The idea that targeting the immune complement pathway could thwart retinal tissue loss associated with age-related macular degeneration (AMD) suffered a major setback in September. Roche of Basel, Switzerland, announced that lampalizumab, an experimental antibody drug directed against complement factor D, fared no better than a sham treatment at slowing atrophic eye degeneration in a 936-person phase 3 trial. Other complement inhibitors--including Soliris (eculizumab) from New Haven, Connecticut-based Alexion Pharmaceuticals and tesidolumab from Basel-based Novartis--have similarly proved ineffective as monotherapies in past AMD trials at reducing the rate of so-called geographic atrophy (GA), a common complication of the'dry'form of the disease, for which there are no approved therapies. By contrast, the'wet'form of AMD, defined by the presence of leaky blood vessels that grow in the choroid layer behind the retina, can be treated with drugs targeting vascular endothelial growth factor (VEGF), a proangiogenic protein.[illus. 1]