Myasthenia gravis (MG) is caused by antibodies directed towards neuromuscular junction proteins and leads to compromised synaptic transmission and disabling weakness. Ultimately, all therapeutics targeting the immune system are designed to moderate the severity of autoantibody injury.

Standard treatments for MG have been copied from other autoimmune diseases, and few have been carefully evaluated by modern-day standards.

Monoclonal antibody therapies under evaluation for MG all have a rationale based on understanding of the autoimmune pathology and have, or are undergoing, rigorously designed clinical trials. None of the agents are designed to reacquire tolerance to the autoantigen and do not specifically target the autoimmune reaction of MG.