Inebilizumab reduces neuromyelitis optica spectrum disorder risk independent of FCGR3A polymorphism.
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.
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