Mechanism of action
Combining the RTK inhibition of LENVIMA® and the mTOR inhibition of everolimus1,2
LENVIMA inhibits the kinase activities of VEGF receptors VEGFR1 (FLT1), VEGFR2 (KDR), and VEGFR3 (FLT4). LENVIMA also inhibits other RTKs that have been implicated in pathogenic angiogenesis, tumor growth, and cancer progression, in addition to their normal cellular functions, including
- FGF receptors FGFR1, 2, 3, and 4
The combination of LENVIMA and everolimus showed increased anti-angiogenic and antitumor activity as demonstrated by decreased human endothelial cell proliferation, tube formation, and VEGF signaling in vitro and tumor volume in mouse xenograft models of human renal cell carcinoma greater than with each drug alone.
RTK=receptor tyrosine kinase; mTOR=mammalian target of rapamycin; VEGF=vascular endothelial growth factor; VEGFR=vascular endothelial growth factor receptor; FGF=fibroblast growth factor; FGFR=fibroblast growth factor receptor; PDGFRα=platelet-derived growth factor receptor alpha.