Good afternoon, ladies and gentlemen, and welcome to the Q2 2023 Kura Oncology, Inc. Earnings Conference Call. At this time, all lines are in listen-only mode. And following the presentation, we will conduct a question-and-answer session. [Operator Instructions]. This call is being recorded on Thursday, August 3, 2023. I would now like to turn the conference call over to Mr. Pete De Spain, the Head of Investor Relations. Please go ahead.

Thank you, Kelsey. Good afternoon, and welcome to Kura Oncology's second 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. With that, I'll now turn the call over to Troy.

Thank you, Pete, and thank you all for joining us this afternoon. Let's jump right in. In June, we reported updated data from the KOMET-001 trial of our menin inhibitor ziftomenib, including durable activity in patients with heavily pretreated and co-mutated relapsed/refractory NPM1-mutant acute myeloid leukemia. These data were featured during a late-breaking oral session at the European Hematology Association Annual Congress in Frankfurt. As of the April 12 data cutoff, seven of the 20 patients with NPM1-mutant AML who were treated at the recommended Phase 2 dose of 600 milligrams achieved complete remission with full count recovery for a CR rate of 35% and an overall response rate of 45%. This represents one of the highest response rates reported for a targeted therapy in the setting of relapsed/refractory leukemia. An eighth patient who had a CR with partial count recovery after treatment with ziftomenib subsequently evolved to a CR with full count recovery after transplant and remained on study as of the date of the EHA presentation. In addition, a patient with NPM1-mutant AML treated at 200 milligrams remained on ziftomenib for 36 cycles as of the cutoff date. The median duration of response for all NPM1-mutant patients was 8.2 months, with a median follow-up of 8.8 months. Continuous once-daily dosing of ziftomenib was well tolerated in the Phase 1 study and the reported adverse event profile remained consistent with features of underlying disease. 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 especially poor. NPM1-mutant AML is further compounded with co-mutations such as IDH and FLT3. Notably, in our Phase 1 study, 33% of…

Thank you, Troy, and good afternoon, everyone. I'm happy to provide a brief overview of our financial results for the second quarter 2023. Research and development expenses for the second quarter of 2023 were $28.2 million compared to $24.3 million for the second quarter of 2022. The increase in R&D expenses was primarily due to the increases in clinical trial costs related to our ziftomenib and KO-2806 programs. General and administrative expenses for the second quarter of 2023 were $11.8 million compared to $11.1 million for the second quarter of 2022. Net loss for the second quarter of 2023 was $37.2 million compared to a net loss of $34.8 million for the second quarter of 2022. This includes non-cash share-based compensation expense of $7 million compared to $6.5 million for the same period in 2022. As of June 30th, we had cash, cash equivalents and short-term investments of $477 million compared to $438 million as of December 31, 2022. This includes net proceeds of approximately $94 million from our public offering completed in June of 2023. We believe that our cash, cash equivalents and short-term investments will be sufficient to fund our current operating plan to mid-2026. With that, I'll 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 and next year. For ziftomenib dosed the first patients in the COMET-008 combination trial in the second half of 2023, preliminary data from the COMET-007 combination trial in the fourth quarter of 2023 for the first quarter of 2024 and dosed the first patients in the post-transplant maintenance program in the first quarter of 2024. For tipifarnib, initiate dose expansion in the current HN trial in mid-2024. And for KO-2806 dosed the first patients in the FIT-001 dose escalation trial as a monotherapy in the second half of 2023 and dosed the first patients in the FIT-001 dose escalation trial in combination with the targeted therapy in clear cell renal cell carcinoma in the second half of 2024. With that, Kelsey, we're now ready for questions.

Thank you. Ladies and gentlemen we'll now begin the question-and-answer session. [Operator Instructions]. And your first question comes from Jonathan Chang from Leerink Partners. Please go ahead.

Hi guys. Thanks for taking my questions. First question, can you give us any more color around enrollment progress and the registration-directed study of ziftomenib and NPM1 mutant AML? And what do you mean by outperforming projections?

