnib at 5 mg and 8 mg. Next slide, please. In the dose escalation, our patients were a mixture of patients who were cabozantinib naive and cabozantinib resistant. For this talk and the poster that's being presented by Dr. Zakharia in IKCS, it was focused on those patients who had been cabo-exposed. All these patients had prior line of cabozantinib or some TKI during their course. About 67% of patients had exposures to other TKIs apart from cabozantinib, and almost 56% or half of these patients had cabozantinib as their immediate prior line of therapy, and all had progressed on cabozantinib. About 56% were what we would consider cabozantinib refractory. A total sample size of around 18. A small population, but still an important population to evaluate. Pretty evenly distributed from all the different cohorts. Important to highlight that a predominant portion of this study includes patients, about 15 of the 18 patients, had cabozantinib at 40 mg, not at 60 mg. Next slide, please. Overall, the safety profile was pretty consistent and tolerable. For the safety profile, we look at the whole dose escalation patients, not just the cabozantinib refractory patients. Here, what we found was that darlifarnib was a pretty tolerable and safe regimen. Now, if you look at any Grade 3 AEs, the most common ones were neutropenia, fatigue, and diarrhea. For the Grade 3 or more AEs from darlifarnib, neutropenia and anemia were by far the most common. Now, it's important to understand that while neutropenia has increased, it is an expected event from farnesyltransferase inhibition, and it is also something that's easier to manage. In comparison to the other side effects from cabozantinib, which are discussed elsewhere in the poster, what we are showing here is that darlifarnib did not add to the toxicity profile of cabozantinib. Neutropenia, anemia, and thrombocytopenia, while are AEs, are usually asymptomatic to the patient's perspective. It did not lead to any significant deterioration in quality of life, which is very important in this patient population. Next slide, please. Overall, darlifarnib was well-tolerated. There were obviously some dose reductions, predominantly due to cytopenias, predominantly neutropenia. There were interruptions in about 60% of patients, but most of them were able to continue on it. 13% had to dose reduce the darlifarnib. A good portion were able to go back without any discontinuation or dose reduction in the darlifarnib. Overall, the number of patients who needed discontinuation of darlifarnib was around six patients, so four out of the 70, so a pretty good number. In comparison, cabozantinib needed dose reduction in about 26%. Cabozantinib needed to be interrupted in about 70%. To put it in context, other trials that have looked at cabozantinib, like the recent LITESPARK-011 trial or the CONTACT-03 trial that had cabozantinib as the control arm, had about dose interruption in about 90%-100% of these patients. We know cabozantinib longer duration is toxic and can have some AEs. Within that context, I think this is pretty reassuring in terms of the tolerability of darlifarnib and how we're able to manage the AEs that arise from it. Next slide, please. The clinical activity is pretty encouraging. What we noticed was that in these 16 patients, about 15 of them had disease control rate, so a disease control rate of about 94%. What was even more promising is that the objective response rate in this population was around 44%. To put it in perspective, these are patients who had prior line of cabozantinib. About 60%, 56% to be precise, had cabozantinib as their immediate prior line and had progressed on cabozantinib. Even among those patients, we had a good amount of response. four out of these seven responders who had cabozantinib as immediate prior line of treatment had an objective response rate on this study. In that context, pretty promising objective response rates of 44%. Next slide, please. What is even more interesting is that the objective responses that were seen on this study seems to be seen along multiple doses of the darlifarnib. You can see darlifarnib at 3 mg also having significant partial responses, and darlifarnib at 5 mg and 8 mg also follow. Now, what's also important to understand is that most of these patients were on cabozantinib 40 mg, as depicted by those polka dot bars. Very few patients, as in the solid bars, were patients who had cabozantinib at 60 mg. Why this is important is that we know cabozantinib 60 mg has a better objective response rate than the 40 mg. It's interesting to see that this combination in a cabozantinib pre-treated or a cabozantinib refractory population still has considerable responses at the lower dose of cabozantinib at 40 mg, which is also the more easier to tolerate dose of the cabozantinib. Next slide, please. Duration of response is still evolving. We don't have a long-term follow-up as of yet, but it's important to note that many of these patients continue to respond. We have a follow-up of around 50-56 weeks for the longest patient in this cohort. The responses do seem to be durable, but we will need to wait to see how durable these responses are in the long term. What we are seeing is that a slow evolution of disease that goes from stable disease to partial response. Some people with partial response pretty early on in the disease course. What we have not identified is a long duration of stable disease before we see a response. Most patients had a partial response by the eight to 10-week mark around the first couple of scans. Important