Pathogenic properties of myasthenia gravis AChR autoantibodies associate with clinical response to efgartigimod.
J Neurol Neurosurg PsychiatrySep 14, 2026 (epub)
Fatemeh Khani-Habibabadi, Fien M Verhamme, Mahan Moshir et al.
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In 30 seconds
This randomized controlled trial investigated the effects of efgartigimod on AChR autoantibody profiles in 50 patients with generalized myasthenia gravis. Efgartigimod significantly decreased all detectable AChR-specific IgG subclasses and associated pathogenic mechanisms, with variability in response. Notably, double responders showed greater reductions in complement activity and AChR internalization.
Key findings
- Efgartigimod decreased all detectable AChR-specific IgG subclasses in treated patients.
- 84% of patients had AChR autoantibody-mediated C3b deposition at baseline.
- Double responders exhibited greater reductions in complement activity and AChR internalization.
- Efgartigimod reduced IgG-dependent IgM binding to AChR.
Why it matters
Understanding the relationship between AChR autoantibody profiles and clinical response to efgartigimod can help clinicians predict treatment outcomes and tailor therapies for patients with myasthenia gravis.