Generalized myasthenia gravis (gMG) is an autoimmune neuromuscular disorder in which pathogenic autoantibodies against acetylcholine receptors or muscle-specific kinase impair neuromuscular transmission, producing fluctuating fatigable weakness. A substantial proportion of patients experience persistent symptoms despite established immunosuppression.

The neonatal Fc receptor (FcRn) recycles IgG; selective FcRn antagonism rapidly reduces circulating IgG — including disease-relevant autoantibodies — with a favorable selectivity profile versus non-specific immunosuppression. Phase 3 ADAPT trial data demonstrated statistically significant improvements in the Myasthenia Gravis Activities of Daily Living scale in AChR antibody-positive gMG patients, with a manageable safety profile. A subcutaneous formulation has further expanded clinical flexibility. Active investigation continues to refine optimal dosing frequency, predictors of sustained response, and long-term immunological effects of chronic FcRn blockade. Positioning FcRn inhibitors relative to established immunosuppressants and complement inhibitors and monitoring long-term IgG effects are evolving practice considerations. Neurologists and neuromuscular specialists managing AChR- or MuSK-positive gMG will benefit from peer discussion of FcRn-targeted therapy integration.

How do you currently position FcRn inhibitors relative to established immunosuppressants and complement inhibitors in gMG, particularly in patients with inadequate corticosteroid or azathioprine responses? What clinical and serological factors most influence your decisions regarding treatment frequency and duration with FcRn-targeted therapy in gMG?