Sure. Thanks, Jonathan, for the question. So, we have guided or I should say, we anticipate full enrollment of the 85 patients in the study approximately the middle of next year. And just to take a half a step back, just to remind everyone, we sized the trial at 85 patients, because it was our view that for a potentially best-in-class therapy, the agency would likely want to see approximately 100 patients worth of safety data at the recommended Phase 2 dose. It's still early days, Jonathan. But in terms of both site activation and now enrollment of patients on the study, we are ahead -- quite a bit ahead of where we expected to be. And we've obviously have enrollment curves under different scenarios. We haven't yet made any adjustments to our guidance in terms of timing of overall enrollment. We want to see how the rest of the summer goes and a little bit into the fall. Sometimes you see a slowdown in the late summer. So, we want to just be mindful of that. But what we want to communicate is there's very strong interest among both physicians and patients. And that seems to be translating directly into enrollment. There are also, Jonathan, appear to be more patients than I think we had anticipated, both from potential competitors and other folks who've tried to enroll trials in the NPM1 space. There was some sort of anecdotal comments out there that it might be challenging to enroll. That hasn't been our experience at all. In fact, quite the opposite. Since through EHA, now on the other side of EHA, we're seeing very, very strong interest, which is translating into enrollment. And I think that's driven, Jonathan, in part because of the data that I just very summarily walked through. The fact that we're seeing activity in patients who failed FLT3, patients who failed IDH patients with various co-mutations. I don't think, we're seeing a siphoning off of patients to those other trials. Instead, they -- we're seeing very strong interest in putting them on the ziftomenib monotherapy study, and we have every expectation that's going to translate into the combos, which is -- it's even earlier days there, but I think we're quite encouraged.

Got it. Thank you. And second question, can you discuss the post-transplant maintenance opportunity for ziftomenib?

Sure. Yes. And let me just clarify there. We're actually going to do both a post-transplant maintenance as well as just the maintenance without requiring transplant. And let's talk about how those are different. So first of all, without needing to get to transplant, our protocols have made allowances for patients to be able to stay on study. So for example, patients who are enrolled in 7+3 plus zifto can stay on zifto in a maintenance type of setting. But -- and that's and we've built that in everywhere we can. So that's obviously important, and I think has the potential to drive value. Our team, I think, is thinking very cleverly of the post-transplant setting, Jonathan. And what we're shooting for is to be able to capture patients no matter how they get to transplant, whether they've had a prior menin inhibitor or not, no matter where they've gotten if they meet the entry criteria and they're on the other side of transplant, they'll be eligible to go into that study. It's our view, Jonathan that given we have such a favorable safety profile, we have no QT prolongation. We have no evidence of drug-induced myelosuppression. We just have a very, very attractive safety profile. We really have the opportunity to be a preferred agent in the maintenance setting. And we've heard from sophisticated parties, that's a very attractive commercial opportunity. If you can keep patients on there for a year or two, that has the potential to drive really significant value, both to the patients as well as for the value of the overall enterprise. So -- and then the final thing, Jonathan, I'll comment on is we're trying -- if people have been paying attention to the way we've laid these studies out, thus far, all the studies we've undertaken are Kura-specific studies, Kura-sponsored studies so that we can drive the timing. And they're all sort of very much value creating. With the maintenance study, we'll do an initial Phase 1 study as an investigator-sponsored study to gather enough data and then we'll flip it over into a Kura-sponsored study if it makes the transition into a Phase 2/3. So, we're trying as much as we can to retain control of the studies to be able to drive timelines and execution. And thus far, that's working quite well.

Understood. Thanks for taking the questions.

Our Pleasure. Thank you.

Thank you. And your next question comes from Roger Song from Jefferies. Please go ahead.

All right. Congrats for all the progress. And thanks for taking the question. I think you mentioned you already start to dose the first combo trial, which is very encouraging. Maybe Troy, you can give us some color around the enrollment progress so far? And how should we think about the expectation for the initial data later this year, early next year in terms of the number, maybe the activity you're looking for? And also, when you will potentially decide the RP2D? Thank you. Multiple part -- sorry.

