Good afternoon, ladies and gentlemen, and welcome to the Q1 2023 Kura Oncology, Inc. Earnings Conference Call. [Operator Instructions]. This call is being recorded on Wednesday, May 10, 2023. I would now like to turn the conference over to Pete De Spain, Senior Vice President of Investor Relations and Communications. Please go ahead.

Great. Thank you, Julie. Good morning, and welcome to Kura Oncology's First Quarter 2023 Conference Call. Joining me on the call are Dr. Troy Wilson, our President and Chief Executive Officer; and Tom Doyle, our Senior Vice President of Finance and Accounting. Before I turn the call over to Dr. Wilson, I'd like to remind you that today's call will include forward-looking statements based on current expectations. Such statements represent management's judgment as of today and may involve risks and uncertainties that could cause actual results to differ materially from expected results. Please refer to Kura's filings with the SEC, which are available from the SEC or on the Kura Oncology website for information concerning risk factors that could affect the company. With that, I'll now turn the call over to Troy.

Thank you, Pete, and thank you all for joining us. Our strong conviction in ziftomenib and its potential to be the best-in-class menin inhibitor continues to increase. This confidence is supported by one of the highest complete response rates reported for a targeted therapy in the setting of relapsed/refractory leukemia and is reinforced by the rapid pace of enrollment in our registration-directed trial. More on that in just a moment. We're also encouraged by the durable remissions in our Phase I trial, driven primarily by single-agent activity of ziftomenib, and we look forward to sharing an update at the European Hematology Association Congress next month. You've got a glimpse of these data in our recently released abstract, which showed that ziftomenib continues to demonstrate significant clinical activity in patients with heavily pretreated and co-mutated relapsed refractory NPM1 mutant AML. As of January 31 data cutoff, 6 of the 20 NPM1 patients treated at the recommended Phase 2 dose achieved complete responses with full count recovery. The abstract showed a median duration of response of 8.2 months with a median follow-up of approximately 8 months. 4 patients were still ongoing at the time of data cutoff. Ziftomenib is well tolerated and the on-target effect of differentiation syndrome is manageable. We are excited by these evolving data, and we look forward to reporting updated data as of an early April data cutoff. Now building on the momentum generated by our positive Phase 1 data, we announced in February that the first patients were dosed in our Phase 2 registration-directed trial of ziftomenib in NPM1 mutant relapsed or refractory AML. Site activation and enrollment in our registration-directed study are outperforming our projections, an indication of the continued enthusiasm surrounding ziftomenib among investigators and patients. As a reminder, NPM1 mutant AML accounts for approximately 30% of new AML cases annually and represents a disease of significant unmet need for which no approved targeted therapy exists. Once the disease becomes relapsed or refractory, the prognosis for NPM1 mutant AML patients is particularly poor, with an overall survival of approximately 6 months after initial chemotherapy. NPM1 mutant AML is further compounded with co-mutations such as IDH or FLT3, notably in our Phase I trial for ziftomenib, 2/3 of NPM1-mutant AML patients who achieved a CR at 600 milligrams had IDH and/or FLT3 co-mutations, all of whom have failed prior treatment with IDH and/or FLT3 targeted inhibitors. A complete response rate with full count I'm sorry, a 30% complete response rate with full count recovery after prior failure of these targeted therapies makes the clinical activity of Ziftomenib even more striking. We're also impressed with the potential for ziftomenib to drive durable remissions as a monotherapy, and additional NPM1 mutant patient who entered the trial with multiple code mutations, including DNMT3A, following 2 prior stem cell transplants achieved a CR with no evidence of minimal residual disease and remains on Ziftomenib for more than 32 cycles as of our January 31 data cutoff. In parallel with our efforts to advance Ziftomenivisim monotherapy, we're preparing to initiate a series of combination studies to significantly broaden the addressable patient population. We believe Ziftomenib is uniquely positioned for these combination strategies. This belief is driven by several key competitive advantages, including no evidence of drug-induced QTC prolongation, no predicted adverse drug-drug interactions and once-daily oral dosing that should enable convenient administration with current standards of care. Our team is working diligently to initiate the COMET 007 and COMT008 trials to evaluate ziftomenib in combination with current standards of care in earlier lines of therapy and across multiple patient populations, including both NPM1 mutant and KMT2A-rearranged AML. We've designed the Phase 1 studies to assess safety, tolerability and antileukemic activity of ziftomenib in combination with key regimens such as venetoclax and azacitidine, the FLT3 