ASH MPN Spotlight

Ivosidenib (AG-120), an IDH1 inhibitor, demonstrated an objective response rate (ORR) of 41.6% in patients&nbsp;with relapsed/refractory&nbsp;<em>IDH1</em>-mutant acute myeloid leukemia (AML), according to findings from a single-arm phase I study.&nbsp;

Treatment with pegylated interferon alfa-2a led to objective responses in about two-thirds of patients with hydroxyurea (Hydrea)-resistant/intolerant polycythemia vera or high-risk essential thrombocytopenia, a phase II study of salvage therapy showed.

Srdan Verstovsek, MD, of MD Anderson Cancer Center, discusses a study of sotatercept (ACE-011) alone and in combination with ruxolitinib in patients with myeloproliferative neoplasm (MPN)-associated myelofibrosis and anemia.

A novel pegylated formulation of interferon alfa-2b achieved a significantly higher rate of complete hematologic response compared with hydroxyurea (Hydrea) in patients with polycythemia vera, according to 2-year findings from the follow-up phase III CONTI-PV randomized trial.

The investigational activin receptor IIA ligand trap sotatercept safely increases hemoglobin levels in patients with myeloproliferative neoplasm (MPN)-associated myelofibrosis, both when used alone and in combination with ruxolitinib (Jakafi).

The investigational Nutlin family antagonist idasanutlin demonstrated significant activity and was well tolerated after multiple cycles of exposure in patients with refractory polycythemia vera.<br /> &nbsp;

Ruben A. Mesa, MD, Director of the UT Health San Antonio Cancer Center, discusses &nbsp;4-year follow-up results from the phase III RESPONSE trial, which investigated ruxolitinib (Jafaki) with best available therapy for the treatment of polycythemia vera (PV) during the 2017 ASH Annual Meeting.

Treatment using BLU-285 (Avapritinib) induced clinically significant activity in patients with an advanced or aggressive form of systemic mastocytosis (ASM), a rare blood disorder that originates in mast cells, according to data from an ongoing phase I trial.<br /> &nbsp;