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Volume 30, Issue 174, August 2026

Advances in Anti-VEGF Therapy for the Treatment of Neovascular Age- Related Macular Degeneration

Agnieszka Kowalska♦

Collegium Medicum at Jan Kochanowski University in Kielce, Poland

♦Corresponding author
Agnieszka Kowalska, Collegium Medicum at Jan Kochanowski University in Kielce, Poland

ABSTRACT

The current standard of care for neovascular age-related macular degeneration (nAMD) heavily depends on anti-VEGF agents. Maintaining early visual gains, however, is a clinical struggle. Recurrent fluid, subretinal fibrosis, and macular atrophy add to a slow decline in sight although ongoing intravitreal injections. This review investigates how modern medicine attempts to lower this treatment burden by adopting next-generation molecules, updated monitoring routines, and sustained-release hardware. Following PRISMA guidelines, I reviewed 14 main English articles from the last 15 years. In the eye, too much VEGF-A damages the blood-retina barrier, causing fluid to leak into the retina. Standard treatments are good at clearing this fluid, but over time, the drugs often become less effective. To counter this, modern drug development focuses on prolonging dose intervals. Although brolucizumab is highly effective at reducing fluid, it carries a risk of intraocular inflammation. Faricimab targets two pathways (Ang-2 and VEGF-A), which strengthens blood vessels and lets certain patients extend their treatment intervals to 16 weeks. Furthermore, OCT imaging confirms that trace amounts of fluid are safe to tolerate. In the future, continuous treatments like permanent surgical ports and gene therapy could completely change long-term care for people with nAMD.

Keywords: "neovascular age-related macular degeneration" (nAMD), "wet AMD", "anti-VEGF therapy", "ranibizumab", "aflibercept", "brolucizumab", "faricimab", "optical coherence tomography" (OCT), and "disease activity criteria".

Medical Science, 2026, 30, e146ms3913
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Published: 12 August 2026

Creative Commons License

© The Author(s) 2026. Open Access. This article is licensed under a Creative Commons Attribution License 4.0 (CC BY 4.0).