Yes, that's okay. I'll take each of them, Roger. And if I miss one, please remind me or correct me. So first of all, just a comment on the design of the trials. So these are dose escalation trials. Each of the genotypes is being treated separately with standard of care. So in the context of 7+3, we have a KMT2A cohort, we have an NPM1 cohort. These are typically six patient escalation cohorts, and we're starting at an N minus 2 dose, a 200 milligram dose. Similarly for the venetoclax containing regimen. I'll remind you that in the Phase 1, there really was no dose dependence within between 200 and 600 milligrams as it pertain to differentiation syndrome. And that's important because you talked about kind of how do we think about data and RP2D. So as with any study, first and foremost, what we're going to focus on, I think, and we're guiding to fourth quarter this year or at the latest first quarter next year is safety and tolerability, specifically with respect to differentiation syndrome. So, can we safely combine with the current standards of care, we believe we can. And importantly, do those standards of care help mitigate the differentiation syndrome that was seen in the KMT2A population. And the question of activity, Roger, is a good one. However, as you appreciate, the backbone therapy has a meaningful level of clinical activity. So that really isn't going to be anything, I think we can speak to. And that's really when you get further on and you take, once you're at a dose that is the optimum biologically active dose or the RP2D, you'll take it potentially into an expansion cohort, and then we can get a better sense of clinical activity relative to the -- backbone…

No, that's great. That's great. Okay. So that's very clear now. Maybe just shift gears to the tipi. So understanding you're figuring out the RP2D for them. In the past, you seems to kind of guide towards the data release around the mid-year for the RP2D. And now you're kind of guiding towards the expansion cohort second half next year. So maybe just let us know what's the current thinking around the tipi? Thank you.

Yes, it's a good question. And it's -- I think it's a reasonable question and the right question. So in short, Roger, the combination is both better tolerated and more active than we expected. That's the short answer. We had -- so if we take a step back, before we ever dosed a patient, when investors and analysts asked me, what's the greatest risk? I said, from my perspective, the greatest risk is the challenges with combining tipifarnib and alpelisib. Particularly, we, as an industry, have not had good success in combining inhibitors of the MAP kinase pathway and inhibitors of the PI3-kinase pathway. We have been, I think, very pleasantly surprised at the safety and tolerability that we've seen with this combination. We have seen evidence of hyperglycemia, but it hasn't been dose limiting. It hasn't inhibited in any way our ability to escalate both tipi and alpelisib. And just to put a point on that, now this final escalation cohort is a full dose of tipi 600 milligrams twice a day and a full dose of alpelisib 300 milligrams daily. Honestly, I was surprised. I wouldn't say shocked, but pleasantly surprised. What -- the other thing, Roger, is we're seeing evidence of clinical activity. Now in this population, that's why I cited to you second line head and neck, you're typically seeing response rates in the teens, 13% to 16% and really challenging PFS and OS, PFS of two to three months. You can assume we are seeing responses. I don't want to get into the granularity of the data, but we're seeing activity at -- and we're seeing, first of all, good safety and tolerability. We're seeing activity at different dose levels. We do need to make sure that we select the optimum biologically active dose, and…

Excellent. Thanks Troy for all the comments. That's it for now. Thank you.

Your next question comes from Peter Lawson from Barclays. Please go ahead.

Thanks so much for taking the questions. Just kind of firstly, a follow-up around the maintenance setting, whether resistance mutations could preclude zifto from being in -- using that maintenance setting? And then other question just around moving zifto and beyond AML and ALL into other hem indications, solid tumors or other diseases? Thank you.

Sure. Yes. Thanks, Peter, for the question. So, we don't think resistance mutations are going to be a big threat to using zifto in the maintenance setting. We've only ever seen one patient of the ones we've tested, the 29 or so we've tested who had a -- who developed a resistance mutation while on zifto. And people might ask the question, Well, was your assay sensitive enough? And my answer would be, we don't see any evidence of resistance mutations driving progression or resistance to zifto. Patients do develop resistance. They do progress, but it doesn't appear to be due to these resistance mutations. That's part one. We've got about a 3% to 4% rate of resistance mutations in the data that we've sampled thus far, Peter. But the other important point is ziftomenib is fully active on two of the three mutants, and it retains meaningful activity on the third, the 327 mutant. So -- and that's in contrast to a number of the other inhibitors in the class. And we've actually seen that as we spoke to around EHA. We've seen that when we treated patients who have come to our study, having failed another menin inhibitor, we do have a measure of clinical activity. Long story short, Peter, I don't think it's -- we don't think it's going to make a difference. We think zifto is very well positioned for the maintenance setting. And importantly, Peter, even probably more importantly, it's very easy to use. It doesn't have any other toxicities that -- thus far that have revealed themselves that would require sort of extra detection or extra vigilance in that setting. So I think, we're looking forward to using zifto in the maintenance setting. And forgive me, Peter, the second part of your question is additional indications.

