Pacritinib occupies a distinct niche within the MF treatment landscape, offering meaningful spleen and symptom benefit in patients with severe thrombocytopenia who historically lacked effective therapeutic options. While no JAK inhibitor has demonstrated clear disease-modifying effects in MF, pacritinib's non-myelosuppressive profile, unique activity against IRAK1, and potential anemia benefit via ACVR1 inhibition suggests potential utility as a backbone for future combination strategies. Ongoing and future studies will be critical to further define its role in phenotype-driven MF management.
Goulart et al. (Wed,) studied this question.