Although laser photocoagulation and PDT destroy pathological vessels, they neither extenuate the primary angiogenic stimuli nor prevent the development of new vessel. Antiangiogenic substances are able to resolve these problems. Antiangiogenic therapy prevents recurrence of AMD by reversing the CNV lesions. Pegaptanib (brand name: Macugen) was the first intravitreal pharmacotherapy approved by the FDA in 2004. It binds to VEGF165 and is responsible for “blood-retinal barrier breakdown and pathological intraocular neovascularisation”, subsequently inhibiting pathological leakage and angiogenesis. According to the results of the
VEGF Inhibition Study in Ocular Neovascularisation (VISION) trial, pegaptanib is proven to be an effective therapy for wet AMD. However, reinjections have to be done regularly as the molecule of pegaptanib is degraded enzymatically by intraocular nucleases. Endophtalmitis, traumatic lens injury and retinal detachment were also observed in the patients receiving this treatment.
In 2006, FDA approved the usage of ranibizumab (brand name: Lucentis), a humanized monoclonal antibody fragment that has a high affinity for VEGF, as a therapeutic option for wet AMD. Ranibizumab is different from pegaptanib as it is not restricted only to binding VEGF165 isoform but binds to all human VEGF isoform. It reduces leakage in vessels as well as decreases retinal and choroidal neovascularisation in animal models. The findings of MARINA study demonstrated that