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FMS-like tyrosine kinase 3 (FLT3) inhibitors act on a receptor tyrosine kinase of early blood cell progenitors. FLT3 and its ligand support the survival and expansion of hematopoietic stem and progenitor cells. In 1996 internal tandem duplications (ITDs) of the FLT3 juxtamembrane region were found in acute myeloid leukemia (AML). These mutations, like kinase domain point mutations such as D835Y, keep the receptor constitutively active. Quizartinib and gilteritinib are widely used FLT3 inhibitors in AML cell models, and gilteritinib also inhibits the receptor tyrosine kinase anexelekto (AXL). Crenolanib also targets platelet-derived growth factor receptors (PDGFRs), and pacritinib inhibits both FLT3 and Janus kinase 2 (JAK2).
FLT3/JAK2/BRD4 ligand-1 is a specific ligand for the FLT3, JAK2, and BRD4 proteins. This compound facilitates the design and synthesis of proteolysis-targeting chimeras (PROTACs), specifically PROTAC FLT3/JAK2/BRD4 Degrader-1. It demonstrates potential applications in targeted protein degradation and cancer research, enabling innovative therapeutic strategies against malignancies associated with these targets.
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