VEGFR, PDGFR, RAF kinase (VEGFR, PDGFR, RAF)

VEGFRs are cell-surface receptor tyrosine kinases primarily responsible for mediating the effects of vascular endothelial growth factors, regulating angiogenesis, vascular permeability, and endothelial cell survival. PDGFRs are tyrosine kinase receptors that respond to platelet-derived growth factors and regulate cell proliferation, migration, and development, especially in mesenchymal cells. RAF kinases (including BRAF and CRAF) are serine/threonine-specific protein kinases that play a key role in the MAPK/ERK signaling pathway, transducing signals from cell-surface growth factor receptors to promote gene expression and cell cycle progression. These receptors and kinases are frequently co-activated or dysregulated in cancer and have become major therapeutic targets; many approved and experimental drugs inhibit multiple family members simultaneously to block redundant or compensatory signaling in tumor cells. Drugs targeting these molecules are used mainly in oncology and occasionally in fibrosis or other proliferative diseases.

Other names

KDRFLK-1FLT-1FLT-4PDGFR-αPDGFR-βCD140aCD140bBRAFCRAFRAF1ARAF

Small-molecule inhibition of kinase activity, blocking ATP-binding site on VEGFR or PDGFR or RAF kinases, suppressing downstream signal transduction, angiogenesis, or cell proliferation. Competitive antagonism with endogenous ligands (mostly for VEGFR/PDGFR).