EHA 2026 | Novel targeted and anti-inflammatory strategies advance MPN treatment landscape

So what’s novel in the MPNs, right? So I’m hoping we are moving more into the targeted era, where the biggest breakthroughs and boons on JAK or RAS-ASH were the chimerical and monoclonal antibodies, where we have preclinical and human data in ET and myelofibrosis on the INCA study, the INCA-909, which is very, very exciting. So these new data and updates from Claire Harrison presented at EHA will also show us how these responses look like in myelofibrosis patients, which already were presented six months ago with very promising and compelling responses in splenetic symptoms and anemias. So that’s a very, very breakthrough, something to watch out for. And they’re more into the space and hopefully more data shown in patients. I do see there’s going to be a role for all of these antibodies for different patient populations. And our next goal for life would be to kind of more discover and prognosticate who would be better fitted with what and in what line and what sequence. And then we had interesting um novel mechanisms, right, there is a lot of effort into which molecules work in MPNs, what’s responsible for disease modification for disease progression, and certainly inflammation, which also comes down to the interferon, plays a significant role in disease propagation. So, for example, to me, very interesting was a presentation by Rebecca Schneider on the anti-inflammatory and anti-fibrotic possible novelties and discoveries of these agents. And she actually mentioned an ongoing study by the Hebart group in Europe that includes an agent that blocks alarmins, which is an NF-kappa-B pathway that shows a role in disease modification progression for patients called tasocitinib, and we actually do have also that compound in the United States as a phase one study for patients with myelofibrosis with a little bit of a broader arm for patients that would be on JAK inhibitors as an add-on, patients without JAK inhibitors but having a need for therapies, as well as refractory and relapsed. So I’m really looking forward to seeing these novel mechanisms. I’m pretty positive they won’t be working as a single agent. So the combinations, how to better design them, where to put them, I hope they will fulfill our goals of modifying MPNs in 2026 and beyond.

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