Bradley Canino: Thank you.
Troy Wilson: You’re welcome.
Operator: Thank you. Your next question comes from Peter Lawson, Barclays. Peter, please go ahead.
Peter Lawson: Hey. Thanks for the taking the questions. Just around the 200-milligram dose in combination, are there any trends emerging from the duration on therapy between the KMT2A versus the NPM1 patients, Troy?
Troy Wilson: It’s early, Peter. It’s early — I mean, the — maybe just to take a step back, it’s too early. If you look at these patients in general though, Peter, the KMT2A are often younger, more typically more frequently go to transplant. The NPM1s, the median age is like 60. So they — and they — oftentimes, they’re older, a little bit more frail. They perhaps don’t go to transplant as readily as the KMT2A. I think it’s too early to say. What we saw from the 200-milligram data, Peter, was even at that dose, which, again, in our view, was a nonoptimized dose, you saw meaningful clinical activity, I think better than many people expected. And it certainly gave us confidence to continue escalating. A big part of the KMT2A, Peter, of driving clinical benefit there is going to be this concept of whole body exposure.
We think that’s critically important. We think it gives the patients the best chance of really differentiating all of the extramedullary disease. And that’s the advantage that zifto has as we look out across the competitive landscape. It’s highly tissue penetrant. It’s extremely well tolerated. It doesn’t have any other toxicities. And in combination, the DS is very well managed, very well mitigated. So I think we’re optimistic, Peter, that as we go higher in dose, that may be — that may provide a benefit to both sets of patients and whether those patients go on to transplant or not. Obviously, we’ll be able to say a lot more when we show you the next data installment here.
Peter Lawson: Got you. And then are you seeing anything in the side effect profile when you combine, is there anything that would be impacting duration of therapy or any quirks from particular regimens?
Troy Wilson: If anything, Peter, I think it’s actually helping with the backbones. Zifto is so active in these populations that people think about — if you think about how do you use this, in the case of 7+3, they’re on for about a week, right, on chemo and then they’re on zifto after that. You don’t have to hit them with a sledgehammer when you’re giving them a potent differentiating agent, and that’s both populations. With ven/aza, the protocol follows ven/aza as it’s labeled, but there’s an openness among investigators to move patients off of these myelosuppressive regimens as quickly as possible. You may actually see better results. We’ll see when you combine with zifto. It’s early days. But Peter, we’re not seeing anything in terms of safety, tolerability, side effect profiles, combinability.
We’re not seeing anything that’s giving us any concern. In fact, if anything, it’s telling us — we use these best-in-class language. We mean it when we say it, zifto. Now that we’ve put the DS question largely to bed, I think zifto is really going to be able to show you what it can do.
Peter Lawson: Great. Thank you so much. Thanks for taking the questions.
Troy Wilson: Pleasure.
Operator: Thank you. Your next question comes from Phil Nadeau, TD Cowen. Phil, please go ahead.
Unidentified Participant: Thank you. This is Ernie Rodriguez for Phil. Thanks for taking our questions. We have one. With the competitors many inhibitors launching, even though it’s in another indication, the KMT2A, is there anything — they’re likely launching soon in this year — later this year, is there anything on that launch that you would be looking to or any metrics or any other aspects that you would expect will be useful or informative to your strategy?
Troy Wilson: Yeah. This may surprise you, but let me take off my Kura CEO hat for a second and just say, if they’re able to get approval and get to market, we’re going to applaud. We’re going to congratulate that. Because at the end of the day, we all do this for patients. And KMT2A, which is the indication you’re talking about is a disease of high unmet need. I think that — and I’ll let them speak to their process and where they are. It is — KMT2A is a much smaller opportunity, but it’s a good indicator of the utility of menin inhibition. We’d certainly be happy that they’re out educating physicians and educating the community when we’re coming along with what we believe is a better menin inhibitor. And whether you look at their combo data or our combo data, you have to believe that combo is the way to go here.
