JAK2 inhibitor treatment of anemia in myelofibrosis

The primary objective of treatment in myelofibrosis (MF) is a prolongation of life, a feat currently realized only by allogeneic stem cell transplantation, with 3-year post-transplant survival reports exceeding 50%, despite increased utilization of alternative donors and older age distribution of recipients.1,2 Non-transplant treatment options in MF are currently palliative in scope and target the triad of quality-of-life (QoL) offenders: anemia, splenomegaly, and constitutional symptoms.3 In addition to its impact on QoL, anemia carries severity-weighted prognostic relevance in MF that is independent of other clinical or genetic risk factors.4–6 Pre-JAK2 inhibitor (JAKi) era treatment of MF-associated anemia included periodic red cell transfusions and the use of erythropoiesis-stimulating agents, androgen preparations, prednisone, danazol, and immunomodulatory drugs (thalidomide, lenalidomide, pomalidomide).3 However, these treatment approaches are modest in their efficacy and often inadequate in controlling other symptoms of the disease, including marked splenomegaly and constitutional symptoms.