Vascular endothelial growth factor receptor 1, 2, and 3; Fibroblast growth factor receptor 1, 2, and 3; Platelet-derived growth factor receptor alpha and beta (VEGFR1, VEGFR2, VEGFR3, FGFR1, FGFR2, FGFR3, PDGFRα, PDGFRβ)

These targets comprise eight distinct receptor tyrosine kinases: the vascular endothelial growth factor receptors (VEGFR1, VEGFR2, and VEGFR3), the fibroblast growth factor receptors (FGFR1, FGFR2, and FGFR3), and the platelet-derived growth factor receptors (PDGFRα and PDGFRβ). All are membrane-spanning proteins characterized by extracellular ligand-binding immunoglobulin-like domains and cytoplasmic tyrosine kinase domains. They are essential regulators of cell proliferation, survival, migration, and differentiation—especially within the vascular, lymphatic, and mesenchymal compartments. Dysregulation is strongly implicated in oncogenesis, metastasis, fibrosis, and other proliferative diseases. The pharmacological blockade of one or several of these receptors is a central strategy of antiangiogenic cancer therapies and treatments for other conditions involving abnormal vasculature formation or tissue remodeling[2][3][4][5][6][7].

Other names

VEGFR1 (Flt-1)VEGFR2 (KDR or Flk-1)VEGFR3 (Flt-4)FGFR1 (CD331)FGFR2 (CD332)FGFR3 (CD333)PDGFRα (CD140a)PDGFRβ (CD140b)

Inhibition of receptor tyrosine kinase activity. - Blockade of ligand-binding, preventing downstream signaling. - Suppression of angiogenesis and lymphangiogenesis. - Inhibition of tumor growth via deprivation of vascular supply. - Reduction of vascular permeability and tissue edema in some contexts.