inhibitor gilteritinib and the chemotherapy regimen of 7 plus 3. Our approach to combinations is to establish ziftomenib as a foundational therapy that can be combined safely with various commonly used regimens and then prioritize those combinations that represent the largest unmet medical need and the greatest potential commercial value, namely venetoclax and FLT3 inhibitor containing regimens. Notably, up to half of NPM1 mutant AML patients also exhibit co-mutations in the FLT3 gene. Given the safety profile of ziftomenib, we believe it may be the ideal menin inhibitor to combine with FLT3 inhibitors to address this population, a difficult-to-treat group that represents approximately 15% of AML. We also believe that rational combination approaches will help to mitigate differentiation syndrome in the KMT2A rearranged population as has previously been demonstrated in the development of IDH inhibitors in combination with azacitidine. We're very excited about the potential for our combination studies to further unlock the value of ziftomenib for patients with acute leukemias. We've begun site activation in the first of these studies, COMET-007, and we're on track to dose first patients this quarter. We're very proud of our team's execution and grateful for the continued support of our studies investigators. Their enthusiasm, coupled with a growing body of clinical data and multiple emerging lines of evidence reinforce our confidence in ziftomenib as the best-in-class menin inhibitor. We look forward to sharing more at our upcoming presentation at EHA. Now let's turn our attention to our farnesyl transferase inhibitor program. Over the past several years, we've pioneered the development of FTIs as combination agents to prevent or delay emergence of resistance to certain classes of targeted therapy in large solid tumor indications. Although targeted therapies have demonstrated meaningful clinical activity across a range of solid tumors, adaptive resistance almost invariably emerges over time, which limits the ability of targeted therapies to drive sustained clinical benefit. We have generated a growing body of preclinical and clinical data that support the combination of SDIs with multiple classes of targeted therapies, including EGFR inhibitors as well as PI3-kinase inhibitors. In April, we presented encouraging preclinical data at the American Association for Cancer Research Annual Meeting, which supports the potential use of FTIs in combination with 2 additional distinct classes of targeted therapy. The first of 2 posters revealed robust synergy between tipifarnib and the standard of care anti-angiogenic TKI, axitinib in cell and patient-derived xenograft models of clear cell renal cell carcinoma. The second poster reported regression of multiple models of KRAS inhibitor resistant non-small cell lung cancer through the addition of tipifarnib either to adagrasib or sotorasib therapy. These promising preclinical data illustrate the potential for FDIs to drive enhanced antitumor activity as well as address mechanisms of both innate and adaptive resistance to targeted therapies. In addition, we believe these data strongly support our rationale to combine our next-generation FTI, KO-2806 with TKIs in clear cell renal cell carcinoma as well as KRAS G12C mutant inhibitors in non-small cell lung cancer. In January, we were pleased to announce FDA clearance of our investigational new drug application for KO-2806 for the treatment of advanced solid tumors, an important next step for this program. Now we intend to evaluate safety, tolerability and preliminary antitumor activity of KO-2806 in a Phase 1 dose escalation study, which we're calling FIT-001. We're now in study startup, and we look forward to dosing the first patients in FIT-001 later this year. Concurrent with the dose escalation as monotherapy, we also plan to evaluate KO2806 in dose escalation combination cohorts in advanced solid tumors. Meanwhile, we continue to evaluate tipifarnib in combination with the PI3 kinase alpha inhibitor, alpelisib, a combination that has potential to address up to half of all patients with recurrent and metastatic HNSCC. We're encouraged by the preliminary activity observed in our ongoing current HN trial, including a durable partial response in a patient with PIK3CA mutated squamous cell carcinoma of the tonsil. We're also very pleased by our ability to combine tipifarnib with another targeted therapy, in this case, alpelisib with no dose-limiting toxicities reported to date. We remain on track to determine the optimal biologically active dose in mid-2023. We continue to unlock the potential therapeutic and commercial value of farnesyl transferase inhibition, the challenging, but we believe increasingly substantial opportunity that has potential to address large solid tumor indications such as renal cell carcinoma as well as cancers of the lung and colorectal system. As with our menin inhibitor program, we believe FTI programs have potential to create significant value for patients, health care providers and our shareholders. We're confident we have the leadership, experience and operational and financial resources to realize that value. With that, I'll now turn the call over to Tom Doyle for a discussion of our financial results.

