They also, we know have different activities against different kinases. So it may turn out to be like some of the other indications where you have multiple kinases that hit different patients with different mutation profiles. But most likely we likely will move it more toward the B-cell arena and also toward inflammation and autoimmunity because we’ve been, as you can tell from the publications we’ve been digging into that area, understanding it, there’s still a need because this drug is different from the other non-COVID and BTK inhibitors. It hits a different set of kinases. It has different activities, and we believe that if we’re able to combine it, for instance, with some of these other drugs that are being developed for the B-cell malignancies like the Venetoclax for instance, then we believe we can see real activity there.
So there are paths for it that do not interfere with Tuspetinib. Does that answer your question?
Operator: Our next question comes from the line of Li Watsek with Cantor Fitzgerald. Your line is open.
UnidentifiedAnalyst: Hi everyone. This is Rosemary Ann for Lee. Thanks for taking my questions. Just a couple here. Firstly, are you able to give some color around early activity that you see from the monotherapy arm in APTIVATE, and then on the RAS pathway, can you talk a bit more about where you can go with this finding if RAS correlates with any other mutations potentially, and whether you see mono or combo therapy potential here?
William Rice: Thanks Rosemary. So, thanks Rosemary for coming on. So I’ll start with this and then maybe Dr. Bejar wanted to jump in. So in terms of early activity, again it is very early in the APTIVATE trial on the monotherapy and as we said in our press release, we are beginning to see what we call an initial anti-leukemic activity. You’ll remember we’re very conservative on what we see in terms of what we’re seeing in the clinic. So yes, if you’re asking us we do see some level of blast reductions, we’re not going to be talking about how much or what we’re seeing or the number of patients. It’s just very early. But are we seeing hints of activity beginning? Yes, it’s early, but we are. You also ask about the RAS mutations.
I find this one very exciting to tell you the truth because many of the other drugs out there, one of the major scape pathways for other drugs is the RAS pathway. But we’ve seen activity, CR, CRHS, these are real responses. Inpatients have NRAs, KRAs, and also other mutations within the RAS pathway. So it’s a real need that I don’t think people have highlighted enough in AML because there hasn’t been a really a good drug to treat these. But, I’m hoping we get more of these patients. I’m hoping that we see activity in these patients and maybe this will be another indication that we can look toward as an accelerated approval. But the data we’ll have to point us in those directions. I’m going to turn over to Dr. Bejar and see if he has any additional comments.
Rafael Bejar: I think that was well put. I think what is exciting about the activity in RAS mutant patients is that RAS mutations in the relapse setting really mean something different than they do in the frontline setting. Even drugs like Venetoclax, you can get responses in patients who have NRAs in that frontline setting. But when patients relapses typically with an expanded NRAs clone or a new NRAs clone or FLT3 clone, that activates that signaling network. So, the ability to target patients that have NRAs mutations is exciting not only to treat potentially refractory patients, but also to treat patients in the frontline and prevent the development of resistance through that pathway. So we’re hopeful that it has benefits in both patient populations.
