Antiangiogenesis effect

The **antiangiogenesis effect** refers to the inhibition of new blood vessel growth (angiogenesis), which is fundamental for tumor development and metastasis. Antiangiogenic therapy primarily targets key molecular drivers such as **vascular endothelial growth factor (VEGF)** and its receptors, but also angiopoietin-Tie2 signaling, integrins, and matrix metalloproteinases. Many antiangiogenic drugs—such as monoclonal antibodies, receptor decoys, and small-molecule tyrosine kinase inhibitors—aim to suppress endothelial cell proliferation, migration, and vessel formation. Such interventions are approved for various cancers and eye diseases but often face limitations, including drug resistance, safety concerns (notably bleeding and hypertension), and the complex adaptability of tumors. Monitoring treatment response and tailoring patient selection often utilize biomarkers like VEGF or ANG2 levels, but clinical benefit can be limited by secondary escape pathways and toxicities[1][2][3][4][5][6][7].

Other names

Anti-angiogenic effectAnti-angiogenesis

Inhibition of vascular endothelial growth factor (VEGF) or its receptor (VEGFR), blockade of angiopoietins (ANG1/ANG2) and Tie2 receptor signaling, inhibition of endothelial cell proliferation, migration, and survival, induction of endothelial cell apoptosis, inhibition of integrin-mediated pathways, disruption of matrix metalloproteinase (MMP) activity, interference with pro-angiogenic signaling molecules (e.g., bFGF, TGF-β), decoy receptor function (e.g., VEGF-Trap binds VEGF), and cyclooxygenase-2 (COX-2) inhibition.