Myasthenia Gravis (MG) is an autoimmune disease caused by the activation of the complement system. Complement-targeting treatments, such as anti-C1q and anti-C6 antibodies, have shown promise in inhibiting complement-mediated destruction and improving the lives of MG patients. The complement system consists of an enzymatic cascade and a lytic pathway that generate proinflammatory molecules critical for immunity and tissue homeostasis. The main complement regulator, CD59, helps prevent osmolysis of healthy cells via autologous complement attack. Targeting specific complement proteins, like C3 and C5, has emerged as a promising therapeutic approach for MG. Eculizumab, a monoclonal antibody that inhibits C5 cleavage, has shown therapeutic effects in treating MG. Ravulizumab-cwvz, a longer-acting derivative of eculizumab, is also being investigated for its potential in treating MG. Zilucoplan, a subcutaneously administered C5 inhibitor, has shown rapid onset of action and sustained improvements in MG patients. Clinical trials have demonstrated the effectiveness of these complement-targeting drugs in improving disease severity and quality of life for MG patients. These advancements offer hope for individuals with MG and contribute to our understanding of autoimmune diseases.

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