Currently we have three approved JAK inhibitors, ruxolitinib, fedratinib and momelotinib. Ruxolitinib was the first drug of its class. Really, it changed the landscape of how we treat the patients. But one of the adverse events, it caused cytopenias or low platelets and anemia. Fedratinib has a similar profile as ruxolitinib and it’s mainly used as second line and then we have momelotinib which not only inhibits JAK but also inhibits ACVR1...
Currently we have three approved JAK inhibitors, ruxolitinib, fedratinib and momelotinib. Ruxolitinib was the first drug of its class. Really, it changed the landscape of how we treat the patients. But one of the adverse events, it caused cytopenias or low platelets and anemia. Fedratinib has a similar profile as ruxolitinib and it’s mainly used as second line and then we have momelotinib which not only inhibits JAK but also inhibits ACVR1. So that makes patients have responses in anemia. So it’s a really good drug for cytopenic patients with myelofibrosis. And the results are quite good. It might take a long time. I mean, we must be patient in order to achieve those responses, but really it has changed the landscape of treatment. And about the unmet needs that we may have in myelofibrosis, I think that we’re seeing in this, indeed, that we’re moving towards combination therapies that might modify the natural history of the disease, which is our main and final goal.
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