So while we believe that ultimately, when we get to market in NPM1-mutant AML, we will be best-in-class. We also think it sets the stage for us to be best-in-class in combination and in maintenance. And that’s how you drive a multibillion dollar peak sales potential. So we’ll be paying — playing — excuse me, we will be paying careful attention, watching, cheering, learning, not necessarily tracking their key performance indicators because the drugs are very different, but it will be instructive of the utility of menin inhibitors. What is clear to us is that there is — 30% of AML patients are NPM1. We’re seeing that in terms of enrollment. It’s going like gangbusters. And the fact that we’re seeing such strong KMT2A enrollment in the combo, I think really speaks to the potential of those regimens to drive activity.
Hopefully that answers your question.
Unidentified Participant: It does. And another quick one on the preclinical data in solid tumors that you expect to disclose in H2. What should we expect on that — are we going to be able to determine like what — which kind of solid tumors would be most amenable — or you will be pursuing on the clinical side or is it more like a broad proof of concept in a broader range of solid tumors.
Troy Wilson: It’s — yes. So it — what we’re talking about really is epigenetic regulator — epigenetic regulation of oncogenes or potential oncogenes, right? That’s what you should be looking for. Are there going to be multiple opportunities? We think so. But each of them is sort of — we’re all still learning about epigenetic regulation. What’s clear to us is that menin, the menin MLL interaction appears to play a critical role both within and outside of AML. When you see this nonclinical data, and we’ve been working on this internally for quite some time, looking not only with zifto, but with other menin inhibitors as well. You’ll know — it will be very obvious to you, the first place that we’re going. Beyond that, I think we have to continue to be data-driven.
We’ve been very good about putting non-clinical data out there and letting that guide the development. We’re going to continue to do that. So we’ve really taken our time, gone to school, done the work and quite excited to share that data with you here in the second half of the year. It will if it works the way it works non-clinically, it’s potentially transformational for that disease type and can only then drive the TAM that much larger.
Unidentified Participant: Got it. Thank you. That’s helpful. Thanks for taking our questions.
Troy Wilson: Sure.
Operator: Thank you. Your next question comes from Ren Benjamin, Citizens JMP. Ren, please go ahead.
Reni Benjamin: Hey, good afternoon, guys. Thanks for taking the questions. Maybe I missed it, Troy, in your prepared remarks, but what’s happening with the post-transplant program? Has that been initiated, maybe I missed it, is one of the upcoming milestones. Just wanted to know how you’re thinking about that.
Troy Wilson: Yeah. Thanks for asking, Ren. You did not miss it. What I can tell you is in contrast to 001 — KOMET-001 and KOMET-007 and KOMET-008, that trial is an investigator-sponsored trial. We’ve done everything as sponsor — or not as sponsor, but as the drug sponsor, if you will, as a company, we’ve done everything we can. We’ve put it into the investigator’s hands. They’re working through the last few bits of red tape. They have everything they need. As with any investigator-sponsored study, it’s their study. They control the conduct, they control the timing, they control the dissemination of data. What I can tell you, Ren, is that the FDA has reviewed it, cleared it. It’s really now just in study startup, but it is in the hands of the investigators.
So we’re not — we’re probably not going to be in a position to guide you on enrollment there, and we’re going to have to rely on them to speak about the trial. But it’s going in the right direction. And let me go one step further. It’s just to remind everybody, we are assessing the safety and tolerability of ziftomenib in the post-transplant maintenance context so that we can have the appropriate discussions with health authorities about what a registration-enabling study would look like. Because we can’t do everything at the same time, we’ve chosen to — we’ve actually accepted a proposal to do it as an IST. And at this point, Ren, they’re just, I think, put — dotting the I’s and crossing the T’s. I will — one other thing — yes, one other thing, Ren, I’ll say is, of course, and this — we do get this question, which is why I wanted to add to it.
