Mechanism of action<unk>  acts as a multiple kinase inhibitor. It inhibits the three main vascular endothelial growth factor receptors VEGFR1, 2 and 3, as well as fibroblast growth factor receptors (FGFR) 1, 2, 3 and 4, platelet-derived growth factor receptor (PDGFR) alpha, c-Kit, and the RET proto-oncogene. Some of these proteins play roles in cancerogenic signalling pathways. VEGFR2 inhibition is thought to be the main reason for the most common side effect, hypertension. Pharmacokinetics<unk>  is absorbed quickly from the gut, reaching peak blood plasma concentrations after one to four hours (three to seven hours if taken with food). Bioavailability is estimated to be about 85%. The substance is almost completely (98–99%) bound to plasma proteins, mainly albumin.<unk>  is oxidized by cytochrome P450 enzymes (CYP), and further metabolized to the quinolinones M2' and M3' by aldehyde oxidase (AO).<unk>  is metabolized by the liver enzyme CYP3A4 to desmethyl-lenvatinib (M2). M2 and<unk>  itself are oxidized by aldehyde oxidase (AO) to substances called M2' and M3', the main metabolites in the feces. Another metabolite, also mediated by a CYP enzyme, is the N-oxide M3. Non-enzymatic metabolization also occurs, resulting in a low potential for interactions with enzyme inhibitors and inducers. Terminal half-life is 28 hours, with about two thirds being excreted via the feces, and one quarter via the urine.
Lenvatinib
Tucatinib
Neratinib
Fostamatinib
Lapatinib
Ponatinib
Selpercatinib
Infigratinib