Biological Treatments for Refractory Myasthenia Gravis

Myasthenia gravis is an autoimmune neuromuscular disorder characterized by fluctuating motor weakness involving ocular, bulbar, limb, and/or respiratory muscles. The weakness is due to an antibody-mediated, immunologic attack directed at proteins in the postsynaptic membrane of the neuromuscular junction (acetylcholine receptors or receptor-associated proteins). Eighty to 90 percent of individuals with myasthenia gravis have autoantibodies against the acetylcholine receptor detectable in serum, and these antibodies are believed to play a central role in disease pathomechanism. Eculizumab (Soliris®) and ravulizumab-cwvz (Ultomiris®) are monoclonal antibodies that are presumed to exert a therapeutic effect in individuals with generalized myasthenia gravis through the reduction of terminal complement complex C5b-9 deposition at the neuromuscular junction. Efgartigimod alfa-fcab (Vyvgart®) is a human IgG1 antibody fragment that binds to the neonatal Fc receptor, resulting in the reduction of circulating IgG in individuals with generalized myasthenia gravis. Vygart Hytrulo is a coformulation of efgartigimod alfa and hyaluronidase (human recombinant) which can be administered subcutaneously. The addition of hyaluronidase increases the dispersion and absorption of co-administered drugs when administered subcutaneously. Rozanolixizumab-noli is a humanized IgG4 monoclonal antibody that binds to the neonatal Fc receptor resulting in the reduction of circulating IgG.