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VEGFR1–3, FGFR1–4, PDGFRα, KIT, RET (Multi-target profile) (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
01
Overview
These are cell-surface receptor tyrosine kinases (VEGFR1, VEGFR2, VEGFR3, FGFR1, FGFR2, FGFR3, FGFR4, PDGFRα, KIT, RET) that collectively regulate key pathways involved in angiogenesis, cell proliferation, migration, and survival. They are frequently dysregulated or overexpressed in cancer and serve as validated targets for multi-kinase inhibitors such as lenvatinib. Pharmacological inhibition of these receptors disrupts tumor angiogenesis and tumor cell growth, providing therapeutic benefit in several solid tumor types. Toxicities are generally related to the on-target suppression of normal physiological angiogenesis and cell signaling, resulting in class effects such as hypertension, hypothyroidism, and increased bleeding risk.
- Other names
- Flt-1 (VEGFR1)KDR/Flk-1 (VEGFR2)Flt-4 (VEGFR3)CD331 (FGFR1)CD332 (FGFR2)CD333 (FGFR3)CD334 (FGFR4)PDGFRA (PDGFRα)CD117 (KIT)c-KIT (KIT)RET proto-oncogene (RET)
02
Mechanism of action
Inhibition of kinase activity; Suppression of angiogenesis; Blockade of mitogenic and survival signaling
03
Biological functions
Signal transductionCell proliferationAngiogenesisCellular differentiationCell migration
04
Disease associations
CancerCardiovascular diseaseInflammationOther proliferative and developmental disorders
05
Safety considerations
HypertensionProteinuriaDiarrheaHypothyroidismFatigueIncreased risk of bleeding, thrombosis, and cardiac events
06
Interacting drugs
Lenvatinib
6 more in the full profile.
07
Biomarkers
Tumor vascularity (microvessel density, MVD)Phosphorylation status of target RTKsCirculating levels of VEGF, FGF, PDGF
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