VEGFR, FGFR, and PDGFR Receptor Tyrosine Kinase Families (VEGFR/FGFR/PDGFR RTK Families)

VEGFR-1, VEGFR-2, and VEGFR-3 (vascular endothelial growth factor receptors 1-3), FGFR-1, FGFR-2, FGFR-3, FGFR-4 (fibroblast growth factor receptors 1-4), and PDGFR-α and PDGFR-β (platelet-derived growth factor receptor alpha and beta) are receptor tyrosine kinases central to the regulation of angiogenesis, tissue development, cell survival, proliferation, and migration. They act as high-affinity signaling receptors for their cognate growth factors (VEGFs, FGFs, and PDGFs). Upon ligand binding and receptor dimerization, they initiate intracellular signaling cascades such as MAPK, PI3K-AKT, and PLCγ. These receptors are highly validated as therapeutic targets, especially in oncology, vascular disorders, sarcomas, and fibrosis. Several multi-kinase inhibitors and selective antibodies have been developed to modulate the signaling of these receptors for the treatment of cancer and other proliferative diseases, but their physiological roles in normal tissues present challenges for therapy due to toxicity, resistance, and biomarker selection [1][2][4][5][6][3].

Other names

FLT1Fms-related receptor tyrosine kinase 1KDRKinase insert domain receptorFlk-1FLT4Fms-related receptor tyrosine kinase 4CD331BEKKGFRCD333CD334PDGFRAPDGFRB

Inhibition of receptor tyrosine kinase activity, leading to suppression of downstream signaling pathways (e.g., MAPK, PI3K/AKT, PLCγ) and inhibition of angiogenesis, tumor growth, and disease progression [2][4][5] Competitive binding at the ATP-binding site of the kinase domain (for small-molecule inhibitors) Monoclonal antibody-mediated neutralization of ligands (for some drugs, e.g., bevacizumab)