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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:

  • Angiogenesis
  • Tumor growth and cellular proliferation
  • Tumor cell metabolism
The mTOR pathway has been implicated in the progression of aRCC, by promoting: angiogenesis, tumor growth and cellular proliferation, and tumor cell metabolism.
*66% (86/130) of metastatic clear cell RCCs obtained from Canadian and US patients. Based on analysis of primary tumor tissues and metastatic lesions. This number does not represent an overall response rate.
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.
  1. AFINITOR [summary of product characteristics]. Novartis Pharma AG; 2017.
  2. 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.
  3. Dancey JE. Inhibitors of the mammalian target of rapamycin. Expert Opin Investig Drugs. 2005;14(3):313-328.