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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.
Abbreviations:
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.
References:
  1. AFINITOR [summary of product characteristics]. Novartis Pharma AG; May 2016.
  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.