Cutting off thetumour’s supply line
Axitinib targets the receptors tumours use to grow new blood vessels.
Axitinib has been shown to inhibit receptor tyrosine kinases including vascular endothelial growth factor receptors (VEGFR)-1, VEGFR-2 and VEGFR-3 at therapeutic plasma concentrations. These receptors are implicated in pathologic angiogenesis, tumor growth and cancer progression.
VEGFR-1
Receptor tyrosine kinase
Inhibited by axitinibVEGFR-2
Receptor tyrosine kinase — phosphorylation inhibited in xenograft models
Inhibited by axitinibVEGFR-3
Receptor tyrosine kinase
Inhibited by axitinibStarving the tumour of its blood supply
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Growing renal tumours release vascular endothelial growth factor (VEGF) — a signal asking nearby blood vessels to grow towards them.
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VEGF docks onto VEGF receptors on the endothelial cells lining the vessel wall, switching on their tyrosine kinase activity.
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Receptor signalling drives endothelial cell proliferation and survival — pathologic angiogenesis that feeds tumour growth and cancer progression.
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Axitinib inhibits VEGFR-1, -2 and -3 at therapeutic plasma concentrations, inhibiting angiogenesis and blocking tumour growth.
Simplified illustration for educational purposes.
What themodels show
VEGF-mediated endothelial cell proliferation and survival were inhibited by Axitinib in vitro and in mouse models.
Axitinib was shown to inhibit tumour growth and phosphorylation of VEGFR-2 in tumour xenograft mouse models.