Thank you, Troy, and good afternoon, everyone. I'm happy to provide a brief overview of our financial results for the first quarter of 2023. Research and development expenses for the first quarter of 2023 were $25.2 million compared to $20.9 million for the first quarter of 2022. The increase in R&D expenses was primarily due to increases in clinical trial costs related to our ziftomenib and KO2806 programs, offset by decreases in clinical trial costs related to our tipifarnib program. General and administrative expenses for the first quarter of 2023 were $11.4 million compared to $11.9 million for the first quarter of 2022. Net loss for the first quarter of 2023 was $34.1 million compared to a net loss of $32.5 million for the first quarter of 2022. This included noncash share-based compensation expense of $6.8 million compared to $6.7 million for the same period in 2022. As of March 31, 2023, we have cash, cash equivalents and short-term investments of $405.9 million compared to $438 million as of December 31, 2022. We believe that our cash, cash equivalents and short-term investments will be sufficient to fund our current operating plan into the fourth quarter of 2025. With that, I now turn the call back over to Troy.

Thank you, Tom. Before we jump into the question-and-answer session, let me lay out our anticipated milestones for the remainder of this year. For ziftomenib, dosed the first patients in the COMET-007 combination trial in the first half, present updated data from our Phase 1 trial in NPM1 mutant AML at EHA in June and dose first patients in the COMMET-008 combination trial in the second half. For tipifarnib, determine the optimal biologically active dose in the current HN trial in combination with alpelisib in mid-2023. And for KO-2806, dose first patients in the FIT-001 dose escalation trial in the second half of 2023. With that, operator, we're now ready for questions.

[Operator Instructions]. Your first question comes from Jonathan Chang from SVB Securities.

First question, can you help set expectations for the upcoming EHA Ziftomenib update and discuss the importance of achieving a good duration of response.

So as you saw from the abstract, which was released, the abstract is focused on the -- the NPM1 mutant AML patients treated at 600 milligrams, which, of course, is the FDA's accepted recommended Phase 2 dose. The abstract Jonathan was as of -- as I said, a January 31 data cutoff. We're going to bring forward all of the clinical data on those patients and reported as of an early April cutoff at EHA. And as we said in the prepared remarks, we're seeing now multiple converging lines of evidence that suggest to us that Ziftomenib is potentially the best menin inhibitor in acute leukemias. And we very much look forward to sharing that data with you and others at EHA. And in terms of your question, Jonathan, on yes, let me follow up on your second question, sorry, I didn't mean to neglect it. In terms of duration of response, so there's 2 things to think about here. The first is what's the bar for registration. And the second is what's clinically meaningful? And how do you think about that, right? So first things first. As we've said consistently, what we understand is that for FDA approval as a monotherapy, you're looking at a 20% to 30% CR/CRH rate as well as a median duration of response of 4 to 6 months. I don't think we've ever deviated from that. The reason that those are meaningful numbers, of course, is you're talking about patients who failed all other options. And the overall survival for NPM1 patients in the relapsed/refractory setting is about 6 months. So if you're driving a duration of response that's in that same time frame, that's clinically meaningful. And nothing has changed in our understanding of that -- those being the registrational bars. In terms of what's important clinically, I would draw your attention to a couple of things. The first is that we are driving CRs with full count recovery. This -- again, not CRIs or even CRHs, but really the full complement of the immune system on the hematopoietic system back. Why is that important? The patients are healthier, right? These patients are at tremendous risk of infection. And all of the docs that we talk to tell us the more you can take patients to full CR, the better off you are. The second, of course, Jonathan, is your question around duration. And I don't want to get in front of the abstract or kind of under the 4 corners. I'll tell you this. We have been very pleasantly surprised by the ability of ziftomenib to drive durable responses as a monotherapy, i.e., without needing to go to either to transplant or to other therapies. We see quite a different sort of mutational profile from what has been reported for other agents. And I think that's going to be important not only in the relapsed/refractory setting, but it will become even more important as we roll forward into combinations. So we'll look forward, as I said, to sharing all of this, both at EHA, Jonathan, and very likely at an associated investor event alongside.

