In in vitro/in vivo studies,
AFINITOR delivered a triple antitumor effect1-3
2/3 of aRCC patients who fail VEGFR-TKIs have a hyperactive mTOR pathway1*
After VEGFR-TKI failure, the mTOR pathway continues to be activated. mTOR has been implicated in the progression of aRCC, by promoting1-3:
- Tumor growth and cellular proliferation
- Tumor cell metabolism
Akt, protein kinase B; IGF-1R, insulin-like growth factor 1 receptor; MOA, mechanism of action; mTOR, mammalian target of rapamycin; P, phosphorus; PI3K, phosphatidylinositide 3-kinases; VEGFR, vascular endothelial growth factor receptor; VEGFR-TKI, vascular endothelial growth factor receptor-tyrosine kinase inhibitor.
- AFINITOR [summary of product characteristics]. Novartis Pharma AG; May 2016.
- Yuan R, Kay A, Berg WJ, Lebwohl D. Targeting tumorigenesis: development and use of mTOR inhibitors in cancer therapy. J Hematol Oncol. 2009;2:45.
- Dancey JE. Inhibitors of the mammalian target of rapamycin. Expert Opin Investig Drugs. 2005;14(3):313-328.