RAF kinases, VEGFR1-3, PDGFR, KIT (RAF (sometimes specified as BRAF, CRAF, etc.), VEGFR1 (FLT1), VEGFR2 (KDR), VEGFR3 (FLT4), PDGFR (PDGFRα or PDGFRβ), KIT (CD117))

This entry covers a set of protein kinases that are frequently targeted by small molecule multi-kinase inhibitors, especially in cancer therapy. **RAF kinases** (e.g., BRAF, C-RAF) are cytoplasmic serine/threonine kinases that transduce signals from membrane receptors to the MAPK/ERK pathway, influencing cell proliferation and survival. **Vascular endothelial growth factor receptors 1, 2, and 3 (VEGFR1-3)** are receptor tyrosine kinases critical for angiogenesis by mediating the effects of VEGFs, and are implicated in tumor neovascularization. **Platelet-derived growth factor receptor (PDGFR)** regulates cell proliferation, survival, and migration, with both alpha and beta isoforms targeted for anti-cancer and anti-fibrotic effects. **KIT** (also CD117 or c-KIT) is a receptor tyrosine kinase important for cell survival and proliferation, frequently mutated in gastrointestinal stromal tumors and leukemia. Inhibitors targeting this spectrum of kinases (e.g., regorafenib, sunitinib) exert anti-tumor and anti-angiogenic effects but can also result in significant adverse events, especially cardiovascular and hematologic toxicities[1][3][4][5].

Other names

RAFRAF1 (C-RAF)BRAFARAFFLT1KDRFLK1FLT4PDGFRαPDGFRβCD140aCD140bc-KITCD117

ATP-competitive kinase inhibition (prevents phosphorylation and downstream signaling) Blockade of angiogenesis (with VEGFR, PDGFR, KIT) Blockade of cell survival/proliferation signaling (with RAF kinases) Downregulation of tumor neovascularization