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Kill 'Em All: Efgartigimod Immunotherapy for Autoimmune Diseases
Jagadeesh Bayry1, Srini V Kaveri1
1Institut National de la Santé et de la Recherche Médicale, Centre de Recherche des Cordeliers, Equipe-Immunopathologie et Immunointervention Thérapeutique, Sorbonne Université, Université Paris Descartes, Sorbonne Paris Cité, Paris, F-75006, France.
Neonatal Fc receptors (FcRns) recycle IgGs by preventing their lysosome degradation. As this process also enhances half-life of pathogenic auto-IgG, inspired from the mechanisms of intravenous immunoglobulin, several inhibitors of IgG-FcRn interface have been conceived for treating autoimmune diseases. Among them, the high-affinity FcRn-binding engineered Fc molecule efgartigimod has recently completed phase I clinical trial.
Neonatal Fc receptors (FcRns) recycle IgGs by preventing their lysosome degradation. As this process also enhances half-life of pathogenic auto-IgG, inspired from the mechanisms of intravenous immunoglobulin, several inhibitors of IgG-FcRn interface have been conceived for treating autoimmune diseases. Among them, the high-affinity FcRn-binding engineered Fc molecule efgartigimod has recently completed phase I clinical trial.
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