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Understanding the Avastin mode of action

Precise VEGF inhibition with Avastin:
understanding the Avastin MoA

Avastin MoA
 

Direct inhibition of VEGF with Avastin blocks the angiogenic cascade1–4

  • Avastin is a humanised MAb that binds specifically to VEGF, preventing activation of the VEGFR.
 
  • Avastin inhibits VEGF extracellularly and may, therefore, inhibit angiogenesis without disrupting targets outside the VEGF pathway.1,2

 

  • Based on preclinical models and clinical observations, it has been proposed that Avastin exerts continuous antivascular effects throughout tumour development
    • rapid regression of existing tumour vessels, as shown by significant reductions in microvascular density5–7
    • normalisation of surviving mature vasculature6,8
    • ongoing inhibition of both new and recurrent tumour vessel growth.9,10
     
  • The net result of the inhibition of VEGF by Avastin is11–13
    • maintenance of a more functional and normal vasculature
    • potentially improved capacity for drug delivery
    • inhibition of tumour growth and metastasis.
     
  • Effects of anti-VEGF agents occur rapidly – sometimes after a single infusion – while the long half-life of the monoclonal antibody allows for a sustained anti-VEGF effect.5
 

For more information on the anti-angiogenic effects of Avastin, please use the links below

Avastin causes regression of tumour vasculature

Avastin normalises existing tumour vasculature

Avastin inhibits new and recurrent vessel growth