VEGFvastased

VEGFvastased, or anti-VEGF agents, are a class of drugs that inhibit vascular endothelial growth factor (VEGF) signaling to suppress angiogenesis. They act by neutralizing VEGF ligands, functioning as decoy receptors, or blocking VEGF receptors on endothelial cells. This reduces the growth of new blood vessels that tumors or diseased tissues depend on.

Mechanisms and examples include monoclonal antibodies (such as bevacizumab, which binds VEGF-A), antibody fragments designed for ocular use (ranibizumab), and fusion proteins that trap VEGF ligands (aflibercept). Other agents are receptor-targeting antibodies (ramucirumab against VEGFR-2) and small-molecule tyrosine kinase inhibitors (sunitinib, sorafenib, pazopanib, axitinib) that block VEGF receptor signaling. Some anti-VEGF therapies are formulated for local delivery (intravitreal injections in eye diseases), while others are given systemically for cancer.

Indications span oncology and ophthalmology. In cancer, anti-VEGF therapy aims to slow tumor growth by hindering blood vessel formation in cancers such as colorectal cancer, non-small cell lung cancer, renal cell carcinoma, and ovarian cancer. In ophthalmology, intravitreal anti-VEGF injections are used to treat neovascular age-related macular degeneration, diabetic macular edema, retinal vein occlusion, and other retinal neovascular conditions.

Administration and safety considerations vary by agent and indication. Systemic anti-VEGF therapy can cause hypertension, thromboembolic events, wound-healing impairment, and proteinuria, while intraocular use carries risks such as endophthalmitis and intraocular inflammation. Resistance and limited responses can occur due to alternative pro-angiogenic pathways.

History notes that anti-VEGF therapy emerged in the late 1990s–2000s, with bevacizumab among the first systemic examples and ocular agents developed subsequently for eye diseases.