Lenvatinib is a multi-target receptor tyrosine kinase inhibitor. Tyrosine kinases are enzymes involved in cellular communication. Certain receptor tyrosine kinases transmit signals that influence cell growth, survival, angiogenesis and other biological processes.
Lenvatinib inhibits VEGFR1, VEGFR2 and VEGFR3, as well as FGFR1 through FGFR4. It also inhibits PDGFRα, KIT and RET.
VEGF signaling
VEGF receptors contribute to the development of new blood vessels. Tumors can use angiogenesis to obtain oxygen and nutrients and support continued growth.
By inhibiting VEGF receptor signaling, lenvatinib can reduce signaling involved in tumor-associated blood-vessel formation.
FGF signaling
Lenvatinib also inhibits fibroblast growth factor receptors. The FGF pathway participates in cell signaling, proliferation and angiogenesis. Blocking several signaling pathways simultaneously may help explain the broad pharmacologic activity of lenvatinib.
RET, KIT and PDGFRα
Lenvatinib also inhibits RET, KIT and PDGFRα. These receptors participate in different biological pathways, including cellular growth and signaling. The combination of target inhibition contributes to lenvatinib’s multi-kinase pharmacology.
Simple explanation
In simple terms, lenvatinib interferes with several molecular signals that cancer cells and tumor-associated blood vessels can use to support disease progression.
This does not mean that lenvatinib affects only cancer cells. Its targets are also involved in normal physiological functions, which helps explain why treatment can produce effects such as hypertension, thyroid abnormalities, proteinuria and other adverse reactions.