to note that so far the responses do seem to be durable, but long follow-up is required. Next slide, please. We'll highlight a couple of different patient vignettes for us to put this in perspective. This is an 80-year-old patient with clear cell RCC diagnosed in 2022, starts frontline treatment with nivolumab and cabozantinib, with a best objective response of stable disease, was on this treatment from around 2023 - 2025. His initial study treatment was on June of 2025, so about three years after he was on nivolumab and cabozantinib. Gets started on cabozantinib 40 mg and daralizumab 8 mg. At week eight he did have a partial response. He had 36% reduction at eight weeks, and these responses seem to be durable. His last scan at 16 weeks shows a partial response with a RECIST score of 32%. Patient continues to remain on treatment, and this highlights that despite progression on cabozantinib as prior line of treatment, patients continue to respond at the lower dose of cabozantinib without significant side effects. Next slide, please. This I think is a little bit more relevant to the ongoing discussion. Here again, another, a younger patient, 53-year-old female diagnosed in 2021, gets started on frontline immune checkpoint inhibition doublets with nivolumab and ipilimumab, progresses to nivolumab and cabozantinib. This was done before we knew that IO beyond progression is not meaningful. Importantly, this patient also had HIF inhibition with belzutifan, the FDA-approved HIF-2 alpha inhibitor, and she subsequently started study treatment in October 2024. What's important is that in this heavily pretreated patient population, prior IO doublet, prior cabozantinib, and prior HIF-2 alpha inhibition, the belzutifan at the lower dose of 3 mg and the cabozantinib at a lower dose of 40 mg caused a PR about 38% reduction at week eight and continues to evolve with a 53% reduction at week 48, indicating an ongoing response in this heavily pretreated population. Pretty promising responses, pretty good safety profile that has got us excited about this novel combination. Next slide, please. This is a little bit exploratory. We're always taught not to make cross-trial comparisons, but in oncology we always end up making cross-trial comparisons, and this is one such scenario. Not to highlight the superiority of any such regimen, but to highlight the tolerability and the safety profile of these different regimens. There has been Phase 2 trials looking at lenvatinib-everolimus showing that they had better outcomes. There was a recent LenCabo trial that was presented at ESMO last year that looked at lenvatinib-everolimus in a randomized manner, and importantly, the control arm on that trial was cabozantinib in a cabozantinib naive patient population. In that trial, what they did show was that cabozantinib objective response rate in a naive patient population was around 40%, and it was inferior to the superior objective response rate of lenvatinib-everolimus. Making big jumps, it's interesting to see that the combination has an objective response rate of 44% in a cabozantinib refractory population compared to cabozantinib monotherapy of 40 and odd responses in a naive population. What's important to understand is that the safety profile seems to be a lot more tolerable. I would want to focus your attention on the second column, which is lenvatinib plus everolimus, an mTOR inhibition combination doublet with TKI and the durvalumab combination to look at the different safety profiles. What we are not seeing here is an increasing toxicity profile from the combination. We are definitely not seeing a significant amount of pneumonitis, arthralgia, and other side effects that we see with everolimus. As demonstrated in the preclinical rationale, the selective mTORC1 modulation via the REDD1 pathway does seem to avoid certain side effects that we don't want while still retaining the efficacy that we want. Next slide, please. Overall, I think it is a very good combination that has a proven safety and tolerability profile. We will need to wait for longer follow-up to evaluate the durability of the responses. It's important to highlight that even in this heavily pretreated population, in this population of patients who are cabozantinib refractory, we had an impressive objective response rate of 44% with a disease control rate of about 94%. The study is now actively enrolling in the expansion phase, which is looking at cabozantinib naive patients in combination, and we're excited to see how the study will fit in the evolving landscape of RCC. Next slide, please. Thank you. All right. Thank you, Dr. Ayana Buckham. With that, I want to discuss the company's next steps. These data are spectacular and we have to ask ourselves, what's next? We are currently in our dose-refining Phase 1b. It is a randomized trial enrolling into two different darlifarnib doses, the 5-mg and 8-mg, as well as a cabo monotherapy arm, where, upon progression, patients can then roll over onto the darlifarnib combination. These patients will have seen IO but be cabo naive and with no more than three priors. Endpoints will include response rate, durability and of course, safety. Going to the next slide. These data encourage us to move forward exploring second-line plus and demonstrate a novel mechanism to add to the RCC armamentarium. We are currently enrolling into this randomized Phase 1b and expect to be able to share data next year. We are excited to be exploring an option for the IO refractory patient population. There are limited options for patients