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Riliprubart (SAR445088, BIVV020) is a humanized IgG4 monoclonal antibody developed as a second-generation classical complement inhibitor. It selectively inhibits the activated form of Complement C1s subcomponent, a serine protease in the classical complement pathway of the innate immune system. By blocking Complement C1s subcomponent, riliprubart disrupts key inflammatory mechanisms that drive demyelination and axonal damage in chronic inflammatory demyelinating polyneuropathy (CIDP) and may also be relevant for other complement-mediated diseases such as cold agglutinin disease (CAD). Riliprubart contains mutations to enhance neonatal Fc receptor binding, promoting antibody recycling and prolonging half-life. The drug is administered intravenously or subcutaneously and has shown promising efficacy and safety in phase 2/3 clinical trials for CIDP, including improvements in disability scores, fatigue reduction, quality-of-life measures, and biomarkers associated with nerve damage[1][2][4][5][6][7].
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