Dr. Mesa on the Role of JAK2 Inhibitors in Myelofibrosis

Ruben A. Mesa, MD
Published: Thursday, Feb 28, 2013

Ruben A. Mesa, MD, Professor of Medicine, Division of Hematology & Medical Oncology, Mayo Clinic, discusses the use of JAK2 inhibitors in patients with myelofibrosis.

Ruxolitinib, as well as several other agents, have been tested in patients with advanced myelofibrosis who are symptomatic and at high risk. Currently, ruxolitinib is approved for use in this population and has shown efficacy to decrease spleen size, minimize symptoms, and likely provide a survival advantage. Mesa believes that phase III trials analyzing pacritinib, CYT387, and SAR302503, will show benefit in the same population.

The question remains, Mesa says, as to whether or not JAK2 inhibitors could show benefit earlier in treatment to help prevent disease progression and if potential improvement to anemia is possible.

With regard to early-stage disease, phase III studies in polycythemia vera are ongoing based on phase II data, which demonstrated ruxolitinib was beneficial for improving symptoms, decreasing need for phlebotomies, and preventing vascular events. Mesa expects that there will be a role for JAK2 inhibitors in polycythemia vera, particularly in patients with problematic disease. Mesa concludes by noting that the path for JAK2 inhibitors in myelofibrosis is clear, while in polycthemia vera and essential thrombocythemia the path is evolving.

Ruben A. Mesa, MD, Professor of Medicine, Division of Hematology & Medical Oncology, Mayo Clinic, discusses the use of JAK2 inhibitors in patients with myelofibrosis.

Ruxolitinib, as well as several other agents, have been tested in patients with advanced myelofibrosis who are symptomatic and at high risk. Currently, ruxolitinib is approved for use in this population and has shown efficacy to decrease spleen size, minimize symptoms, and likely provide a survival advantage. Mesa believes that phase III trials analyzing pacritinib, CYT387, and SAR302503, will show benefit in the same population.

The question remains, Mesa says, as to whether or not JAK2 inhibitors could show benefit earlier in treatment to help prevent disease progression and if potential improvement to anemia is possible.

With regard to early-stage disease, phase III studies in polycythemia vera are ongoing based on phase II data, which demonstrated ruxolitinib was beneficial for improving symptoms, decreasing need for phlebotomies, and preventing vascular events. Mesa expects that there will be a role for JAK2 inhibitors in polycythemia vera, particularly in patients with problematic disease. Mesa concludes by noting that the path for JAK2 inhibitors in myelofibrosis is clear, while in polycthemia vera and essential thrombocythemia the path is evolving.




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