Its primary mechanism of action is thought to be vascular endothelial growth factor receptor 1-3, c-KIT and PDGFR inhibition, this, in turn, enables it to inhibit angiogenesis (the formation of new blood vessels by tumours). It was also proposed that it might act by inducing autophagy, as some other tyrosine kinase inhibitors, like sorafenib. It has also been shown to bind (in a different conformation from the VEGF binding) to the BCR-ABL fusion protein, specifically inhibiting the drug-resistant T315I mutant isoform. + The effect of<unk>  on tyrosine kinases Protein IC50 (nM) VEGFR1 0.1 VEGFR2 0.2 VEGFR3 0.1-0.3 PDGFR 1.6 c-KIT 1.7
Axitinib
Ceritinib
Abrocitinib
Upadacitinib
Sunitinib
Afatinib
Erdafitinib
Dacomitinib