Obexelimab

Obexelimab (XmAb5871) is a bifunctional monoclonal antibody that binds to both CD19 and FcγRIIb, inhibiting the activity of B cells, plasma cells, and plasma cell precursors. Obexelimab is used in the study of autoimmune diseases such as systemic lupus erythematosus.

Obexelimab induces the expression of genes associated with apoptotic pathways and promotes B-cell apoptosis. [1]
A 10 μg/mL solution of Obexelimab, applied for 3 minutes, inhibits B-cell activation and function by suppressing BCR-mediated calcium influx and promoting FcγRIIb phosphorylation. [2]
Methods: Human resting B cells were isolated and purified from tonsils. Cells were pretreated with 10 μg/mL obexelimab for 30 minutes, then stimulated for 30 minutes with 2.5 μg/mL anti-Ig (BCR activation), 1 μg/mL CpG ODN (TLR9 activation), or a combination of both. Western blot analysis was performed to detect the phosphorylation levels of FcγRIIb (Y292), AKT, and ERK1/2 phosphorylation levels.
Results: Obexelimab induced phosphorylation at the FcγRIIb Y292 site and significantly inhibited AKT and ERK phosphorylation induced by BCR and TLR9 activation, either alone or in combination. [3]
Methods: Purified B cells were isolated from ACPA-positive RA patients; after treatment with obexelimab (10 μg/mL), the cells were stimulated with R848 (1 μg/mL) and IL-2 (10 ng/mL) for 3 days; ELISPOT was used to detect IgG AFC specific to citrullinated filamentous protein peptides.
Results: Obexelimab significantly reduced the number of cells secreting citrullinated filamentous protein-specific autoantibodies in RA patients, directly inhibiting the production of pathogenic autoantibodies.[4]

10 mg/kg Obexelimab, injected intraperitoneally twice weekly, suppressed autoimmune responses in immunodeficient mice implanted with peripheral blood mononuclear cells (PBMC) from rheumatoid arthritis (RA) patients. [2]

Human

Monoclonal

Unconjugated