Inebilizumab reduces neuromyelitis optica spectrum disorder risk independent of <scp><i>FCGR3A</i></scp> polymorphism-Reference-Cited by-同舟云学术

Inebilizumab reduces neuromyelitis optica spectrum disorder risk independent of FCGR3A polymorphism

Published:2023-10-07 Issue:12 Volume:10 Page:2413-2420
ISSN:2328-9503
Container-title:Annals of Clinical and Translational Neurology
language:en
Short-container-title:Ann Clin Transl Neurol

Author:

Kim Ho Jin¹^ORCID,Aktas Orhan²,Patterson Kristina R.³,Korff Schaun³,Kunchok Amy⁴,Bennett Jeffrey L.⁵,Weinshenker Brian G.⁶,Paul Friedemann⁷^ORCID,Hartung Hans‐Peter²⁸⁹¹⁰,Cimbora Daniel³,Smith Michael A.³,Mittereder Nanette³,Rees William A.³,She Dewei³,Cree Bruce A. C.¹¹^ORCID

Affiliation:

1. Department of Neurology Research Institute and Hospital of National Cancer Center Goyang South Korea

2. Medical Faculty Heinrich Heine University Düsseldorf Düsseldorf Germany

3. Horizon Therapeutics Illinois Deerfield USA

4. Department of Neurology Mellen Center for Multiple Sclerosis, Cleveland Clinic Ohio Cleveland USA

5. Department of Neurology, Programs in Neuroscience and Immunology University of Colorado School of Medicine, Anschutz Medical Campus Colorado Aurora USA

6. Department of Neurology University of Virginia Virginia Charlottesville USA

7. Experimental and Clinical Research Center, Max Delbrück Center for Molecular Medicine and Charité Universitätsmedizin Berlin, Corporate Member of Freie Universitat Berlin and Humboldt‐Universitat zu Berlin Berlin Germany

8. Brain and Mind Centre University of Sydney New South Wales Sydney Australia

9. Department of Neurology Medical University Vienna Vienna Austria

10. Department of Neurology Palacky University in Olomouc Olomouc Czech Republic

11. Department of Neurology, UCSF Weill Institute for Neurosciences University of California San Francisco California San Francisco USA

Abstract

AbstractInebilizumab, 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.

Publisher

Wiley

Subject

Neurology (clinical),General Neuroscience

Link

https://onlinelibrary.wiley.com/doi/pdf/10.1002/acn3.51911

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