C5 and myasthenia gravis: Taken together, these data support a dual mechanism of action by which zilucoplan inhibits the activation of the terminal complement cascade via binding C5, including wild-type C5 and R885 variants, to prevent C5 convertase-mediated C5 cleavage into C5a and C5b, and additionally through remaining on the C5 TED moiety to hinder the formation of C5b6, efficiently blocking MAC formation that is central to targeting diseases such as acetylcholine receptor autoantibody-positive myasthenia gravis (33).