The Fc Receptor and Mechanisms of Efgartigimod


A. Gordon Smith, MD, FAAN, explores the rationale for targeting the neonatal Fc receptor and the mechanisms for efgartigimod for use in the treatment of myasthenia gravis.

A. Gordon Smith, MD, FAAN: One of the more exciting developments, therapeutically, in myasthenia gravis, and I would say for potentially many other antibody-mediated disorders, are agents that target the neonatal Fc receptor or FcRn which is really interesting physiology. The FcRn system serves really three purposes. One is this is the mechanism by which maternal antibodies cross the placenta into the fetal circulation. It is also the way that neonatal gut transports the antibodies from breast milk into the fetal circulation. FcRn is important for all of us when we are fetuses and when we're neonates. It turns out that the system is also important for regulating antibody levels and so these drugs and the one that's been approved so far is called efgartigimod, bind to and block the FcRn receptor, which leads to degradation of antibodies and so treatment with efgartigimod results in very quick reduction in immunoglobulin levels in the blood. In the clinical trial, this is associated with significant improvement in myasthenia gravis symptoms. It's interesting that the long-acting complement inhibitor ravulizumab is long-acting because it has been engineered to have greater affinity for the neonatal Fc receptors. So, therefore, it sticks around longer, therefore it lasts longer but one of the exciting areas in myasthenia therapeutics is not the available of efgartigimod but a number of other similar agents in the therapeutic pipeline.

Transcript edited for clarity

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