Understood. And second question, can you provide any more granularity on what you mean by the Phase 2 NPM1 study enrollment outperforming projections. Yes, I'm happy to. So I'll just remind everyone that last year, we reported that we had enrolled 14 patients in our Phase 1b study in approximately 3 months. And here's where we are today. So our total goal for this trial is 62 clinical sites in the U.S. and Europe. We're now open, Jonathan, in a majority of those sites. And we've seen site activation in both the U.S. and Europe that has exceeded our expectations. And the only thing we can attribute that to is excitement of the investigators, the sites, the patients for getting their hands on ziftomenib. As you know, and an obvious competitor of ours has extended its time lines for recruitment of NPM1. We're not ready yet, Jonathan, to pull time lines in. What I can tell you is the investigators on the Phase 1b study as well as the new investigators has picked up exactly where they left off. So -- and site activation is always a leading indicator, but we've seen both site activation and now enrollment that exceeded are already pretty aggressive goals. So I think we're seeing a continuation of the excitement, the enthusiasm from the Phase 1b. And I think it positions us very well not only to come forward with potentially best-in-class data, but to be very competitive on time lines in the NPM1 setting.

Your next question comes from Roger Song from Jefferies. Great.

Maybe just a follow-up on your earlier Troy to your earlier comment related to the best-in-class profile, particularly in the emerging resistance data on the main inhibitor. So maybe just tell us a little bit more about this, how the manager will differentiate in this kind of resistant mechanism, and why you think it's better suited.

So let's start with kind of what we see and then we can talk about the implications for what it means. First, what we see. One of our competitors was reported that they're seeing the emergence of resistance mutations at roughly 30% to 40% of patients, and they're seeing it very early on, cycle 1, cycle 2. It's not -- we've known for a long time about the potential for resistance mutations. But what have we seen? By comparison, and we're still analyzing our data, Roger. But to this point, having analyzed quite a number of patient samples, I can tell you we've seen 3 examples of resistance mutations. 2 of them were patients who presented with the 327 methionine mutation as soon as they presented to the study, having failed revue. So do we see them? Yes, we do. What's interesting is we don't seem to see them nearly at the same frequency as perhaps our competitors do. Now what's the implication of that? Well, as we know from EGFR, pick any other small molecule oncology target, right, the emergence of resistance mutations typically means the therapy is becoming less effective. And what I think this is going to mean, Roger, I should say what we think is it will be important as a monotherapy. And again, I'll stress to you we're seeing durable responses just in the presence of ziftomenib. But as you now go forward into combinations, that's going to become incredibly important because if those menin clones can get away with resistance mutations, now you've lost -- now you've lost that therapeutic activity. So I think it sets up very nicely. There are a number of both biochemical and drug-like properties that we think are contributing. But it's very clear, Roger, that these compounds have very different profiles. And again, as I said to Jonathan, look forward to sharing much more of this data at and around EHA. Excellent.

And then moving on to the tipifarnib or your STI franchise. Since you're planning to announce the biologically optimized dose for applicant tumble in the year. So what would be the next step for the program and also how that will play into your 2806 overall FTI franchise?