that have progressed on IO HIF-2 alpha combinations, and adding darlifarnib to these combination backbones provides new options for patients. We recognize that the field is appropriately moving to combination approaches in the advanced setting. As HIF-2 alpha continue to move towards the frontline, we believe darlifarnib combinations offer a potentially new way to address disease after failure of HIF-2 alpha. We believe that darlifarnib and cabozantinib have the potential, as a combination, to establish a new standard in IO-refractory second-line-plus clear cell renal cell carcinoma. With that, I will turn it over to Troy. Thanks, Mollie. We can go to the next slide. As Mollie said, we're really pleased with this data. This is just the first of multiple data updates on our precision combinations. You can see them laid out here. It's going to be an eventful year. From our perspective, we couldn't be happier. We have a strong launch. We have outstanding execution on the Phase 3s, and we have a lot of upcoming clinical data of these precision combinations that will help us figure out how do we position them in order to achieve the best outcomes for patients. In particular, I'll draw your attention to. This is the kidney cancer side of the darlifarnib story. We expect to present to you the KRAS side of the story here before too long, in the context of an upcoming major medical meeting. With that, if we can go to the next slide. We're happy at this point, Jenny, to turn it over, and open it up for questions and answers. We will now move to our question- and- answer session. If you have joined via the webinar, please use the raise hand icon, which can be found at the bottom of your webinar application. When you are called upon, please unmute your line and ask your question. We will now pause a moment to assemble the queue. Again, we ask that you please limit yourself to one question. You're welcome to re-enter the queue for any follow-up questions. Our first question comes from Charles Zhu with LifeSci Capital. Please unmute your line and ask your question. Hello, and thank you very much for taking my question. Congrats on the data. Recognizing that these data are from about 4.5 months ago and not that many patients were evaluable at 60 mg Cabo combinations, could you talk about the decision to expand at some of these 60 mg Cabo combinations? Maybe what you've seen. Is there a potential to see enrichment in response rates as you treat patients at these higher doses and potentially introduce prophylactic G-CSF? Thanks. Yeah, Charles, thanks for the question. I'm going to ask Mollie to speak. You have a couple of sub-parts in there, but Mollie can take the question. Yeah. I just want to remind you that what we're showing you here are the patients that had already seen cabozantinib therapy, so it is not the full data set. By the time we got to the 60 mg portion of that dose escalation, we were not enrolling patients that had seen Cabo previously. That's why you see less data at the 5 and 8 60 mg combination doses. When we present the updated Phase 1b data a little bit later this year, you'll see the full patient profile. You'll see all the patients that were treated, and it'll be clear to you why we think that the 60 mg dose with either 5 mg or 8 mg of darlifarnib makes the most sense. With regards to your safety-related question, now that we're done with the dose-limiting toxicity portion of the trial, meaning we're done with kind of the initial dose finding and safety portion, we'll be able to do prophylactic treatment. We will be able to use G-CSF or give a transfusion, et cetera, in order to mitigate these events. I expect patients to be able to stay on at least as long, if not longer, and again, continue to have an easier time on treatment, because we'll be able to use prophylaxis. Next question. Our next question comes from Jonathan Chang with Leerink Partners. Please unmute your line and ask your question. Hi, guys. Thanks for taking my question. Maybe for Dr. Adeyemi Onabanjo, where do you envision darlifarnib fitting into the RCC treatment landscape, and how has that changed with HIF-2 alpha inhibitors? Thank you. Thanks for the. Dr. A? Yeah. Thanks for the question, and I think it's an important question, and it's something that's very promising from a treating a kidney cancer doc, because now we have a lot of options. I think the landscape is evolving, and it's evolving really quickly, and we're going to change how we do stuff over the next few years. We have seen in the LITESPARK-022 trial that looked at adjuvant therapy with HIF inhibition, pembrolizumab plus belzutifan. We know that there are frontline trials looking at IO combination with HIF-2 alpha inhibition. There's also a triplet approach, IO plus TKI plus HIF-2 alpha inhibitors in the frontline setting. Triplet therapy in frontline kidney cancer has been an elusive strategy. This is not the first time we've tried it, but we've not had success before. Maybe things will change, and we will move on to combination therapies. As of now, I would argue that there is a combination therapy that's recommended in the frontline setting, and two important trials have looked at combination therapy against the best TKI second line that we had, which is cabozantinib, which are LITESPARK-011 and also the LenCabo trial. The LenCabo looked at lenvatinib, bevacizumab versus cabozantinib. The other trial, lenvatinib belzutifan, looked at cabozantinib as the control arm. In both of the trials, objective responses with cabozantinib was around 40%. Median