VEGFR, FGFR, and PDGFR Family Receptor Tyrosine Kinases (VEGFR/FGFR/PDGFR RTKs)

These targets are receptor tyrosine kinases that transduce signals from extracellular growth factors (VEGF, FGF, PDGF) into cells, mediating critical biological functions such as angiogenesis, cell proliferation, migration, and survival. Their dysregulation or aberrant activation is implicated in multiple diseases, especially cancer, where they support tumor growth, angiogenesis, and metastasis. Therapeutic strategies frequently focus on inhibiting their kinase activity, ligand binding, or dimerization. Their structural and signaling similarities allow for "cross-family" interactions, and multi-target inhibitors are often developed to simultaneously block several receptors to overcome resistance. Clinical use of their inhibitors carries significant safety concerns due to their central physiological roles, particularly in vascular and developmental processes. Each receptor within the VEGFR, FGFR, or PDGFR families may play distinct roles depending on tissue expression, ligand specificity, and downstream pathway context.

Other names

FLT1KDRFLK1FLT4FGFR1-4JTK2CD140aCD140b

Inhibition of kinase activity: Prevents downstream signaling and cellular responses (cell proliferation, angiogenesis). Blockade of ligand binding: Interferes with the receptor-ligand interactions. Disruption of receptor dimerization or autophosphorylation: Essential steps in receptor activation. Cross-family blocking: Some drugs (multi-targeted TKIs) inhibit several RTKs simultaneously.