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ASH 2025 | An update on BET inhibition in myelofibrosis: data presented at ASH 2025
In this video, Claire Harrison, MD, FRCP, FRCPath, Guy’s and St Thomas’ NHS Foundation Trust, London, UK, provides a brief update on BET inhibition for the treatment of myelofibrosis (MF). Prof. Harrison highlights several studies presented at the ASH 2025 meeting, including PROMise (ISRCTN12451433) and MANIFEST (NCT02158858), that demonstrate the efficacy and tolerability of BET inhibitors in combination with JAK inhibitors. This interview took place at the 67th ASH Annual Meeting and Exposition, held in Orlando, FL.
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Transcript
BET inhibitors, by targeting NF-kappa B, inflammation pathways, and potentially also JAK/STAT signaling, have been an interesting combination partner with JAK inhibitors, predominantly being investigated with ruxolitinib. And there’s several pieces of data presented at ASH, actually. So the first was a Chinese presentation with a Chinese JAK/ROK inhibitor in combination with a BET, showing some good tolerability and efficacy...
BET inhibitors, by targeting NF-kappa B, inflammation pathways, and potentially also JAK/STAT signaling, have been an interesting combination partner with JAK inhibitors, predominantly being investigated with ruxolitinib. And there’s several pieces of data presented at ASH, actually. So the first was a Chinese presentation with a Chinese JAK/ROK inhibitor in combination with a BET, showing some good tolerability and efficacy. Secondly, we presented an academic study called PROMise with OPN-2853 BET inhibitor in combination with ruxolitinib, showing the usual responses we expect to see as an add-on, so patients still on ruxolitinib and then benefiting more with spleen and symptoms. And then finally, we also presented the 96-week data from the MANIFEST study. So this is really profoundly interesting in the field because we’ve still got patients who are in the randomized study. So we’ve still got a running comparison at 96 weeks. So it’s a big study and the longest ever randomized study. And what we saw was continuation of deep spleen responses, still a doubling of patients who are benefiting from both spleen and symptoms, ongoing improvements in hemoglobin, and then really importantly, also reductions in bone marrow fibrosis and improvements in mutational burden. So also importantly, because there was a slight imbalance in leukemia events in that study, we showed that actually these imbalances no longer exist. So that’s important in addressing a safety signal.
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