Dr. Gabriela Hobbs discusses important new developments in myelofibrosis treatment from the American Society of Hematology annual meeting. Dr. Hobbs highlights emerging therapies, novel combination approaches, and encouraging trial results that are aimed at improving symptoms, spleen size, and blood counts in people with myelofibrosis.
Dr. Gabriela Hobbs is a hematology-oncology physician specializing in the care of patients with myeloproliferative neoplasms (MPN), chronic myeloid leukemia, and leukemia. Dr. Hobbs serves as clinical director of the adult leukemia service at Massachusetts General Hospital. Learn more about Dr. Hobbs.
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Transcript
Jamie Forward:
Dr. Hobbs, we’re just coming off the American Society of Hematology Annual Meeting. What are the most important updates in myelofibrosis that came out of that meeting?
Dr. Gabriela Hobbs:
Sure. So, there’s a lot of different medications that are being developed for myelofibrosis. I think that just seeing the variety of different medications that are being developed and studied for MF, I think, was probably the most exciting part of the meeting. Specifically, I think we were all really eagerly awaiting results of the Incyte monoclonal antibody that’s being developed for CALR-mutated MPNs. This year, at EHA, we saw the presentation of the CALR antibody for ET patients, and at ASH this year we saw the presentation for patients with myelofibrosis, both as monotherapy as well as in combination with ruxolitinib (Jakafi).
And so, although I would say the data for myelofibrosis was not quite as exciting or as profound as it was for ET, it definitely still seems to be an active compound. It seems to still be really safe and well tolerated, which is especially important in myelofibrosis patients that are much more likely to have cytopenias, for example.
So, that was one presentation that I think we were all waiting for. In terms of other drugs that are being developed, so there are still several medications that are being developed in combination with JAK inhibitors.
And this year at ASH, we saw a presentation of nuvisertib, an oral PIM kinase inhibitor, that was presented in combination for the first time not with ruxolitinib but for momelotinib (Ojjaara). So, that was the first time that we saw a novel combination therapy being utilized with a JAK inhibitor that wasn’t ruxolitinib.
And those data looked really promising also actually. The combination seemed to be well tolerated. Patients seem to have really impressive rates of spleen volume reduction and symptom improvement as well as some improvements in their blood counts. The other presentation that I think we were all waiting for is the 96-week data of the Pelabresib MANIFEST-2 Study, and encouragingly there don’t seem to be any new safety concerns. There was concerns before that maybe there was a higher rate of blast phase transformation, but that really doesn’t seem to be the case.
And importantly, patients continued to have excellent spleen volume reductions over time, so the responses seem to be durable. And there were also several other compounds that are being studied mostly for anemia, one of them being elritercept, which in addition to helping with hemoglobin seemed to improve with platelets as well.
And that would be exciting, if that pans out in larger studies because we really don’t have any medications for myelofibrosis that help with thrombocytopenia.
And there’s also another agent being developed from Disc Medicines also helping with anemia, although maybe the responses there were a little bit more modest.
Jamie Forward:
Okay, wonderful. So, you’ve kind of alluded to this, but are there new therapies or clinical trials that look promising for symptom improvement, like fatigue, spleen enlargement, et cetera? You mentioned anemia.
Dr. Gabriela Hobbs:
Yeah, so all of these therapies are aiming to improve the disease. And for example, the nuvisertib study, I think, was the one that showed the most improvements in spleen in symptoms as well as the MANIFEST-2 Study. But I would say that really the field should be asking for more than spleen in symptom improvement. We should be asking for medications that modify the underlying disease biology, that eliminate the malignant stem cells with these mutations that lead to the disease.
And ultimately over time, we should see that other things that are manifestations of the disease, like splenomegaly symptoms, get better once you get rid of the disease initiating clone.