Abstract
The neonatal Fc receptor, FcRn, is responsible for controlling the half-life of IgG antibodies. As a result, inhibitors of FcRn have been investigated as a possible way to modulate IgG half-lives. Such inhibitors could have possible applications in reducing autoantibody levels in autoimmune disease states. To date, monoclonal antibodies, engineered Fc domains, and short peptides have been reported to inhibit FcRn function and modulate IgG half-lives in vivo.
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