Inebilizumab reduces neuromyelitis optica spectrum disorder risk independent of FCGR3A polymorphism
Authors
- H.J. Kim
- O. Aktas
- K.R. Patterson
- S. Korff
- A. Kunchok
- J.L. Bennett
- B.G. Weinshenker
- F. Paul
- H.P. Hartung
- D. Cimbora
- M.A. Smith
- N. Mittereder
- W.A. Rees
- D. She
- B.A.C. Cree
Journal
- Annals of Clinical and Translational Neurology
Citation
- Ann Clin Transl Neurol 10 (12): 2413-2420
Abstract
Inebilizumab, a humanized, glycoengineered, IgG1 monoclonal antibody that depletes CD19+ B-cells, is approved to treat aquaporin 4 (AQP4) IgG-seropositive neuromyelitis optica spectrum disorder (NMOSD). Inebilizumab is afucosylated and engineered for enhanced affinity to Fc receptor III-A (FCGR3A) receptors on natural killer cells to maximize antibody-dependent cellular cytotoxicity. Previously, the F allele polymorphism at amino acid 158 of the FCGR3A gene (F158) was shown to decrease IgG-binding affinity and reduce rituximab (anti-CD20) efficacy for NMOSD attack prevention. In contrast, our current findings from inebilizumab-treated NMOSD patients indicate similar clinical outcomes between those with F158 and V158 allele genotypes.