Lenvatinib’s target

Lenvatinib exerts its mechanism of action by inhibiting multiple receptors of tyrosine kinases: VEGFR-1 (FLT1), VEGFR-2 (KDR), VEGFR-3 (FLT4), FGFR-1, FGFR-2, FGFR-3, FGFR-4, PDGFRa, RET and c-KIT. Tumor growth depends on the development and proliferation of new blood vessels (neovascularization). Tumor growth and angiogenesis occur when ligands bind to their respective tyrosine kinase receptors in the cell membrane, initiating intracellular signal transduction phosphorylation cascades that promote angiogenesis and cell proliferation. Inhibiting VEGF receptors prevents tumor angiogenesis, and inhibiting FGFR, RET, PDGFRα, and KIT prevents further proliferation of malignant cells. Simultaneous inhibition of both receptor pathways results in inhibition of nuclear signaling and concomitant inhibition of the activity of tumor growth-related factors.