Precise VEGF inhibition with Avastin:
understanding the 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