Prior research has implicated strong roles for inflammation, and complement in particular, mitochondrial dysfunction, oxidative stress, lipid abnormalities, and cell death in dry AMD pathobiology, but their precise mechanisms are unclear. The lack of preventive measures and treatment for dry AMD underscores the importance of gaining a better understanding of its pathobiology. A number of other approaches for treating GA have failed in human trials (e.g., visual cycle inhibitors, emixustat, Acucela, sustained release of neurotrophic factors, NT501, Neurotech, and complement pathway inhibitors, eculizumab, Soliris) 7, 9. A Phase 2 study conducted by Apellis using an inhibitor of complement factor 3 activation (APL-2) demonstrated a reduction in the rate of GA progression but was also associated with an increased risk of wet AMD in a subset of patients 8. Recently, lampalizumab, an inhibitor against complement Factor D, showed some efficacy in slowing GA progression in a Phase 2 study 7, but this result was not confirmed in a Phase 3 study. The Age-related Eye Disease Study (AREDS) trials demonstrated that antioxidant micronutrient supplements given to intermediate AMD patients modestly reduced the risk of developing advanced disease, and in particular, wet AMD 5, 6. While successful treatment using anti-vascular endothelial cell growth factor treatment is available for wet AMD 4, no effective prevention or treatment is available for dry AMD. When GA involves the fovea, vision loss is severe. In late, dry AMD or geographic atrophy (GA), patches of RPE cell loss become confluent. Multiple medium-sized drusen, large-sized drusen, RPE pigmentary changes, and AMD duration are independent risk factors for developing late AMD 3. These pigmentary abnormalities are the clinical manifestation of RPE degeneration, which can ultimately culminate in death of the RPE and of the overlying photoreceptors. Dry AMD is defined clinically by the presence of at least intermediate-size yellow sub-RPE deposits called drusen (63 µm or larger in diameter), RPE pigmentary abnormalities, and subretinal deposits called reticular pseudodrusen 3. In dry AMD, vision loss is typically gradual. In the wet form, rapid, severe vision loss can occur due to the development of new blood vessels from the choroid into the subretinal space, within Bruch’s membrane, or in the subretinal pigmented epithelial (RPE) space that can leak fluid, hemorrhage, and with time, develop fibrosis around these neovascular tufts. In the US alone, approximately 11 million people have AMD, a prevalence that is similar to that of all invasive cancers combined, and more than double of that of Alzheimer’s disease 2.ĪMD is classified into two forms, a non-neovascular or “dry” form and a neovascular or “wet” form (Fig. While AMD is currently more prevalent in Europe and North America than Asia, given that Asia accounts for more than 60% of the world’s population, the largest projected number of AMD cases will occur in Asia 1. It is projected that the number of people with AMD worldwide will be 196 million in 2020, increasing to 288 million in 2040, with the pooled prevalence of early, late, and any AMD to be 8.01% (95% CI 3.98–15.49), 0.37% (0.18–0.77), and 8.69% (4.26–17.40), respectively 1.

Age-related macular degeneration (AMD) is the world’s leading cause of blindness among the elderly 1.

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