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| Item Type: | Article |
|---|---|
| Title: | Inebilizumab reduces neuromyelitis optica spectrum disorder risk independent of FCGR3A polymorphism |
| Creators Name: | Kim, H.J., Aktas, O., Patterson, K.R., Korff, S., Kunchok, A., Bennett, J.L., Weinshenker, B.G., Paul, F., Hartung, H.P., Cimbora, D., Smith, M.A., Mittereder, N., Rees, W.A., She, D. and Cree, B.A.C. |
| 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. |
| Keywords: | Aquaporin 4, Humanized Monoclonal Antibodies, IgG Receptors, Immunoglobulin G, Neuromyelitis Optica |
| Source: | Annals of Clinical and Translational Neurology |
| ISSN: | 2328-9503 |
| Publisher: | Wiley |
| Volume: | 10 |
| Number: | 12 |
| Page Range: | 2413-2420 |
| Date: | December 2023 |
| Official Publication: | https://doi.org/10.1002/acn3.51911 |
| PubMed: | View item in PubMed |
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