The second half of the question was expanding outside hem indications or other hem indications into solid tumors and other diseases, just your thoughts there and where you are?

Sure. So, I think there, Peter, you want to be data driven. There are other opportunities that we see beyond acute leukemia for menin inhibitors. I think one needs to be very mindful of the potential impact of the Inflation Reduction Act. And long story short -- the best analysis we have, and we've talked to all the experts, including CMS, is that we can do anything within AML. And we stay out of the Inflation Reduction Act by virtue of having an orphan designation that covers AML. Once you go to another indication, be it ALL, be it any of the others, you potentially put your program at risk of being included in the IRA. And I think -- we think, Peter, the appropriate way to mitigate that risk is we have a next-generation menin inhibitor program. We've taken everything about zifto that we think can be improved, and the team -- has a very attractive compound -- that would be the one we would probably take into additional indications. Be those other solid or liquid tumors be that potentially diabetes. We've got multiple opportunities for additional menin inhibitors. And just given the evolving sort of legal and regulatory and pricing landscape, I think one wants to be thoughtful there. We think we can drive significant value just in AML alone, and you hear us, right? We're talking about frontline relapsed/refractory maintenance. We really think you can transform the standard of care and transform the market. And we're going to do everything we can with zifto in that setting. If there's additional opportunities, I think we might do some early exploration, but we'd likely pick those up with a second generation compound. And that way, you can really drive the full commercial value for the franchise.

Great. Thank you so much. Really appreciate it.

Pleasure.

Thank you. And your next question comes from Li Watsek from Cantor. Please go ahead.

Hey, congrats on the quarter. And thank you for taking our questions. I guess first one is on the Phase 2 pivotal study of zifto. Troy, can you maybe just clarify if you have seen greater traction in terms of patient enrollment after your EHA update in June, I mean, especially for some of the EU sites that you have? And also for the potential combo data later this year or early next year, can you give us a sense of the variables here? Is it just a matter of enrollment speed? Or you want to reach a certain number of patients or certain period of follow-up before you disclose the data?

Yes, Li, thanks for the question. So on the first question, it's -- when you do this with any trial, you do feasibility studies and you have an enrollment curve. And that enrollment curve is driven by the feedback that you get from the sites. How many patients do they see, how many do they think they can put on, et cetera. And our clinical operations group has done that very well with the 001 study. We are ahead of our projections, Li. And I think there are a lot of reasons for that. I think it's physician excitement. I think it's the data itself. I think there's more patients than perhaps we expected and we're not losing them to other studies. It's hard to say kind of -- it's hard to isolate one variable. What we're communicating is for people who think there's going to be a big gap in terms of time to market. I think we have a different view that's perhaps informed by data, particularly in that NPM1 setting. And you fully expect if the combination trials go well, and we have good safety and tolerability that you would expect that traction to continue. Because everyone acknowledges that as these molecules eventually go in front of the FDA and potentially come to market, we're still -- AML is a disease of combination therapy. So the party that can get to the combinations with the highest -- the best safety, best tolerability, combined ability and activity is ultimately going to be the market leader. And we think that sets up very nicely for zifto. So I expect that excitement and enthusiasm will pull through into the combo studies. With respect to the second part of your question, Li, in terms of how we think about data release.…

Yes. Okay. Thank you. I have a second question. So in terms of the patients that you're enrolling into the pivotal study with co-mutations. Do you have a sense of the -- in terms of the breakdown for FLT3 versus IDH co-mutations?

No. At least I don't think so. You're talking Li about the breakdown of co-mutations in patients enrolled on the study. Is that what you're asking?

Yes, yes.

We are seeing -- so I think it's early days. We're seeing very high levels of co-mutation. That's why I highlighted for you, if you go pull the quizartinib label, 50% of the FLT3 are NPM1 co-mutated right? So you need to be able at some point to combine with the FLT3 inhibitor or you've given up 15% of the population. We're seeing that as well Li, both FLT3, IDH, DNMT3A, all the central actors. It's exactly -- it's very similar to what we've seen in the Ib. I don't have -- I don't think we have specific breakdowns yet in terms of the co-mutational content in the population.

Okay. Thank you.