So stepping back, just for a second, a number of our analysts and shareholders have been with us for a number of years, and they know this is a program that we've been very passionate about. I don't think, Roger, that it's an overstatement to say that STIs may turn out to be one of the ideal combination agents for targeted therapy. People have looked at SHIP 2, they've looked at . People have been trying to drug both the MAP kinase and the PI3 kinase pathway for at least the past couple of decades. And you might ask why did nobody discover this sooner. But by the time most of the FDI programs were discontinued, that was right at the dawn when a lot of these targeted therapies were discovered, and it wasn't really until our team began doing first preclinical and then clinical work on the combinations that we really began to see the opportunity. When we started, we naively said we need to go after farnesylated onco proteins, HRAS being the most obvious and perhaps the only. What we've learned is, actually when you stress the cell with EGFR inhibitors, KRAS inhibitors, TKI the cell responds in a very organized, highly choreographed way and it exposes farnesylated proteins such as REV and those become ideal targets for drug synergy. And I think it's that, Roger, that's driving the biology that you see in the 2 posters at AACR, just incredible synergy both in the context of RCC and KRAS mutant inhibitors. So to your question now, because I think that's important background. We've -- I think the most immediate takeaway from our Alpelisib combo is we can actually take these 2 drugs I think, to their full dose with no dose-limiting toxicities. I think most investors, and in fact, even many people at KURA would not have expected that would have been the case. But that bodes extremely well for combining 2806 with these various targeted therapies. If you can combine with alpelisib, that sets a pretty high bar. For that program specifically, Roger, we're going to do 2 things. The first thing is, I mean, we know we have adequate safety and tolerability. The question is, is the clinical activity sufficient to support continued development of tipifarnib and alpelisib or do we perhaps prioritize KRAS-driven tumors, RCC as potential next steps, next investments. The good news is I think we're going to have options. We're going to have choices. The team is doing a lot of work to get 2806 into those targeted combinations as quickly as possible. It's really not about the monotherapy. It's how quickly can you get into the combos. How quickly can we see if we can replicate that preclinical data. So that's the data that we're expecting, Roger. And the way that we're going to -- the lenses that we're going to use to look through it, as we say, is the next investment, one in head and neck, perhaps lung cancer with KRAS or perhaps RCC or in a perfect world, more than 1.

Your next question comes from Peter Lawson from Barclays.

This is Alex on for Peter. Just given the comments on the pace of site activation and enrollment in the pivotal study. Any color you could provide around when enrollment could complete in that study?

Yes, Alex, thanks for the question. So we've guided that -- maybe taking a step back. The Phase 2 study is designed to enroll a total of 85 relapsed/refractory NPM1 mutant patients. The reason we're -- the reason it's 85 is we felt that, that was an appropriate safety database to support a best-in-class menin inhibitor. Typically, the FDA wants to see about 100 patients at your recommended Phase 2 dose just from a safety perspective. Obviously, from an efficacy perspective, you probably don't need 85 patients. And within the context of those numbers and that trial design, Alex, we've guided that full enrollment of the 85 is probably middle of next year. But given that we are -- given that our initial site activation and enrollment is exceeding our expectations, although we're not yet ready, Alex, to pull the time lines in, I can tell you we're going to take advantage of every possible opportunity to be competitive, I think we'll have best-in-class data. The question is really going to be where are we in terms of timing. And at this point, I think we're neck and neck potential to even pull ahead of that. We've just been really pleasantly surprised by what we're seeing in the ongoing COMMET registrational trial.

And then just a second question on EHA. Now the focus is on NPM1, but should we expect any updated data from the MLL patients you've treated so far?

At this point, I'll just refer you back to the abstracts. Again, I don't want to get ahead of the abstract or sort of get under the Four Corners. We'll focus, at this point, I'm giving you an update on what's laid out in the abstract. As I mentioned, we're intending to provide an investor event in connection with EHA. And as I've said, we're seeing multiple lines of evidence really that are supporting ziftomenib as being a best-in-class inhibitor in acute leukemias. We look forward to sharing that data with you and the rest of the folks on this call at that time.

Your next question is from Brad Canino from Stifel.

Strategic ziftomenib question for me, Troy. You've been open in the past about the requirement for a global pharma partner to capitalize on the valuable frontline AML setting. So as I look at it now, you're in a position where you have NPM1 data evolving positively. You've got this pivotal trial progress that's ahead of schedule as you state, and you're moving to dose optimize the combos as quickly as possible. ahead of you, you've got competitor pivotal data and combo safety data in second half '23. I look at your cash burn guide, that would suggest even with all the planned trial additions that you have laid out in your press release, you expect the cash burn to cap at about a 50% increase from the current levels this past quarter as I look through 2025. And -- so as you think about the evolution of all of these pieces, how are you currently weighing the ideal time for such a transaction?

