Inebilizumab reduces neuromyelitis optica spectrum disorder risk independent of FCGR3A polymorphism

被引：5

作者：

Kim, Ho Jin ^{[1
]}

Aktas, Orhan ^{[2
]}

Patterson, Kristina R. ^{[3
]}

Korff, Schaun ^{[3
]}

Kunchok, Amy ^{[4
]}

Bennett, Jeffrey L. ^{[5
,6
]}

Weinshenker, Brian G. ^{[7
]}

Paul, Friedemann ^{[8
,9
,10
,11
]}

Hartung, Hans-Peter ^{[2
,12
,13
,14
]}

Cimbora, Daniel ^{[3
]}

Smith, Michael A. ^{[3
]}

Mittereder, Nanette ^{[3
]}

Rees, William A. ^{[3
]}

She, Dewei ^{[3
]}

Cree, Bruce A. C. ^{[15
]}

机构：

[1] Natl Canc Ctr, Res Inst & Hosp, Dept Neurol, Goyang, South Korea

[2] Heinrich Heine Univ Dusseldorf, Med Fac, Dusseldorf, Germany

[3] Horizon Therapeut, Deerfield, IL USA

[4] Cleveland Clin, Mellen Ctr Multiple Sclerosis, Dept Neurol, Cleveland, OH USA

[5] Univ Colorado, Sch Med, Dept Neurol, Program Neurosci, Anschutz Med Campus, Aurora, CO USA

[6] Univ Colorado, Dept Neurol, Program Immunol, Sch Med, Anschutz Med Campus, Aurora, CO USA

[7] Univ Virginia, Dept Neurol, Charlottesville, VA USA

[8] Max Delbruck Ctr Mol Med, Expt & Clin Res Ctr, Berlin, Germany

[9] Charite Univ Med Berlin, Berlin, Germany

[10] Free Univ Berlin, Berlin, Germany

[11] Humboldt Univ, Berlin, Germany

[12] Univ Sydney, Brain & Mind Ctr, Sydney, NSW, Australia

[13] Med Univ Vienna, Dept Neurol, Vienna, Austria

[14] Palacky Univ Olomouc, Dept Neurol, Olomouc, Czech Republic

[15] Univ Calif San Francisco, UCSF Weill Inst Neurosci, Dept Neurol, San Francisco, CA 94143 USA

来源：

ANNALS OF CLINICAL AND TRANSLATIONAL NEUROLOGY | 2023年 / 10卷 / 12期

关键词：

FC-GAMMA-RIIIA; TREATMENT OUTCOMES; RITUXIMAB; ANTIBODY; BINDING; DESIGN;

D O I：

10.1002/acn3.51911

中图分类号：

R74 [神经病学与精神病学];

学科分类号：

摘要：

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.

引用

页码：2413 / 2420

页数：8

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