Complement regulation and role of eculizumab and ravulizumab. The alternative, lectin, and classical pathways of complement converge at C3 activation at which point CD55 typically exhibits an inhibitory effect on the formation of the C3 convertase to prevent the formation of C3b. C5 is cleaved by the C5 convertase to C5a and C5b, and then C5b may join with C3b and other complement proteins to form the membrane attack complex (MAC). CD59 inhibits the formation of the MAC. Without CD55 and CD59, complement-mediated cellular destruction leads to increased inflammation, hemolysis, and thrombosis. Both eculizumab and ravulizumab inhibit terminal complement activation by binding to C5, which prevents the formation of C5b and therefore the MAC.