Anti-Abatacept ELISA Kit

Sample

Serum, Plasma (EDTA, Heparin)

Species Reactivity

Human

Detection Method

sELISA

Intended Use

Enzyme immunoassay for determination of quantitative antibodies to Abatacept in serum and plasma samples.

Storage

The kit is shipped at ambient temperature (10-30°C) and should be stored at 2-8°C for long term storage. Keep away from heat or direct sunlight. The strips of microtiter plate are stable up to the expiry date of the kit in the broken, but tightly closed bag when stored at 2-8°C.

Precision

Intra-assay and inter-assay CVs < 30%

Sensitivity

The lowest detectable level (Lowest detection limit, LOD) that can be distinguished from the zero standard is 50 ng/mL
Functional sensitivity (Limit of quantification-LOQ): 62.5 ng/mL

General Description

Abatacept is licensed for the treatment of rheumatoid arthritis (RA) in combination with methotrexate. The indication includes moderate to severe RA unresponsive to other diseasemodifying antirheumatic drugs including at least one tumour necrosis factor (TNF)- a blocker, or where patients have been intolerant of such drugs. Abatacept (CTLA4Ig) is a fusion protein of the extracellular domain of the human cytotoxic T-lymphocyteassociated antigen 4 (CTLA-4) linked to a modified Fc of human immunoglobulin 1 (IgG1).
Abatacept inhibits the activation of T lymphocytes that play an important role in the early stages of pathogenesis of RA.Activation of a T cell requires two signals from the antigen-presenting cell (APC). The first signal is antigen specific and arises when antigenic peptides are presented to the T cell through the Major Histocompatibility Complex. A second signal, so-called co-stimulation, develops from the interaction between CD80 or CD86 antigen on the APC and CD28 antigen on the T cell. Abatacept binds with the extracellular domain of CTLA-4 to CD80 or CD86 antigen on the APC with a higher affinity than CD28, preventing the essential second signal for T-cell activation. T-cell activation and the 3 production of inflammatory mediators and cytokines (TNF-a, interferon-gamma and interleukin-2) are consequently reduced. Trials in patients with RA have shown that Abatacept slows progression of joint damage and improves function. An increased incidence of all kinds of infections caused by Abatacept is explained by its mechanism of suppressing the immune response. Headache, hypertension, dizziness, gastrointestinal disorders and rash are other common adverse effects. A small percentage of treated patients develop antiAbatacept antibodies.