Michael Schmidt: In the NPM1 cohort, how many patients had overlapping co-mutations, other genetic alterations and potentially have had received other target agents prior to receiving revumenib and how do you expect that dynamic to play out in the pivotal cohort and ultimately on the market?
Michael Metzger: Michael, thanks for the question. So we didn’t break out that data in the swimmer’s lane, but I will tell you, as you noticed in the, we did say that a lot of obviously, a lot of prior therapy for these patients. In terms of co-mutations, I think the vast majority, if not all, were co-mutated. So, there were obviously, there is variations on the theme of what we saw, but we didn’t break that out. But I think, suffice to say, we had most patients were co-mutated. Yes, and it is obviously representative of what you would think.
Michael Schmidt: And in order to how does that affect potential sequencing of therapies? Should the data be replicated in your pivotal study, if approved, in your opinion?
Michael Metzger: Yes. I think what you are getting at is whether or not physicians will look at targeting these specific mutations for treatment. And obviously, the paradigm for NPM1, at least in the unfit population or the fit population, they get chemo or they get Ven/Aza upfront and then physicians look to target their mutations with either a FLT3 or an IDH inhibitor. And we do expect that if these patients have those co mutations, that is what’s going to happen in the real world and in trial as well. So, that is what ends up resulting, and I think the remarks that I made suggest this that physicians will be reaching for second or third line revumenib, after they’ve taken action against, obviously, frontline and then they are going after their targeted mutation to the extent they have one.
So, I think the data that we presented today shows that, right? It shows that patients do extremely well, treated in, call it, the 3rd line, 4th line setting on our drug, and as they progress and get into very, very late lines of therapy, which we have had some patients also like that, they don’t do as well. So I think the targeting of these mutations will likely come before revumenib.
Operator: Our next question is from Kalpit Patel at B. Riley. Your line is open. Please ask your question.
Kalpit Patel: Maybe a couple more questions related to the maintenance use of revumenib. Now that you have all the post transplant data here, how are you seeing the median duration of treatment for revumenib between the, KMT2A populations and the NPM1 populations? Do you expect them to be very similar to each other?
Michael Metzger: Yes, I think we do think it is going to be very similar. It is interesting how the data converges a bit. So you have patients in the KMT2A population that a great percentage go get a high, overall response rate, get taken to transplant and put back on drug and stay on drug and do very, very well. The speed at which they get a best response first and best response and then move to transplant is noteworthy in KMT2A. It is a beat slower, with NPM1, which probably allows their accounts to recover, as I mentioned earlier. But the paradigm is seems to be similar. At least in relapsed refractory disease, where physicians are interested in putting them back on, once you get to a CR, you take them to transplant and you put them back on drug.
I think that is also new and it is a new paradigm, but it is actually a very positive back pattern for the drug in terms of the ability to treat patients for a long time and keep them in remission. So we are actually very encouraged by what we are seeing, both by the from the efficacy standpoint and the tolerability and safety standpoint to allow this to be the new paradigm. So it is quite interesting how it is turned out to be pretty similar.
Kalpit Patel: It is nice to see the additional responses in the NPM1 patient population. I’m just curious if you have any more, NPM1 patients after that, I believe July cutoff in that data in that Phase 1?
Michael Metzger: We do not, this is final data in terms of patients, that is all we have. We were looking to complete the pharmacokinetic work in the Phase 1 and we had talked about that in the past and this was these are the remaining patients to accomplish that.
Operator: Our next question is from Justin Zelin at BTIG. Your line is open. Please ask your question.
Justin Zelin: Hi, thanks for taking the question and congrats on the progress here. Maybe a question just on the SAVE AML study, I think the abstract show there wasn’t much differentiation Syndrome seen here. Can you comment on whether you would expect, differentiation syndrome to be reduced in the combination setting moving forward? Thank you.
Michael Metzger: Yes. Thanks, Justin. The answer is yes. I mean, the data, as we have discussed are highly encouraging. And I think that clearly, the combination with Venza, of reviuminib with Venza and the hydromethylating agent is extremely well tolerated. So there is no reason to spec that, we would see a different pattern as we advance, for instance, as we advance combinations of Sennheypomethylating agents into earlier lines therapy. So I think it is both expected and gratifying to see.
Justin Zelin: Thanks. And congrats again on the plenary for axatilimab. Anything additional we should look out for at ASH beyond what we saw at the top line?
Michael Metzger: Justin, I think, yes, thank you. We obviously have the plenary for axitilumab, which is very exciting. I think we had five abstracts out today, so a lot of information saved, as we talked about, but also some of the combinations. And so, yes, just a lot of interesting information coming your way and obviously, we will have lots to say at our event at ASH as well. So, looking forward to seeing everybody there.
Operator: Our next question is from George Farmer at Scotiabank. Your line is open. Your line is open. Please ask your question.
George Farmer: Hi, good afternoon. Thanks for taking my question. Neil, you mentioned that the 6.4 month DOR in the AUGMENT-1 trial, could get better. I’m wondering if it is it possible it could get worse? We haven’t seen any capital minor curves, so just wondering what your thoughts are there. And then also in the SAGE trial, alluded to a previous question about the myelosuppression. Wondering if those patients got any growth factor support and if growth factors were effective. Perhaps maybe revumentum had an impact on recovery or anything like that, if you could comment. Thanks.