Yes. Brad, I appreciate the thoughtfulness with which you laid out the question. So I can tell you that the discussions that we've had with sophisticated parties that do research, development and commercialization of products in heme have reinforced the idea that we have a best-in-class compound. And not only are they drawn to the clinical activity, but very much some of the other properties that we've continued to highlight the lack of QT, the lack of drug-drug interactions, the oral once-a-day dosing, the ability to not have to vary dose as you're changing SIP regimen -- ASL regimens or others is very appealing. In particular, you'll hear us in our prepared remarks stressing the opportunity with the FLT3 inhibitors. That's fully half of NPM1, and you want to hit that head on as early as you possibly can because you have a real potential to drive durable responses in those NPM1-3 patients. All of that, Brad, is saying, we -- the team is doing everything you've said and even more behind the scenes. I think there comes a point where we KURA will need additional operational resources to fully maximize the value of Zifto. What we see is Zifto to be the preferred combination agent across the continuum of care, from frontline to maintenance combination with every other approved agent as well as emerging agents. And clearly, at some point, you need global scale to be able to do that. But we also very much -- we prioritize patients. We also prioritize our shareholders. And so we want to make sure that anything we do ensures that our shareholders are appropriately rewarded. I can't be a lot more specific than that, obviously. But I can tell you, those of you who know me know I have a history of -- on both the business side and the science side. And I would say there's a lot of excitement about ziftomenib kind of across the continuum. And as we have more to say, we'll give updates throughout the year.

Your next question comes from Li Wastek from Cantor Fitzgerald.

I guess for the dealer that you just shared with us. Just wondering if you could put this into perspective for us relative to your competitor? And then second, in terms of the combinations, you mentioned that you will dose the first patient this quarter. And I guess just based on the past enrollment you've seen so far for your NPM1 patients, do you think that's going to translate into your studies as well?

Yes, in terms of excitement. So yes, a very good question. So your first question is -- Li, I'm sorry, can you tell me your first question again?

Yes, duration of response, maybe just share your perspective relative to our competitor.

Yes. Okay. Thank you. I wanted to make sure I answer the question you're asking. So if you'll indulge me, if you look at the Phase 1b study, right, this is what we're updating. I just want to underscore something for everyone. We're reporting data on 20 patients, 20 NPM1 mutant patients at our recommended Phase 2 dose. And that's nearly between 3 -- between 25% and 1/3 of the way to a registrational study just in terms of pure patient numbers. So both you and the analysts -- the other analysts and investors on the call are getting a very good look into potentially what a pivotal data set might look like if things continue on the current trajectory. And I want to just underscore that because you want to make sure you're comparing apples-to-apples. The competitor is 3 patients, right? 2 of whom went to transplant almost immediately. And so I'll highlight that to you, Li. I'm not going to give you an exact number. I'm going to wait for EHA to do that. But what you'll see is the duration of response being driven by ziftomenib. As you saw from the abstract, we have had a couple of patients who luckily for them, gone on to transplant with good results. But it's clear both the efficacy, the potency of Zifto, the ability to drive full count recovery and the ability to avoid these resistance mutations we're driving very good durability. And I think, Lee, it's that entire package that is what is driving the excitement among investigators. So to your other question of, is that -- do we think that's going to pull through to the combos? Yes, very much. Again, we've seen -- our combo strategy is we believe ziftomenib has the potential to be a cornerstone of therapy for acute leukemia. And our goal is to transform AML the way, for example, I think it might sound cliche, but the way Gleevec transformed CML, right, turned it from a devastating disease into kind of a chronic condition. Menin inhibitors may be the first thing to come along in AML that have the potential to do that. And we've seen similar levels of excitement and enthusiasm among investigators who are joss ling to either get into the 007, the 008 study or both. Our goal though Li, is to try to give as many sites around -- in both the U.S. and Europe, the opportunity to work with ziftomenib. So that enthusiasm where people actually use it with their own patients that, that continues to build. That's what's, I think, driving those exceeded expectations, and we fully expect that to pull through into the compass.

[Operator Instructions]. Your next question comes from Phil Nadeau from TD Cowen.

