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Abstract

Age-related macular degeneration (AMD) is the leading cause of blindness among people aged over 50 years in the western world. Verteporfin (Visudyne) is the first light-activated drug indicated for the treatment of patients with AMD caused by subfoveal choroidal neovascularization (CNV). This form of AMD is characterized by the development of abnormal blood vessels on the back of the retina that leak and cause scarring, resulting in central vision loss. Following intravenous administration, verteporfin selectively accumulates within proliferating tissue, including neovasculature, probably via low density lipoprotein receptors. The verteporfin is then activated by shining a specific wavelength of light with a nonthermal laser on the affected area in the eye. This process, called photodynamic therapy (PDT), generates reactive free radicals and highly reactive singlet oxygen in the target cells in the eye, causing damage and occlusion of the CNV and resulting in closure of the abnormal vessels and cessation of leakage. In experimentally induced CNV in animal models and in randomized, controlled clinical trials of patients with CNV due to AMD, verteporfin PDT has been shown to selectively occlude abnormal vessels without significantly altering overlying photoreceptors. Verteporfin therapy for CNV in Japanese patients had a similar or better angiographic and vision effect as that observed in Caucasian patients, with the same safety profile.