VEGFR, FGFR, PDGFR, c-Kit, c-Met Group (VEGFR, FGFR, PDGFR, c-Kit, c-Met)

These molecules are all members of the receptor tyrosine kinase (RTK) family, transmembrane proteins that transmit extracellular growth, survival, and angiogenic signals across the cell membrane in response to binding of their respective ligands (VEGF for VEGFR, FGF for FGFR, PDGF for PDGFR, stem cell factor for c-Kit, and hepatocyte growth factor for c-Met). They regulate key processes such as angiogenesis, cell proliferation, migration, and survival. Dysregulation—by mutation, overexpression, or autocrine signaling—drives the development and progression of many cancers and other diseases. These receptors are established targets of numerous cancer drugs, especially multi-kinase inhibitors that can block several simultaneously to prevent tumor angiogenesis, growth, and escape via parallel signaling pathways. Because they are distinct genes/proteins, each is associated with unique and overlapping biological functions and pathologies as well as diverse, drug-specific resistance and safety profiles. The listing of all five together is commonly seen in the context of multi-kinase inhibitors used to treat advanced or refractory cancers, but each should ideally be annotated with specificity to maximize clinical and mechanistic clarity.

Other names

VEGF receptorFLT1 (VEGFR-1)KDR/FLK1 (VEGFR-2)FLT4 (VEGFR-3)FGF receptorFGFR1FGFR2FGFR3FGFR4PDGF receptorPDGFR alphaPDGFR betaCD140aCD140bKITCD117stem cell factor receptorMEThepatocyte growth factor receptorHGFR

Inhibition of ATP binding to receptor tyrosine kinase domains. Prevention of receptor phosphorylation and downstream signaling. Induction of endothelial cell apoptosis (anti-angiogenic effect). Blockade of tumor vascularization and direct inhibition of tumor cell growth/proliferation.