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Inebilizumab reduces neuromyelitis optica spectrum disorder risk independent of FCGR3A polymorphism.
Kim, Ho Jin; Aktas, Orhan; Patterson, Kristina R; Korff, Schaun; Kunchok, Amy; Bennett, Jeffrey L; Weinshenker, Brian G; Paul, Friedemann; Hartung, Hans-Peter; Cimbora, Daniel; Smith, Michael A; Mittereder, Nanette; Rees, William A; She, Dewei; Cree, Bruce A C.
Affiliation
  • Kim HJ; Department of Neurology, Research Institute and Hospital of National Cancer Center, Goyang, South Korea.
  • Aktas O; Medical Faculty, Heinrich Heine University Düsseldorf, Düsseldorf, Germany.
  • Patterson KR; Horizon Therapeutics, Illinois, Deerfield, USA.
  • Korff S; Horizon Therapeutics, Illinois, Deerfield, USA.
  • Kunchok A; Department of Neurology, Mellen Center for Multiple Sclerosis, Cleveland Clinic, Ohio, Cleveland, USA.
  • Bennett JL; Department of Neurology, Programs in Neuroscience and Immunology, University of Colorado School of Medicine, Anschutz Medical Campus, Colorado, Aurora, USA.
  • Weinshenker BG; Department of Neurology, University of Virginia, Virginia, Charlottesville, USA.
  • Paul F; 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.
  • Hartung HP; Medical Faculty, Heinrich Heine University Düsseldorf, Düsseldorf, Germany.
  • Cimbora D; Brain and Mind Centre, University of Sydney, New South Wales, Sydney, Australia.
  • Smith MA; Department of Neurology, Medical University Vienna, Vienna, Austria.
  • Mittereder N; Department of Neurology, Palacky University in Olomouc, Olomouc, Czech Republic.
  • Rees WA; Horizon Therapeutics, Illinois, Deerfield, USA.
  • She D; Horizon Therapeutics, Illinois, Deerfield, USA.
  • Cree BAC; Horizon Therapeutics, Illinois, Deerfield, USA.
Ann Clin Transl Neurol ; 10(12): 2413-2420, 2023 12.
Article in En | MEDLINE | ID: mdl-37804003
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.
Subject(s)

Full text: 1 Collection: 01-internacional Database: MEDLINE Main subject: Neuromyelitis Optica Type of study: Etiology_studies / Risk_factors_studies Limits: Humans Language: En Journal: Ann Clin Transl Neurol Year: 2023 Type: Article Affiliation country: South Korea

Full text: 1 Collection: 01-internacional Database: MEDLINE Main subject: Neuromyelitis Optica Type of study: Etiology_studies / Risk_factors_studies Limits: Humans Language: En Journal: Ann Clin Transl Neurol Year: 2023 Type: Article Affiliation country: South Korea