Anti-angiogenesis

Anti-angiogenesis broadly refers to therapeutic strategies aimed at blocking the formation of new blood vessels (angiogenesis) essential for tumor growth and metastasis. Most anti-angiogenic therapies in oncology target the VEGF/VEGFR axis using monoclonal antibodies, small-molecule tyrosine kinase inhibitors (TKIs), or soluble decoy receptors. While these strategies can slow tumor progression, challenges such as acquired resistance, lack of predictive biomarkers, and notable adverse effects—especially hypertension, bleeding risks, and impaired wound healing—limit their effectiveness. Anti-angiogenic therapy is not a molecular target per se, but rather an approach addressing multiple targets within the angiogenic signaling network.

Other names

Angiogenesis inhibitionAngiogenesis inhibitor therapyInhibition of angiogenesis

Anti-angiogenic therapies primarily function through the inhibition of VEGF/VEGFR signaling, which subsequently blocks endothelial cell proliferation and new vessel formation. This can involve tyrosine kinase inhibition, particularly for small-molecule drugs like sunitinib and sorafenib. Monoclonal antibodies such as bevacizumab operate by binding circulating VEGF, while agents like aflibercept act as a VEGF trap (decoy receptor). Some drugs, like thalidomide and lenalidomide, also contribute by modulating the immune response.