OJJAARA has a novel combination MOA that inhibits JAK1/JAK2* and ACVR11,2

Myelofibrosis (MF) is an MPN associated with constitutive activation and dysregulated JAK signaling that contributes to inflammation and hyperactivation of ACVR1. 

MOA JAK1/JAK2 infographic
  • JAK1 and JAK2 contribute to signaling of a number of cytokines and growth factors that are important for hematopoiesis and immune function 
  • OJJAARA and its major human circulating metabolite, M21, have higher inhibitory activity for JAK2 compared to JAK3 and tyrosine kinase 2 (TYK2)
MOA ACVR1 infographic
  • OJJAARA and M21 additionally inhibit ACVR1, also known as ALK2, which produces subsequent inhibition of liver hepcidin expression and increased iron availability, resulting in increased red blood cell production

OJJAARA has a multi-modal mechanism of action that inhibits signaling pathways important in MF1

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ACVR1=activin A receptor type 1; ALK2=activin receptor-like kinase-2; BMP=bone morphogenetic protein; EPOR=erythropoietin receptor; JAK=Janus kinase; MPL=myeloproliferative leukemia virus; MPN=myeloproliferative neoplasm; p=phosphorylation; SMAD=suppressor of mothers against decapentaplegic; STAT=signal transducer and activator of transcription.
*Momelotinib is an inhibitor of wild-type Janus kinase 1 and 2 (JAK1/JAK2) and mutant JAK2V617F.


  1. OJJAARA (momelotinib). Prescribing Information. GSK; 2023.
  2. Chifotides HT, Bose P, Verstovsek S. Momelotinib: an emerging treatment for myelofibrosis patients with anemia. J Hematol Oncol. 2022;15(1):7. doi:10.1186/s13045-021-01157-4