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VEGFR1-3, FGFR1-4, PDGFRα, KIT, RET (VEGFR1, VEGFR2, VEGFR3, FGFR1, FGFR2, FGFR3, FGFR4, PDGFRα, KIT, RET)
- Target
- VEGFR1, VEGFR2, VEGFR3, FGFR1, FGFR2, FGFR3, FGFR4, PDGFRα, KIT, RET
- Molecular classification
- Receptor tyrosine kinase, Cell surface receptor, Protein kinase (Enzyme family)
01
Overview
This panel refers to a group of receptor tyrosine kinases that mediate key cellular processes such as growth, angiogenesis, and differentiation. They are frequently activated or overexpressed in various cancers. Multi-targeted drugs (e.g., lenvatinib) are designed to inhibit several of these kinases concurrently, thereby blocking cancer progression through multiple pathways. The receptors are homologous transmembrane proteins with intrinsic kinase activity, responsible for initiating complex intracellular signaling cascades upon ligand binding. Their central role in tumor biology makes them prime targets for anticancer therapy, but combined targeting increases the risk of adverse effects and therapeutic resistance[1][2][3][5].
- Other names
- Flt-1 (VEGFR1)KDR/Flk-1 (VEGFR2)Flt-4 (VEGFR3)CD331 (FGFR1)Bek (FGFR2)JTK2 (FGFR3)TKF (FGFR4)CD140aCD117Stem cell factor receptorCD350
02
Mechanism of action
Inhibition of kinase activity, blocking ligand-mediated receptor activation; Suppression of downstream signaling pathways such as: MAPK/ERK, PI3K/AKT, JAK/STAT; Anti-angiogenic effects (inhibit new blood vessel formation); Induction of apoptosis in tumor cells
03
Biological functions
Signal transductionCell proliferationCell migrationAngiogenesis (formation of blood vessels)Survival and apoptosis modulationDevelopment and tissue remodelling
04
Disease associations
Cancer (including thyroid, renal cell carcinoma, hepatocellular carcinoma)Cardiovascular diseaseDevelopmental disordersInflammation
05
Safety considerations
HypertensionDiarrheaHypothyroidismFatigueOff-target toxicities due to inhibition of multiple kinasesPotential development of resistance
06
Interacting drugs
Lenvatinib
6 more in the full profile.
07
Biomarkers
Expression or mutation/amplification of the respective receptor genes (VEGFR, FGFR, PDGFRα, KIT, RET) in tumorsFusion mutations, e.g. FGFR2 fusionPhosphorylation status of specific tyrosine residues in these receptors
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