Inebilizumab reduces neuromyelitis optica spectrum disorder risk independent of FCGR3A polymorphism
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 (...
| Main Authors: | , , , , , , , , , , , , , , |
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| Format: | Article |
| Language: | English |
| Published: |
Wiley
2023-12-01
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| Series: | Annals of Clinical and Translational Neurology |
| Online Access: | https://doi.org/10.1002/acn3.51911 |
| _version_ | 1797389793859993600 |
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| author | Ho Jin Kim Orhan Aktas Kristina R. Patterson Schaun Korff Amy Kunchok Jeffrey L. Bennett Brian G. Weinshenker Friedemann Paul Hans‐Peter Hartung Daniel Cimbora Michael A. Smith Nanette Mittereder William A. Rees Dewei She Bruce A. C. Cree |
| author_facet | Ho Jin Kim Orhan Aktas Kristina R. Patterson Schaun Korff Amy Kunchok Jeffrey L. Bennett Brian G. Weinshenker Friedemann Paul Hans‐Peter Hartung Daniel Cimbora Michael A. Smith Nanette Mittereder William A. Rees Dewei She Bruce A. C. Cree |
| author_sort | Ho Jin Kim |
| collection | DOAJ |
| description | 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. |
| first_indexed | 2024-03-08T23:01:09Z |
| format | Article |
| id | doaj.art-117e79e5e7134a03b6b3f3c65a13a5f5 |
| institution | Directory Open Access Journal |
| issn | 2328-9503 |
| language | English |
| last_indexed | 2024-03-08T23:01:09Z |
| publishDate | 2023-12-01 |
| publisher | Wiley |
| record_format | Article |
| series | Annals of Clinical and Translational Neurology |
| spelling | doaj.art-117e79e5e7134a03b6b3f3c65a13a5f52023-12-15T16:39:24ZengWileyAnnals of Clinical and Translational Neurology2328-95032023-12-0110122413242010.1002/acn3.51911Inebilizumab reduces neuromyelitis optica spectrum disorder risk independent of FCGR3A polymorphismHo Jin Kim0Orhan Aktas1Kristina R. Patterson2Schaun Korff3Amy Kunchok4Jeffrey L. Bennett5Brian G. Weinshenker6Friedemann Paul7Hans‐Peter Hartung8Daniel Cimbora9Michael A. Smith10Nanette Mittereder11William A. Rees12Dewei She13Bruce A. C. Cree14Department of Neurology Research Institute and Hospital of National Cancer Center Goyang South KoreaMedical Faculty Heinrich Heine University Düsseldorf Düsseldorf GermanyHorizon Therapeutics Illinois Deerfield USAHorizon Therapeutics Illinois Deerfield USADepartment of Neurology Mellen Center for Multiple Sclerosis, Cleveland Clinic Ohio Cleveland USADepartment of Neurology, Programs in Neuroscience and Immunology University of Colorado School of Medicine, Anschutz Medical Campus Colorado Aurora USADepartment of Neurology University of Virginia Virginia Charlottesville USAExperimental 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 GermanyMedical Faculty Heinrich Heine University Düsseldorf Düsseldorf GermanyHorizon Therapeutics Illinois Deerfield USAHorizon Therapeutics Illinois Deerfield USAHorizon Therapeutics Illinois Deerfield USAHorizon Therapeutics Illinois Deerfield USAHorizon Therapeutics Illinois Deerfield USADepartment of Neurology, UCSF Weill Institute for Neurosciences University of California San Francisco California San Francisco USAAbstract 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.https://doi.org/10.1002/acn3.51911 |
| spellingShingle | Ho Jin Kim Orhan Aktas Kristina R. Patterson Schaun Korff Amy Kunchok Jeffrey L. Bennett Brian G. Weinshenker Friedemann Paul Hans‐Peter Hartung Daniel Cimbora Michael A. Smith Nanette Mittereder William A. Rees Dewei She Bruce A. C. Cree Inebilizumab reduces neuromyelitis optica spectrum disorder risk independent of FCGR3A polymorphism Annals of Clinical and Translational Neurology |
| title | Inebilizumab reduces neuromyelitis optica spectrum disorder risk independent of FCGR3A polymorphism |
| title_full | Inebilizumab reduces neuromyelitis optica spectrum disorder risk independent of FCGR3A polymorphism |
| title_fullStr | Inebilizumab reduces neuromyelitis optica spectrum disorder risk independent of FCGR3A polymorphism |
| title_full_unstemmed | Inebilizumab reduces neuromyelitis optica spectrum disorder risk independent of FCGR3A polymorphism |
| title_short | Inebilizumab reduces neuromyelitis optica spectrum disorder risk independent of FCGR3A polymorphism |
| title_sort | inebilizumab reduces neuromyelitis optica spectrum disorder risk independent of fcgr3a polymorphism |
| url | https://doi.org/10.1002/acn3.51911 |
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