Sure.

Thank you. And your next question comes from Bradley Canino from Stifel. Please go ahead.

Hi, this is Bijan on for Brad Canino. Congrats on the progress. So first question is on tipifarnib glad to see responses in some limited safety issues. How should we be thinking about the contribution of parts for tipi and PIK3 in the next data? And then will we be getting data in both the HRAS overexpressed population in PIK3CA?

Yes, Bijan. So let's -- if I may, let's take those in opposite order. So earlier this year, we announced that we were not going to continue enrolling in the HRAS overexpressing cohort. We were going to focus our effort in the PIK3CA mutant -- and that was really for a couple of reasons. Number one, we -- as with every company, we have finite resources. And we have more things we can invest in, then we have funds with which to invest. So particularly, as you hear us articulate everything we're doing with systematic. If one wants to identify the OBAD, the best place in our experience to go is in those patients who have driver mutations in the target oncogene, whether they be HRAS mutant in the case of the RUN and the AIM studies or PIK3CA mutants in the case of the current studies. If you're going to define the OBAD, go there because that's where you're going to have the potential of the greatest level of activity, because the closer you get to a driver mutation. I should say, gain of function mutation in a driver oncogene, typically, that's where you see the highest activity. That doesn't, Bijan, preclude that once we get the OBAD, we would come back and investigate either HRAS overexpressed or PIK3CA amplified. We just want to do it in stages. And we want to be good stewards of capital, good fiduciaries and be smart about doing drug development. So we are -- the picture is coming into focus in the PIK3CA mutant. Your question around contribution of parts. There -- so tipifarnib, you would expect it has no ability to drive responses in a PIK3CA mutant population as a monotherapy. That I can say with great confidence. Alpelisib in the experience…

Yes, great. Thanks for the comments there.

Sure. Appreciate the question.

Thank you. And your next question comes from Justin Zelin from BTIG.

This is Julian on for Justin. Thanks for taking our question. I was just looking to get your take on your view on menin for diabetes based on recent competitor data at ADA? And I had a follow-up question.

Sure. So we're following, as many are, we're following that data with interest. There's certainly a relationship between menin inhibition and beta cell regeneration. I think in our minds, there's still a lot of gaps and questions as to what exactly is going on there. What we've decided to do is to -- we'll continue to watchfully wait that data set. We're actually evaluating ziftomenib as well as a number of other menin inhibitors in the appropriate models of diabetes, both as monotherapy and in combination. And I'm hopeful that we'll have some data later this year to make an assessment as to do we see an opportunity. And if so, how do we make sure we take advantage of it. If there's an opportunity for menin inhibitors in diabetes, I'll tell you today, we'll find a way to maximize that value for shareholders, either through a partnership or an out-licensing. I doubt will become Kura diabetes, but we will find a way to get the value in it. But importantly, and this is an answer I gave previously -- our view is you probably want to do that with another menin inhibitor, both because you don't necessarily want your diabetes compound and your oncology compounds to have the same safety database. And #2, from the standpoint of the Inflation Reduction Act, you kind of shot yourself in the foot. So we have, as I said, a next-generation menin inhibitor that we've been bringing along, that may -- if the data supports it. And we're going to look for the recommendation from our translational research and clinical colleagues, that's how you'll see us generate value with menin inhibitors in diabetes is through a next-generation compound. And I'll tell you this, if it's there, I have no doubt we can generate a best-in-class compound. It's just a matter of let's be disciplined, let's do the right experiments and let's generate the data and see.

Makes sense. And just as a follow-up, I was hoping you can maybe just clarify the number of patients being treated for the head and neck expansion cohort for tipifarnib. And secondly, what other indications outside of head and neck and RCC numbers are promising for FTIs in your view?

