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What Is the Future of Myeloproliferative Neoplasm Treatments?

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Published on February 28, 2020

Key Takeaways

  • At ASH, long-term follow-up was presented on a European study of the new variation of interferon with less side effects.
  • Fedratinib (Inrebic) might be better for newly diagnosed myelofibrosis (MF) patients, patients with lower platelet counts or those who are no longer responding to ruxolitinib (Jakafi). 
  • A novel agent that’s being investigated in a Phase II study is a bromodomain (BET) inhibitor. It can help manage anemia for myelofibrosis patients on ruxolitinib.

Myeloproliferative neoplasm expert Dr. Laura Michaelis from the Medical College of Wisconsin shares highlights on updated treatment options as part of our roundtable discussion at the American Society of Hematology (ASH) Conference 2019. Watch as she provides insight on JAK inhibitors, interferon and managing anemia.

This program is sponsored by Incyte. This organization has no editorial control. It is produced by Patient Power. Patient Power is solely responsible for program content.

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Transcript | What Is the Future of Myeloproliferative Neoplasm Treatments?

Please remember the opinions expressed on Patient Power are not necessarily the views of our sponsors, contributors, partners or Patient Power. Our discussions are not a substitute for seeking medical advice or care from your own doctor. That’s how you’ll get care that’s most appropriate for you.

Andrew Schorr:           

Laura, I want to start with you. So, you are the editor of one of the main publications for the medical society, the American Society of Hematology, and you have a journalism background.

Dr. Michaelis:              

I do.

Andrew Schorr:           

So, we’re brother and sister journalists. So, from your point of view in MPNs, what are things that have impressed you?

Dr. Michaelis:              

Yeah. So, one of the things I think about before I come is how am I going to categorize the new data, the new information and the way I’ve been thinking about it is I’ve been looking through the posters or the oral abstracts is what are we learning about the ways to use the JAK inhibitors that we have; for example, ruxolitinib (Jakafi) or fedratinib (Inrebic). What are we learning about what we can add to the JAK inhibitors to use them in combination and what are we learning about new agents that maybe have nothing to do with JAK inhibitors, maybe a new way to attack myelofibrosis.

We also, of course, have information about transplantation; information about lower risk diseases like essential thrombocythemia and polycythemia vera. So, a couple of things that stood out, and I did a little bit of review before I came here and that was first off, I’m pretty impressed with some of the information we’re seeing in the long-term follow-up of the new variation in interferon out of Europe. So, this is a study called the PROUD-PV study, and we’re now looking at three to four years of follow-up. And it doesn’t use peginterferon alfa-2a (Pegasys), which many of have heard about, right, which is a pegylated interferon. 

It uses even a new variety of interferon, which is purportedly even less toxic to patients; fewer with fatigue, a little bit less of the side effects, and we’re seeing not only very low amounts of blood clotting in patients who got that versus hydroxyurea (Hydrea) and had a diagnosis of PV, but also lower levels of the JAK2 allele burden, which I just think is interesting. So, that new data is going to be presented tomorrow.

In terms of combinations with the drugs that we already have, so we know that approved for myelofibrosis is the medicine ruxolitinib, which we’ve had now for I guess nearly a decade and fedratinib (Inrebic), which is the newest kid on the block and may be better for patients with a little bit lower platelet count, so that we don’t know. And it is really approved not only for newly diagnosed patients but mostly for patients where they’ve already been on ruxolitinib, and they’ve lost their response for some reason.

So, we have some follow-up data on fedratinib on what happens in people with low platelet counts, and we also have in the ruxolitinib space evidence of what we can add to ruxolitinib to help patients. In my practice, one of the most impactful things was a publication from this year, not here at ASH, but from this year about how you can safely add anti-leukemia therapy in the form of hypomethylating agents to ruxolitinib which is something that that safety data is…

Andrew Schorr:           

…like what kind of drug?

Dr. Michaelis:              

Like azacitidine (Vidaza) or decitabine (Dacogen) so, in patients where you maybe are a little concerned about transformation that’s it’s very nice to have safety data on how to combine those two agents.

Andrew Schorr:           

When you say transformation, transformation to acute myeloid leukemia.

Dr. Michaelis:              

Exactly. From myelofibrosis when you see somebody with maybe a small increase in the number of blasts that they have in their bone marrow rather than from their spleen. This is something we’ve sort of done in practice a lot. But now we’re seeing more and more published data on that combination.

Another combination that I think is really attractive is how do we manage anemia in people on Jakafi or ruxolitinib, and there is a novel agent that’s being investigated in a Phase II study called a bromodomain inhibitor or BET inhibitor and that’s also I think pretty exciting. I think dealing with anemia is one of really the unmet needs in myelofibrosis and is not addressed even in people with—even in some of our most modern drugs.

In terms of other agents, people are looking at sort of old fashioned agents, something like metformin (Glucophage) which is a drug we use for diabetes. People are looking at a new medicine that was really effective in anemia in thalassemia and myelodysplastic syndrome, a medicine called luspatercept (Reblozyl) that’s being investigated in myelofibrosis again as a single agent. Nothing’s really hit a home run yet, so we’ve still got some work to do.

Please remember the opinions expressed on Patient Power are not necessarily the views of our sponsors, contributors, partners or Patient Power. Our discussions are not a substitute for seeking medical advice or care from your own doctor. That’s how you’ll get care that’s most appropriate for you.

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