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.

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

Department of Neurology Medical University Vienna Vienna Austria

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

Department of Neurology Palacky University in Olomouc Olomouc Czech Republic

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

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

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

Department of Neurology University of Virginia Virginia Charlottesville USA

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

Horizon Therapeutics Illinois Deerfield USA

Medical Faculty Heinrich Heine University Düsseldorf Düsseldorf Germany

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