
Efgartigimod is an Fc fragment engineered for increased affinity for the neonatal Fc receptor (FcRn) to outcompete endogenous IgG binding, thereby preventing recycling and causing increased IgG degradation.In previous phase II studies in primary immune thrombocytopenia and myasthenia gravis, as well as in a phase III study in myasthenia gravis, efgartigimod induced reductions in all IgG subclasses with corresponding clinical efficacy and was well tolerated.In this phase II, open‐label study of efgartigimod in patients with pemphigus vulgaris and pemphigus foliaceus, efgartigimod induced early decreases in serum total IgG, as well as disease‐specific anti‐desmoglein 1 and 3 autoantibodies, and was well tolerated.The clinical results of this study demonstrate that efgartigimod represents a well‐tolerated potential means of achieving early disease control and complete clinical remission of pemphigus while allowing early corticosteroid tapering.
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