Autoantibodies against the acetylcholine receptor (AChR) are often found in patients with generalized myasthenia gravis (gMG), which destroy the post-synaptic membrane of the neuromuscular junction (NMJ) via aberrant complement cascade activation.¹ Humanized monoclonal antibodies with a high affinity to the human terminal complement component C5 such as ravulizumab inhibit the membrane attack complex formation.¹ Previously, the 26-week randomized controlled period (RCP) of the phase 3 CHAMPION MG study demonstrated the efficacy and safety profile of ravulizumab in adult patients with anti-acetylcholine receptor antibody-positive (AChRAb+) gMG.¹

Long-term ravulizumab allowed more patients to achieve MGFA-PIS with or without MM at week 60, when compared with week 26 in both the ravulizumab-ravulizumab and the placebo-ravulizumab arms