This on-demand virtual symposium brings together expert clinician-researchers to discuss the role of B-cell pathways in the pathophysiology of generalized myasthenia gravis and how this provides therapeutic targets and will potentially expand the array of novel therapies available for patients...

In generalized myasthenia gravis (gMG), pathogenic antibodies activate the terminal complement cascade at the neuromuscular junction, leading to membrane attack complex–mediated damage of the postsynaptic membrane. Complement C5 inhibition directly blocks this mechanism, addressing a central driver of disease rather...

The neonatal Fc receptor (FcRn) preserves IgG by preventing lysosomal degradation, thereby extending IgG half-life. Inhibition of FcRn enhances the clearance of pathogenic IgG autoantibodies, resulting in rapid and reversible reductions in circulating AChR and MuSK antibodies without causing broad...