ASH 2025 | Pivekimab sunirine in combination with venetoclax plus azacitidine in unfit, newly diagnosed AML

I think we’re all excited by the molecular targeted therapy. There’s multiple triplet combinations that are looking exciting, particularly in the FLT3 space, the NPM1, and KMT2A. But the challenge is there’s still over half of AML patients that won’t have a mutation that’s targetable. So we really need our next new therapy that’s going to be the game changer for frontline non-intensive AML-based backbones as really this is a majority of treatment patterns within the United States. So pivekimab is a CD123 antibody drug conjugate that’s been now studied quite extensively both as single agent and now as combination. So the data we present is looking at a standard frontline triplet. I think what’s nice is we did look at different venetoclax durations. I would say out of all molecular agnostic subsets, we actually present really the highest composite CR response rate that we’ve ever seen, actually pushing well above 80% to 90%. So the vast majority of patients are responding. We’ve not really seen significant increased toxicity. There are some infusion reactions and some edema tox that’s manageable. Fortunately, grade three events or higher are quite rare. I do think that optimizing venetoclax duration is a big push amongst the field. So 14 days did have a little bit quicker count recovery, although both the 14 and the more continuous venetoclax were both well tolerated. I do think in the sort of next phase, which we’re now moving into a potential phase two, three trial, you know, doing early bone marrow biopsies, holding venetoclax and quicker dose reductions down are going to be key. I think the big question is what about mutant versus wild type? And I think the field really needs to separate these groups for all pivotal strategies. I’d say the wild type or P53 wild type group looks really exciting. Actually, survival data look quite favorable over doublet, especially because there’s not many super responders. I think the P53, I’m not as convinced. Does CD123 targeted therapy add a lot or not? The data look a little bit better than historical, but I think we need to be cautious with maybe a little bit more longer follow-up. But I think especially the wild type quite excited, maybe limiting the number of P53 mutant patients on a more pivotal strategy or even excluding them maybe the route to go when we think about regulatory approval.

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