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Fedratinib is an oral small molecule kinase inhibitor with higher selectivity for JAK2 over other JAK family members, including JAK1, JAK3 and tyrosine kinase 2.1-3 Myelofibrosis is a life-threatening myeloproliferative neoplasm (MNP) that occurs due to the proliferation of mutant hematopoietic stem and progenitor cells and can be caused by alterations in the JAK/STAT pathway.4,5 Approximately 60–65% of patients with primary myelofibrosis have a mutation in JAK2, typically JAK2V617F.5 An additional 20-30% of patients with primary myelofibrosis have abnormalities in markers mutant Calreticulin or the thrombopoietin receptor, also known as the myeloproliferative leukemia protein (MPL), which also signal through the JAK2/STAT pathway.5 Preclinical studies have suggested that fedratinib may inhibit both mutant and wild-type JAK2, thus blocking abnormal hyperactive JAK/STAT signaling and inhibiting proliferation in hematopoietic stem cells with or without mutations in JAK2.2,6,7
Preclinical studies using mouse models of JAK2V617F-driven myeloproliferative disease have suggested that fedratinib blocked phosphorylation of STAT 3/5 and improved survival, white blood cell counts, hematocrit, splenomegaly, and fibrosis, supporting the clinical development of fedratinib in myelofibrosis.1