Yes. Great question. So within head and neck, you probably won an expansion cohort of sort of -- and I'm just -- I'm spitballing here, sort of six to 12 patients. Similar to what we did with ziftomenib in the Phase 1b, we want to have enough clinical data there that you've got a strong steer on how to think about future development. So that's that. In terms of other indications, we've got, I think, very good and evolving clinical data, both with tipifarnib as a monotherapy and increasingly tipifarnib and alpelisib. Although we terminated enrollment in our AIM study, we terminated it for operational feasibility. The compound is active. It's actually quite active. But again, in a world of limited resources, you have to make some difficult choices. And we would do our best to try to capture both the HRAS mutant and the PIK3CA-mutant population, which is about one-fourth of head and neck. For that, I would think about tipifarnib and alpelisib. You would then want to come with a second and possibly third FTI and think about RCC and how you crack the KRAS riddle. At this point, you want to generate data, you want to make sure you have optionality. But -- there have been questions about tipi, the composition of matter patent has expired. But once you bundle it up with alpelisib, our IP colleagues have done a great job of building a strong patent estate around FTIs and head and neck cancer that we can leverage. And if we could beat it, if we could get tipi and alpelisib to market for patients like that would be an amazing accomplishment. There's no targeted there -- no small molecule targeted therapy approved. If you then wanted to come along with another FTI and try to beat it, great. But I always joke walk then then run the four minute mile. So let's keep tipi and alpelisib moving along. You'll see us put increasing resources on 2806 -- and at this point, we don't have to make a decision. We want to generate data in both RCC and KRAS and continue to mine the chemical space for more FTIs and see where we go. Those are three very significant solid tumor indications. And I think the data set is coming together nicely. It's turning out to be -- who knew that the killer application of FTIs was going to be back to KRAS where it all started, but just as a combination therapy. That would be sort of coming home, if you will. I hope that's where we end up.

Makes sense. Thank you so much.

Sure.

Thank you. And our last question comes from Reni Benjamin from JMP Securities. Please go ahead.

Hey guys, thanks for taking the questions. Troy, can you talk to us a little bit about maybe the strategic rationale for starting off with RCC and what's the unmet need there versus starting off with KRAS and KRAS mutant and NSCLC. And then a question for kind of all your combination programs. Are you in any sort of discussions with the companies that are marketing the approved drugs that you're combining either zifto or tipi with -- in order to set up an MTA or try to get some free drug? I mean how important is that for kind of cost mitigation and maybe enrolling patients quickly and getting the clinical trials off the ground?

Sure. It's a great question, Reni. And let me take it in parts. So with respect to RCC going first, we are improving as an organization fundamentally different than where we were just a few years ago and really have a great cross-functional effort as we think about going from sort of preclinical R&D all the way through to life cycle management. And so we've done the work on renal cell carcinoma. We've talked to the KOLs, we've done the market research, we understand the landscape. And we'll speak more to our specific partner in RCC probably a little later this year. But that's ran a relatively more mature space. We know what -- it's still evolving, but it's relatively more mature. -- for example, the docs were very clear if they could -- if we could enable them to use TKIs in the second line, that would be phenomenal. And if you look at the preclinical data that Francis' group has generated, there's really potent synergy between tipifarnib and TKIs, most notably exitinib in that setting. So it's a great setup. The docs love it. We -- in my view, we can't get there fast enough. Now take KRAS. KRAS is an emerging area. It's -- I know it's got a lot of heat, a lot of light. It is a rapidly evolving area. It's clear that resistance is going to be something that everybody is going to have to contend with. And our target of rapamycin, which is what we -- one of the targets that we deal with, with tipi 806. That seems to be a central actor in driving resistance to TRS inhibitors across the board, whether they're mutant selective, whether they're Raton, whether they're G12C or G12D, if you hit KRAS, tour gets engaged and tries to develop resistance, the tumor tries to find a workaround. So it's taking -- we're just being run very deliberate and making sure that we're making the right decisions with respect to your last question, are we trying to build clinical collaboration or supply agreements? The answer is yes. Ideally, you either want the drug to be reimbursed or you want to work with the sponsor to try to get a drug sharing agreement or a clinical collaboration. We did that, of course, with Novartis initially with the tipifarnib alpelisib trial, and you can assume we are taking a similar strategy as we think about the opportunities for 2806.

Perfect. Thanks for taking the questions.

Sure.

Thank you. There are no further questions at this time. Mr. Troy Wilson, you may proceed with closing remarks.

Thank you. And thank you all for joining our call today. We'll be participating in the Cantor Healthcare Conference next month and hope to see a number of you there. In the meantime, if you have any additional questions, please contact Pete, Tom, or me. Thank you again for attending our call, and have a good evening, everyone.

Ladies and gentlemen, this concludes your conference call for today. We thank you very much for participating and ask that you please disconnect your lines. Have a great day.