Biologic
RCSB PDB 7Q3P
Efgartigimod
Vyvgart
- Mechanism of action
- Neonatal Fc receptor (FcRn) antagonist (antibody Fc fragment)
- In plain language
- Blocks a receptor that normally recycles antibodies, so the body clears out disease-causing antibodies faster.
- How it works
- Efgartigimod is an engineered fragment of the human IgG1 antibody's Fc region, modified for enhanced binding to the neonatal Fc receptor (FcRn). FcRn ordinarily binds circulating IgG inside cells and recycles it back into the bloodstream rather than routing it for degradation, which is why IgG has an unusually long half-life among plasma proteins. By competitively occupying FcRn, efgartigimod blocks this recycling step, so both normal and pathogenic IgG — including the anti-acetylcholine receptor (anti-AChR) and anti-muscle-specific tyrosine kinase (anti-MuSK) autoantibodies implicated in myasthenia gravis — are instead degraded, lowering circulating total IgG and autoantibody levels. Clinical studies measured this effect directly: patients treated with efgartigimod showed reductions in both total IgG and disease-relevant autoantibody levels relative to baseline.
- Therapeutic applications
- Indicated for the treatment of generalized myasthenia gravis (gMG) in adult patients.
- Class
- Fc fragment
- Therapeutic area
- Neurology / Immunology
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