Taylor Schreiber: Sure. Yes, good morning Yigal. Thanks for the questions. As Lini mentioned, 88% of the patients enrolled to date in the PROC study progressed within the first six months of platinum. And so this is a fairly homogeneous poor prognosis group with rapid kinetics of disease. And we really – as Lini alluded to before, the size of the data set is not large enough where we can try to distinguish between did it make a difference if the patient progressed on platinum within one to three versus three to six months. All that we can say is that all of these patients were rapidly resistant to primary platinum. And then with regard to whether there’s a difference in the subpopulations or TP53 mutant AML versus higher-risk MDS in conjunction with azacitidine, we’re looking forward to sharing more data there soon with the frontline cohorts.
And what I can say is that it’s always been a little bit of a mystery why the TP53 mutant AML patients with some prior studies seem to do a bit better than the TP53 wild-type patients because otherwise, those are quite similar diseases. And one of the hypotheses that’s been out there in the literature is that the TP53 mutant patients seem to have a higher mutational burden. Perhaps there were more tumor-infiltrating CD8+ T cells, i.e., perhaps it was a more immunogenic tumor to start than some of the TP53 wild-type patients. And part of the value proposition of adding a CD40 agonist to a CD47 inhibitor was framed around the expectation that some of those characteristics might be normalized because of the immune-activating potential of CD40.
And so it’s certainly something that we’re looking at. And a priori, we can’t necessarily say that, that would indeed be the case, but we’ll be sharing data soon and following that over the next six to nine months.
Yigal Nochomovitz: Okay. Thank you.
Taylor Schreiber: You’re welcome.
Operator: And your next question comes from the line of Gil Blum of Needham & Company. Your line is open.
Gil Blum: Hey, good morning and thanks for taking our question. So maybe just to focus here on the ovarian cancer. What would you gauge as a go/no-go decision on PLD plus SL-172154? And – how relevant is PLD these days and PROC? I mean you faced some enrollment challenges here. So I’d love your $0.02 here. And I have a follow-up.
Taylor Schreiber: Yes, good morning Gil and thanks for the question. I mean, I can tell you that when we first started this study, there were many investigators who only joined the study because of the ELAHERE arm because as is highlighted by the JAVELIN study, PLD doesn’t help very much in these patients. And – it’s now – it took us about as long to enroll the first five patients in the study as it has to now complete this – complete enrollment in the study. And perceptions can be changed by data, right? And I think we’re starting to see that SL-172154 is adding something in both heme and solids. And certainly, and – people always seem to shy away from the word synergy, and we can’t say that quite yet. But if these data hold, then that’s what this will mean in the PLD setting.
This is an all-comer population and a response rate in excess of 25% in an all-comer PROC setting, non-biomarker selected in and of itself could be meaningful and could be very meaningful if it is accompanied by a duration of response that exceeds five months. And so those are benchmarks that we will be looking toward as we – as the data mature over the first half of next year. And similar to my comments on the TP53 mutant AML cohort in terms of what the next step would be, we’d be looking at an incremental expansion of the current study somewhere between adding 20 and 40 patients or so to confirm the results and to enroll those patients with our current momentum. And that would be the basis then of a regulatory discussion for the first registration-direct study.
