C5 is a central component of the complement system, an integral part of the innate immune response. Its activation, typically at the convergence point of the classical, lectin, and alternative pathways, leads to the generation of C5a (a potent anaphylatoxin that recruits and activates immune cells, causing inflammation) and C5b (which initiates the assembly of the MAC, a pore-forming complex that lyses target cells). In the diseases treated by eculizumab, dysregulated or excessive complement activation via C5 causes catastrophic damage to the body's own cells—namely red blood cells in paroxysmal nocturnal hemoglobinuria (PNH) and atypical hemolytic uremic syndrome (aHUS), or myasthenia gravis (MG) and neuromyelitis optica spectrum disorder (NMOSD) patient cells expressing specific antigens.