A follow-up perhaps on the last question. In terms of those earlier lines of therapy in the combination regimens, when we've discussed the opportunity for inhibitors with our consultants in the earlier lines, some have questioned what trial design would be necessary to support approval and use. Do you have any thoughts on what a registration trial would look like for an early line combo regimen in particular, what endpoints do you think would be meaningful and likely to be hit?

Yes. Phil, it's a good question. And I don't want to get ahead of the team on this. It is very much an active topic of discussion. I don't think we've said much publicly about what registrational studies would look like in the front line. Clearly, you're going to need to have I think it's --unlikely you can rely on MRD negativity. You may be able to go on the basis of response rate with survival. But as for specific parameters, it's obviously going to depend on the specific combination and the line of therapy. I will tell you, we're -- we've highlighted trying to do 2 things simultaneously, provide a data set so that physicians can use ziftomenib with whatever regimen they want to use, whether it be venetoclax, chemotherapy, other targeted therapies. That's our first goal. Our second goal is to go where there's the greatest unmet need and the greatest commercial opportunity that's going to be venetoclax. I think Phil will learn as we begin to get experience on those patients. For example, is there the potential for either synergy or resensitization I think we're cautiously optimistic, but it's just a bit early to speak to specific registrational designs at this point. Let us get a little bit more experience in Phase I and build up that data set. And then as we've started to lock it down with the investigators and the KOLs, we can communicate it. But it's very topical for our team internally.

And then second question is I'm wondering whether you have any new visibility on the potential competitors, obviously, not the competitors that are coming from the public companies, but investors have an eye out for those potential competitors, the menin inhibitors either at big pharma or foreign pharma. Any visibility on when the first data from any of those programs could be announced? Or are you running into any of them as you enroll your studies?

I'll tell you, we're not running into them. No. I think there are 3, right? There's Janssen, Dai-ichi and Dainipon Sumitomo. We don't hear a lot about them. We don't bump into them as you would say. We're not -- we're careful not to put our investigators in a position where we ask them for data because for obvious reasons, we wouldn't want them to share data on our programs. But we've been impressed, Phil, to this point, as I said, by the pace of site activation and the pace of enrollment in the NPM1 setting. And I think that's as much of a biomarker as we probably have. And I'll go even a step further and say, -- my prediction as we go into KMT2A, you're going to see the activity pick up significantly based on what we've seen with NPM1. And I'm cautiously optimistic we'll be best-in-class there as well. The ability to drive durable responses without necessarily needing to go to transplant so quickly. But obviously, the proof is in the pudding on that one. But that's what we're hearing back as we go out and we talk to investigators -- our investigators both in the U.S. and Europe.

And last question from us is one that we get from investors. We're curious to hear your thoughts on it. Any -- does Cure have any desire to go into diabetes? Yes, it's a good question. So I would say the following. We are doing work -- we're doing preclinical work with not only ziftomenib, but next-generation menin inhibitors that are reversible. And we're doing them in diabetes models. And we're doing that to try to feel sort of be very data driven. I think the data that you're referring to, it's provocative. But it's just -- it's very incomplete. I can tell you this, if there is a connection there, and there's a biological rationale for why one would use a menin inhibitor in diabetes. The question is really the effect size, the safety, et cetera. I would tell you this, we believe Ziftomenib is the best-in-class menin inhibitor in acute leukemia. If you want to go into, whether it's diabetes or solid tumor indications, both from a safety perspective and from the perspective of the IRA, you want to take a different chemotype, -- you want to take a different compound forward. And I believe, based on the work that our chemistry group has done, we'll have a best-in-class reversible inhibitor to take into diabetes, but let us do the work and really validate that as a meaningful opportunity because as you know, it's a completely different development paradigm.

There are no further questions at this time. I will turn the call over to Troy Wilson, President and CEO, for closing remarks.

Thank you, Julie, and thank you all once again for joining our call today. We'll be participating in the JMP Life Sciences Conference next week in New York and look forward to seeing a number of you there. In the meantime, if you have any additional questions, of course, please feel free to contact Pete, Tom or myself. Thank you again, and have a good evening, everyone.

Ladies and gentlemen, this concludes your conference call for today. We thank you for joining, and you may now disconnect your lines.