Jim Dentzer: Yes. So we’re continued to look at those data and learn more about emavusertib in that population. As you know as we have made more public, we now have a very clear strategy going forward as a result of our discussions with FDA. We know that this drug very consistently from mechanism of action to preclinical data to clinical data works exactly where we would expect it would as a single agent. It works in patients with FLT3 or spliceosome mutation and so that’s where we’re going for monotherapy. But you also remember that IRAK4 Long is not just the single largest genetic driver of disease in this AML/MDS spectrum, but it’s also over expressed in the entire population. Half the population has so much of it, that monotherapy works, the other half still has a significant amount, it’s just not quite as much as the monotherapy crap.
So what we’re planning on doing with this drug is in the rifle shot genetic populations where this drug ought to be differentially active and so far looks to be, we’re going to go single agent relapsed/refractory setting, again, FLT3 and spliceosome. For everybody else, we’re going to go frontline combination because we think that that’s what makes sense. In AML, the standard of care is aza/ven. So we are going to go aza/ven frontline in combination with emavusertib, all comers, doesn’t matter what mutation you have. In MDS with the recent magro release from Gilead, I would say the standard of care question is a little more open. We’re still waiting for the output of the aza/ven study, but it’s not clear exactly what that standard of care regimen is.
So it’s also not clear what we would want to add emavusertib to. So we – at this point, what we’re doing is engaging our physicians and KOLs to try and figure out what is the most appropriate strategy for this drug. But long-term, our review generically is this drug is going to get used as a single agent wherever it makes sense, that’s going to be spliceosome and FLT3 mutation, and everywhere else it’s going to go frontline, all comers, no filter needed. That was a really long answer. I hope that was helpful.
Soumit Roy: No, that was incredibly helpful. Thank you. Thank you again for taking the questions and congratulations.
Jim Dentzer: Thank you. I really appreciate it. Thank you for calling in.
Operator: The next question will come from Yale Jen with Laidlaw & Co. Please go ahead.
Yale Jen: Good afternoon, and I also add my congrats on the progress.
Jim Dentzer: Thank you.
Yale Jen: My first question is in terms of TakeAim Lymphoma regarding the PCNSL. Could you give us a little bit more color in terms of the current study design process and eventually that the timeline in terms of data release? And any other color, so would be very helpful.
Jim Dentzer: Sure. So in primary CNS lymphoma, so let’s step back for a second. Just as in AML and MDS IRAK4 is important because it binds really hard to the myddosome and MYD88 in particular in the toll-like receptor pathway and shuts it down. That’s important on the AML/MDS side, because IRAK4 Long is the largest genetic driver of disease. On the lymphoma side, it’s an indirect target. So NF-κB is the problem in primary CNS lymphoma and NHL more broadly. The current treatment is ibrutinib that shuts down the BCR pathway, which is one of two pathways driving NF-κB. Our drug emavusertib shuts down the toll-like receptor path, which is the other pathway driving NF-κB. So our strategy in lymphoma is these patients who really want to downregulate NF-κB over activity, today they’re looking at using ibrutinib or a BTK inhibitor to do that work.
