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Myasthenia gravis (MG) is an autoimmune disorder caused by immunoglobulin G (IgG autoantibodies directed against acetylcholine receptors (AChRs) or, less commonly, other components of the neuromuscular junction. Removal of IgG autoantibodies, for example by plasma exchange, results in rapid clinical improvement. By contrast, neonatal Fc receptors (FcRn) bind IgG and prevent its degradation, thereby prolonging the availability of pathogenic autoantibodies. This manufacturer-funded, randomized, placebo-controlled, double-blind study, tested the efficacy for generalized MG of efgartigimod, an investigational modified human Fc fragment that blocks FcRn, resulting in greatly shortened persistence of IgG. The 167 participants were given 4 weekly …