Li Watsek: Thank you.
Operator: Your next question comes from the line of Yale Jen with Laidlaw. Your line is now open.
Yale Jen: Good morning. And thanks for taking the questions. I just want to have on the last question, just asked which you mentioned that the aza-ven is the — I guess, fair line for three inhibitor patients. So you mentioned about the survival. What about the ORR because I think that probably will be a benchmark actually you might have compared to as well.
Jim Dentzer: Yes. Actually, again, Bob, you’re probably better to take that one.
Robert Martell: So the response rate sort of — there’s not a lot of data on splicing factor mutation post aza-ven. There is one really interesting study looking at first-line treatment with AML that demonstrates splicing factor mutations have an extremely low response rate. So patients who don’t have a splicing factor mutation have approximately 80% response rates. And only maybe — 20% who can achieve that, whereas almost 80% of the patients with a splicing factor mutation are unable to achieve a [CR] (ph) in the first-line, it’s dramatically reduced. In terms of a FLT3 subset of population that is roughly similar, although there aren’t as detailed data on that. Does that answer your question?
Jim Dentzer: Yes. And that was frontline by the way, Yale. So of course, in relapsed refractory, it gets far worse across the board, right? So it’s one of the reasons why we’re excited about the populations that we’re going after is that they’re cylinder served. The hurdle to show something is lower. And we are excited to talk about the age and activity that we’re seeing in that population. Again, it’s relapsed/refractory, in our case not front-line. Even though in both settings, there is a dramatic drop-off in performance for existing therapies.
Yale Jen: Right. And it’s just a hypotheses to think what are these patients will be — I mean, in this patient population, would you anticipate potentially accelerate growth pathway if the data was robust?
Jim Dentzer: So it’s interesting that you say that. The — we look at the precedents in AML, specifically for gilteritinib for IDH1 and for IDH2. In all three cases, the FDA approved those drugs on four trials that were single-arm studies, based on a CR/CRh endpoint and that led to full approval, not even accelerated approval. So we can’t, of course, put words in the FDA’s mouth. We need to have the discussion with the FDA. But we believe that those precedents reflect an understanding at FDA that these diseases are really underserved by existing therapies, and these patients are in need of new therapies. So our hope would be that if we can bring a data set to FDA that can show that we can see single-agent activity and pair it with early but still indications of survival that the FDA will hopefully be in a position to agree to a registration path that can get these drugs in the hands of physicians and patients as quickly as possible.
Yale Jen: Maybe last question here, again a little bit forward-looking type of thoughts, which is that in terms of the FLT3 patients would you — I mean if the data is robust, would you consider a combination in other words to move up to the first-line instead of in the refractory patients at this stage of development.
Jim Dentzer: Yes. So in fact, the answer is we’ve already started that, right? And it’s not just for FLT3, it’s for all comers, whether you have a FLT3 mutation or not. And the reason for that, of course is that our drug, emavusertib, will start to target does target FLT3, but it also targets IRAK4. It targets the CLKs, CLK 1, 2 and 4, targets [derek] (ph), mean this is a multi-targeted drug to hit a number of targets of interest in the context of AML. So — and that is precisely why we’ve already started the frontline study, the triplet study of EMA in combination with aza-ven. So our hope would be with this initial study that we can chose safety. And with those safety data in hand, by the time we get to year-end, we’ll be in a position to have the drug be what I would call partner ready.
We’ll have a mature data set in splicing factor patients and FLT3 patients as a monotherapy, and we will have shown hopefully, by the time we get to ASH, and even though it’s just in a handful of patients that adding Ema to the aza-ven doublet in frontline is safe. And if we can do that I think we can make the case with the regulatory authorities that we are prepared to go simultaneously in the relapsed/refractory setting as a monotherapy and the frontline setting in combination. And I think we’ll be in a position to have a conversation with partners to get access to, obviously, non-dilutive financing, but access to a broader clinical infrastructure so that we can accelerate the pace of clinical development and increase our ability to maximize commercial launch.
So all of those things are part of our thinking at this point in time.
Yale Jen: Okay. Great. That’s very helpful. And I look forward to see the data next week and congrats.
Jim Dentzer: Thank you very much. Appreciate it.
Operator: Your next question comes from the line of Bill Jahangiri with Truist. Your line is open.
Billal Jahangiri: Hi, congratulations on progress. I have a couple of questions here. Your split for FLT3 and spliceosome patients inside the study, is that representative of the [real world] (ph). And then also — I’m going to move on over to the triplet study. Is there a way to, I don’t know maybe pick a subgroup of patients to derisk on the safety since this is the first time we’ll be seeing a triplet. And, I guess that’s a question. And then for PCNSL, are you guys still enrolling BTK — BTK-naive patients as well that we can compare and contrast those two data sets between experience [indiscernible] later this year.