PFS was around 10 months or so. The CONTACT-03 trial, which had cabozantinib in the control arm, all these three trials had cabozantinib at 60 mg, so they're very strong control arms. All of them, objective response of 40%, PFS of 10 months, showing that a combination approach is probably better. As more people start using pembrolizumab or lenvatinib up front, maybe with another HIF-2 alpha, depending on how that other trial pans out, and as people start using lenvatinib belzutifan more, it begs the question of what other options there are. We know that the mTOR pathway is an important pathway to inhibit, an important pathway that adds to mechanism of resistance. I see this as being a doublet strategy for second-line and above. Whether this combination is sequenced before lenvatinib belzutifan or after lenvatinib belzutifan depends on if the patient has had HIF-2 alpha inhibition before or not. It'll be interesting to see, but this is probably in subsequent or in sequence with the combination with HIF-2 alpha. Got it. Thank you. Our next question comes from Etzer Darout with Barclays. Please unmute your line and ask your question. Great. Thanks for taking the question and congrats on the data. Just given what we've seen here from an efficacy safety standpoint, maybe your view around the mechanism translating into sort of the KRAS update on both efficacy and safety, if you could comment on that. Thank you. Mollie, you want to take that? Sure. For us, just as well as our PIK3CA data that we've presented last year now, I believe it was, this is showing that the mechanism is what we say it is. That this inhibiting the ability of Rheb to activate mTOR is really shutting down that additional pathway that cancer uses to evade treatment with targeted therapies, including KRAS inhibition. I think you should take away from this that that mechanism of action, we have yet once again, shown you evidence of its activity in this particular combination in PIK3CA, and we'll be moving forward into that KRAS inhibitor, where we think that you'll take away the same message, that this works. This is an appropriate combination partner to help get rid of some of the acquired resistance mechanisms that these cancers use to evade. Thank you. Thanks, Etzer. Our next question comes from Daniel Bronder with Cantor Fitzgerald. Please unmute your line and ask your question. Hi, team. This is Daniel Bronder on for Louise Chen. Thanks so much for taking our question. Could you elaborate on the 10 patients of the 18 that you had noticed had disease progression on prior cabo, and what were the reasons the other patients discontinued cabo, and whether or not you see responses across the whole spectrum of prior cabo exposure? Thank you. Just in answering the last part of your question first, yes, we see responses across the continuum of how and when and where they've received cabozantinib previously. For the patients, especially in the 40 mg group, they either came off for progressive disease or potentially intolerance. That makes sense with why they would want to come back on a 40 mg combination, because that's usually how they re-expose these patients to cabo after they've previously seen it. I think the most important piece to recognize is that of the seven responders, all of them had had progressive disease on their cabo, and four of those seven had come directly onto our trial from cabo therapy, so from a cabo failure, and were able to have their responses rescued from use of darlifarnib as well. Their best response on their prior cabo was only stable disease. We were able to actually not only get them out of a progression, but move them into a response using a combination, where the monotherapy was not able to even get them into a response originally. Great. Thank you so much. Our next question comes from Erik Lavington with Mizuho Securities. Please unmute your line and ask your question. Eric on for Salim. Congrats on the progress and thanks for taking our question. Recognizing it's really early days yet, just curious about the dosing of darlifarnib. If you have any interest or capacity in protocol to look at dosage above 8 mg, your thoughts on that? Thanks. Sure. We did a monotherapy dose escalation in addition to these combination dose escalations of the cabo, one of which you're seeing right now. In the monotherapy dose escalation, as we've previously described, 10 mg appeared to be really the maximally tolerated dose, but you have a very wide therapeutic window with anywhere from 3 mg-10 mg producing efficacy in expected patient populations and being safe enough to keep patients on. We would be able to increase the dosing between that 3 mg and 10 mg in any combination that we're looking at. That's probably the escalation pattern we would look at. Here we felt that the 8 mg offered the appropriate safety and efficacy and really moving to 10 mg would've only increased the toxicity. That's why we're moving forward with the 5 mg and 8 mg. Yeah. Eric, just to add to Mollie's comments, I mentioned that darlifarnib is a next-generation FTI and that really is kind of on three axes. One is significantly greater potency, relative to Tipifarnib. Tipifarnib was dosed at 600 mg twice a day, and one really needed to be at that dose in order to see activity in HRAS-mutant solid tumors. As Mollie indicated here, we have obviously a much more potent compound, beginning with activity at 3 mg. But we also interestingly have this window between 3 mg-10 mg, probably 3 mg-8 mg, where we can balance safety, tolerability, and activity. It gives