EHA 2026 | Which emerging therapeutic approaches have the potential to transform patient outcomes in MF?

I’m eternally optimistic about all of these things because I think that all of them have value. I don’t think that there’s any one particular agent that we are developing, particularly late stage at this point, that doesn’t have a potential niche or application. I would say at a high level, the drugs that I think have clearly demonstrated from preclinical to early clinical now to Phase III results is selinexor, which is an XPO1 inhibitor approved, of course, in myeloma, but repurposed in myelofibrosis. Very relevant to multiple pathways. The SENTRY data, I think, really speaks volumes to the ability to augment response and spleen response, but also the potential for survival benefit, which we’re already seeing early on, tied into SVR. So to me, that’s quite exciting. And it’s new data. It’s really only at ASCO and EHA and now JCO. So they’ve got to let people sink their teeth into that one. It has to be followed out longer. But that is quite, I think, quite compelling. And not surprising, because I think these drugs are hitting the mechanisms that matter. The other drug, navtemadlin, clearly an active drug. We have an immense amount of data, again, pre-clinically and clinically and from correlatives, that it really hits the clone and you get very deep responses. I very much look forward to seeing the results of the POIESIS study. So you get patients on rux, JAK inhibitor-naive, and then only after 18 weeks do you then assess for response. Suboptimal responders, you add navtemadlin on versus placebo. And the question is, can you improve upon and deepen that response? It’s a brilliant study in the sense that it probably replicates how myelofibrosis is actually treated in the community. You would start rux and then you would add on. The fundamental question between the SENTRY study, the POIESIS study, the MANIFEST-2 is really great, great agent too. PAN-BET inhibitor, we’ve got beautiful data from MANIFEST-2 demonstrating not just doubling of spleen and improvement in symptomatology, even if it wasn’t statistically significant, I would still say it was clinically meaningful, but it’s the durability. It’s the first study, we have 96-week durable data. We have 144-week coming out at some point, demonstrating that you can give these drugs, improve outcomes, and extend the durability, which is what really matters. The question is, how do we do it? Should it be upfront? Should it be add-on? These are nice problems to have. We don’t have the answers quite yet. We don’t quite have yet biomarkers that would tell us, well, this patient probably would do best with navtemadlin, this patient with selinexor, this patient with pelabresib or nuvisertib or, you know, where does the CALR antibody? We’re going to get to a point where we’re going to have a lot of options and maybe not so much clarity on how best to use them. But I would still say that’s a better point than having no options or limited options.