Expert: FcRn (neonatal Fc receptor) inhibition. FcRn is present on endothelial cells and many immune cells, rescuing IgG from lysosomal degradation by binding it in acidic endosomes (pH ~6.0) and recycling it to the cell surface (release at pH ~7.4). This recycling mechanism gives IgG its uniquely long ~21-day half-life. Efgartigimod (Vyvgart) blocks FcRn competitively, preventing IgG rescue. ALL IgG — including pathogenic autoantibodies — undergoes accelerated catabolism, reducing total IgG by ~70-80%. In MG, this addresses ALL THREE pathological mechanisms: complement activation (by reducing complement-fixing IgG1/IgG3), antigenic modulation (by reducing cross-linking antibodies), and direct receptor blockade (by reducing blocking antibodies). Unlike complement inhibitors which only address complement-mediated damage, FcRn inhibition is mechanism-agnostic with respect to IgG subclass.
Everyday: Speeds up the destruction of antibodies in the blood. Normally, a special receptor (FcRn) acts like a recycling system that rescues antibodies from being broken down, giving them a long 3-week lifespan. Vyvgart blocks this recycling receptor, so ALL antibodies — including harmful autoantibodies — get broken down much faster, reducing their levels by 70-80%. This works regardless of WHICH type of damage the autoantibodies cause. Think of it as shutting down the antibody recycling plant — the bad antibodies (autoantibodies causing disease) get destroyed faster, providing relief.
Targets: ["FCRN"]
Rozanolixizumab, a subcutaneous anti-FcRn monoclonal antibody for generalized myasthenia gravis. Reduces pathogenic IgG autoantibodies by blocking neonatal Fc receptor; weekly self-administered SC injection.