Likewise, targeting downstream C5—either with intravitreal (LFG316, NCT01527500; [75]) or systemic (eculizumab; NCT00935883; [76]) administration—or by targeting C5 in combination with the alternative pathway (LFG316 + CLG561; NCT02515942) were also not successful in early phase clinical studies, potentially suggesting that the alternative or common lytic pathways are not key drivers of pathology in AMD; however, these latter studies were either small (n < 40/arm; LFG316/CLG561) or of limited duration (6 months; eculizumab). This evidence concerns the gene C5 and age-related macular degeneration.