Troy Wilson: Yeah, Brad, so 2 good questions there. On the €“ what does it take, it’s probably a little larger than a handful, just to be colloquial maybe a couple of handfuls. But if you’ve got €“ if you’re not seeing €“ or if you’re seeing sort of mitigated DS, i.e. grade 1, grade 2, you’re not seeing the more severe forms of DS; you can calculate the posterior probabilities and figure out, what’s needed. The more patients you have, the more confidence you have. But, we were seeing a 30%-plus rate of DS, so it won’t take too long. In terms of the contributions of efficacy that obviously will require more patients to parse them out. But I’ll just remind folks, neither 7+3 nor venetoclax are particularly effective at driving durable responses in these patients, particularly in the KMT2A patients.
So you should get a signal fairly early on. And I’ll just remind you, Brad, we were seeing all of €“ many of the other correlates of disease control blast count reduction symptomatic improvement and so forth. So we’re pretty confident that this is going to solve the problem. And as far as the NPM1 is concerned, we’re in good shape there. We don’t really have to take anything beyond the traditional measures to manage the DS. This is really just a question now about KMT2A.
Bradley Canino: I appreciate that. If I can sneak in one on the FTI decision to de-prioritize the EGFR combination, how should we read that to the potential KO-2806 combination partners? Because you previously mentioned you’d be using new targeted therapy combo partners for that drug early on? Well, those combo partners being types where you’re trying to enhance ORR and we can see that earlier or versus delaying response like an EGFR combo? Are there
Troy Wilson: Yeah, Brad, I appreciate €“ yeah, sorry to step on your question there. I appreciate the way you ask the question, because you’ve already with your question anticipated the answer. So we’re seeing pre-clinically, the potential to combine FTIs and, most notably, 2806 with a number of different targeted therapies. And I listed EGFR inhibitors, PI3 kinase alpha inhibitors; you’ve now heard us reference TKIs, specifically in renal cell carcinoma and KRAS inhibitors. And to your specific question, one of the things that we’re always doing is taking in data, scientific data, clinical data, business data, find macroeconomic data. We realized that we want to get to clinical datasets that will show the ability for FTIs to realize the promise of the potential for additive or synergistic activity.
We think there may be opportunities, Brad, to do that more quickly than was the case with osimertinib. So it was not in any way a lack of interest or enthusiasm on our part, but really a recognition that we need €“ we operate in a world, where we have to show data as quickly as possible. The amount of value that we can create per dollar and per unit time is a measurement of our success, and we want our shareholders to understand. We think we’ve got a winner with zifto. We think that 2806 is looking very strong and coming on more quickly than we expected. So I think it’s appropriate particularly in these times to look at the portfolio and, say, where can you create the greatest amount of value in the shortest amount of time and the fewest dollars.
And that’s exactly what we did.
Bradley Canino: Okay. Thanks, again.
Troy Wilson: Sure.
Operator: Our next question is from Tiago Fauth with Credit Suisse. Please proceed with your question.
Unidentified Analyst: Hey, this is on the line for Tiago. Thanks for taking our questions. So we’ve heard a lot about discussion about the relative value of an MRD positive CR versus an MRD negative CRh in the relapsed/refractory setting. So what’s your perspective on that? And are there any data that really addressed that question? And then is there any read through to durability?
