Antiangiogenic

Antiangiogenic refers to therapies or agents that inhibit angiogenesis, the process by which new blood vessels form from existing vasculature. By limiting blood vessel growth, antiangiogenic strategies aim to reduce tissue perfusion, tumor growth, and edema in diseased states. These agents can target endothelial cell proliferation, migration, or survival, and may act at various steps of the angiogenic cascade. They include monoclonal antibodies, receptor fusion proteins, small molecule tyrosine kinase inhibitors, and gene therapies.

Most widely used targets are the vascular endothelial growth factor (VEGF) pathway and VEGF receptors. Other pro-angiogenic factors such as fibroblast growth factor (FGF), platelet-derived growth factor (PDGF), and angiopoietins can also be inhibited. Agents may sequester VEGF, block receptor signaling, inhibit downstream kinases, or degrade pro-angiogenic proteins. In oncology, antiangiogenic therapy can transiently normalize abnormal tumor vasculature, improving oxygenation and the delivery of chemotherapeutics.

In cancer, antiangiogenic drugs are used to treat renal cell carcinoma, colorectal cancer, hepatocellular carcinoma, non-small cell lung cancer, glioblastoma, and others. In ophthalmology, intravitreal anti-VEGF therapy is used for neovascular age-related macular degeneration, diabetic macular edema, and retinal vein occlusion. Examples include bevacizumab, ranibizumab, aflibercept, and small molecule inhibitors such as sunitinib, sorafenib, pazopanib, and axitinib.

Adverse effects and resistance are considerations. Potential side effects include hypertension, thromboembolism, hemorrhage, wound healing impairment, and proteinuria. In the eye, local infections or inflammation can occur with injections. Tumors may adapt via alternative pro-angiogenic pathways or vessel co-option, limiting lasting benefit.