An orally bioavailable inhibitor of Janus kinase 2 (JAK2), the JAK2 mutant JAK2V617F and FMS-like tyrosine kinase 3 (FLT3; CD135; STK1; FLK2), with potential antineoplastic activity. Upon oral administration, pacritinib competes with JAK2 and the JAK2 mutant JAK2V617F for ATP binding, which may result in inhibition of JAK2 activation, inhibition of the JAK-signal transducer and activator of transcription (STAT) signaling pathway, and the induction of apoptosis. In addition, pacritinib targets, binds to and inhibits the activity of FLT3. This inhibits FLT3-mediated signaling and the proliferation of FLT3-expressing cancer cells. JAK2, often upregulated or mutated in a variety of cancer cells, plays a key role in tumor cell proliferation and survival. The JAK2V617F gain-of-function mutation involves a valine-to-phenylalanine modification at position 617. The JAK-STAT signaling pathway is a major mediator of cytokine activity. FLT3, a class III receptor tyrosine kinase (RTK), is overexpressed or mutated in most B-lineage neoplasms and in acute myeloid leukemias. In addition, JAK2 and FLT3 play a key role in the regulation of the inflammatory response and dendritic cell (DC) proliferation, differentiation and function. Inhibition of JAK2- and FLT3-mediated signaling may suppress the generation and differentiation of DCs, and may regulate inflammatory and immune responses.