Amer Zeidan, MBBS, and Rami Komrokji, MD, offer closing remarks on recent advances in MF and MDS, and look towards the future of treatment.
Rami Komrokji, MD: Several drugs are moving into a combination with ruxolitinib up front, trying to improve the responses or durability. Some are in patients who have suboptimal response. We still have an unmet need with fewer drugs at the time of all those JAK2 failures. We need some studies in the accelerated, or blast phase, of MPN; that’s challenging. Finally, in terms of cytopenias, we have better JAK2 inhibitors in the setting of cytopenia, like pacritinib and momelotinib, that could see some anemia response. Those drugs shouldn’t be mildly used for patients who are just cytopenic. If they don’t have splenic or constitutional symptoms, then it’s going to worsen their anemia. There are ongoing studies with luspatercept in combination with ruxolitinib for anemia, which is an area of unmet need. We need drugs for the cytopenic profile of myelofibrosis. There are plenty of activities and clinical trials, and we encourage our audience to refer their patients to enroll on those trials.
My take-home message on MDS [myelodysplastic syndrome] is regarding the IPSS-M [International Prognostic Scoring System–Molecular]. We have to think of molecular profiles from a practice-changing perspective and think of lenalidomide earlier on. The luspatercept data and real-world data duplicate what’s seen in the MEDALIST trial. Look for imetelstat in data early next year. Maybe that will be the next drug to be approved. We need to make something better than the backbone of hypomethylating agents in patients with higher-risk MDS.
Amer Zeidan, MBBS: I completely agree. Thank you so much, Rami. This was fantastic in terms of overviewing everything that’s happening in the myelofibrosis landscape, which is quite amazing. The future for MDS and myelofibrosis is quite bright. Many drugs are being tested, and we’re all hopeful that we’re going to have some new drugs come in. We’ve had hypomethylating agents and JAK inhibitors forever in both of those diseases. We look forward to having other agents from novel classes that can continue to improve the outcomes of our patients. We hope to see more updates in the upcoming ASH [American Society of Hematology] meetings.
Rami Komrokji, MD: Absolutely. It’s always a pleasure chatting with you. We could talk for hours about MDS and myelofibrosis, but we’ll stop here. Thank you to the audience for listening. Hopefully this is helpful translating some of the ASH data into clinical practice. Thank you very much, Amer.
Amer Zeidan, MBBS: Thank you so much.
Transcript edited for clarity.