us a lot more flexibility, and it's also once daily dosing versus the twice daily dosing of Tipifarnib. It really is an ideal set of properties for these precision combinations, whether it's cabozantinib, adagrasib, as you'll see, or other TKIs and KRAS PI3 kinase inhibitors in the future. Super helpful. Thank you very much. Our next question comes from Jason Zemansky from Bank of America Securities. Please unmute your line and ask your question. Jason Zemansky, you should now be live. We will come back to Jason Zemansky. Our next question comes from Roger Song with Jefferies. Please unmute your line and ask a question. Hey, good morning, team. Thanks for taking our question. This is Nabil on for Roger. Congrats on the data updates. Curious on the treatment durations, we still have a couple of patients on therapy. How are we interpreting durability at this stage? Yeah, it's a great question. It's still early, but you saw that there's patients that have been on, even in this subset of the Phase 1, that we're showing you for getting close to a year. It's an evolving story, with the patients still on. I think that it'll be nice for you to get a broader picture when we show you the additional Phase 1b data in coming weeks where you'll be able to see even more patients, even more patient stories, and even more of the durability story. Testing. Thank you. Our next question comes from Roger Song with Jefferies. Please unmute your line and ask your question. Apologies, that is Jason Zemansky with Bank of America. There we go. Hello? Can you hear me? Hi, Jason. We can hear you. Perfect. Wonderful. Thanks for taking our question, and congrats on the progress. Maybe just a quick follow-up to Mollie regarding the mechanism, but appreciating RCC as just one indication of a broader strategy. Has the dataset changed your outlook about which indications to pursue next? Are there any read-throughs to other solid tumors here that make them more attractive indications? Thank you. What it does is reassure me that we can do this with any of the compounds, that we can really. It's more than just indication, it's really the combination partner. Anywhere cabo can go, we can go. Anywhere lenva can go, we can go. I would generalize that also to the KRAS inhibitors and the PI3CA inhibitors. That's really your landscape. Wherever those particular compounds can go, we can make them better, and that's why we'll continue to evaluate potential options, and pick the right one to get this to the patients as quickly as we can. Yeah. Jason- Great. Thank you. Just to add to Mollie's comment, again, you should be seeing the KRAS data, hopefully here, before too long. I think after we show you that, we may be in a better position to talk about the balance between going fast and getting to registration versus going broad. If anything, this data reinforces that there's a significant opportunity here, in solid tumors. We are actively working through what's the right development strategy for Kura, both alone and in collaboration with others. We'll be in a position kind of as the year goes on, I think, to speak more to that. Great. Thanks for the color. Sure. As a reminder, if you would like to ask a question or would you like to ask a follow-up, please use the raise hand function at the bottom of your webinar application. Our next question comes from Phil Nadeau with TD Cowen. Please unmute your line and ask your question. Morning. Congrats on the data. Thanks for taking our question. We wanted to follow- up on the activity in the refractory patients. It seems like based on our math, approximately four patients to 10 patients who were refractory to cabo had a response. That's a very similar response rate to the three or eight, roughly, who weren't refractory to cabo. Is that analysis correct, that you're relatively seeing the same efficacy across those two populations? If so, I guess our question is, for the next trial, you're looking at cabo-naive patients. Why not continue in cabo refractory given the pretty strong efficacy there? Thanks. Yeah. What we do think is that this combination gets the cabo exposed up to what you'd expect to see with cabo monotherapy, in the naive patient population. I think that actually, more of the patients were refractory than maybe your calculations are taking into account. Like I said, of the seven responders, all of them were refractory to cabo at the time of coming onto trial. Excuse me. As for our Phase 1b trial, it's part of the reason we're doing the cabo monotherapy arm is, one, to establish a good baseline in this patient population that has this ever-evolving landscape. We wanna see what our patients look like now today with HIF-2 alpha IO, et cetera. Having that rollover potential, really allows us to continue to demonstrate the mechanism of being able to save or induce responses in patients that progress on the monotherapy. We'll still be able to see additional data in that regard. To get the clearest signal, we wanted to make it so that we had cabo-naive patients. There are no more questions at this time. I'd now like to turn the call over to Troy Wilson for closing remarks. Great. Thank you, Jenny, and thank you to everyone who participated in the call today. We will look forward to the next time we talk to you, I think, will be our earnings call, in early May. Look forward to that. If in the meantime you have any questions, feel free to reach out either to Greg or me. We appreciate it. We hope everyone enjoys the Friday and the weekend. With that, we'll adjourn the call. Thanks very much.