In Vitro Neuromuscular Junction Models to Functionally Dissect Anti-AChR Pathogenic Mechanism in Myasthenia Gravis

Time: 12:30 pm
day: Track A - Day 1 AM


  • Exploring three mechanisms of neurotransmission impairment by anti-acetylcholine receptor (AChR) autoantibodies in myasthenia gravis, including complement activation, antigenic modulation, and functional blockade
  • In vitro NMJ (neuromuscular junction) models may offer an opportunity to dissect the contribution of pathogenic autoantibodies and may allow a tailored therapeutic strategy
  • Sharing how Zilucoplan, an investigational macrocyclic peptide inhibitor of complement C5, prevented functional impairment induced by AChR+ myasthenia gravis patient sera in an in vitro neuromuscular junction model