Catalog No.
KDB95803
Description
PRINCIPLE OF THE ASSAY This assay employs the quantitative competitive enzyme immunoassay technique. Recombinant Human CD25 has been pre-coated onto a microplate. Standards or samples are premixed with biotin-labeled antibody and then pipetted into the wells. Daclizumab in the sample competitively binds to the pre-coated protein with biotin-labeled Daclizumab. After washing away any unbound substances, Streptavidin-HRP is added to the wells. Following a wash to remove any unbound enzyme reagent, a substrate solution is added to the wells and color develops in inversely proportion to the amount of Daclizumab bound in the initial step. The color development is stopped and the intensity of the color is measured.
Applications
Used for the quantitative determination of Daclizumab concentration in serum and plasma.
Detection method
Colorimetric
Sample type
Plasma, Serum
Assay type
Quantitative
Range
125 - 8,000 ng/mL
Sensitivity
15.36 ng/mL
Precision
Intra-Assay Precision (Precision within an assay): <20%
Three samples of known concentration were tested sixteen times on one plate to assess intra-assay precision.
Inter-Assay Precision (Precision between assays): <20%
Three samples of known concentration were tested in twenty four separate assays to assess inter-assay precision.
|
Intra-Assay Precision |
Inter-Assay Precision |
||||
Sample |
1 |
2 |
3 |
1 |
2 |
3 |
n |
16 |
16 |
16 |
24 |
24 |
24 |
Mean (ng/mL) |
3628.6 |
1096.4 |
247.6 |
5413.0 |
1458.1 |
198.3 |
Standard deviation |
162.1 |
117.1 |
44.8 |
897.3 |
260.3 |
40.0 |
CV (%) |
4.5 |
10.7 |
18.1 |
16.6 |
17.9 |
20.2 |
Recovery
80-120%
Shipping
2-8 ℃
Stability and Storage
When the kit was stored at the recommended temperature for 6 months, the signal intensity decreased by less than 20%.
Alternative Names
BIIB019, DAC HYP, CAS: 152923-56-3
Background
Daclizumab (DAC) is a humanized, monoclonal antibody that blocks CD25, a critical element of the high-affinity interleukin-2 receptor (IL-2R). DAC HYP blockade of CD25 inhibits effector T cell activation, regulatory T cell expansion and survival, and activation-induced T-cell apoptosis. Because CD25 blockade reduces IL-2 consumption by effector T cells, it increases IL-2 bioavailability allowing for greater interaction with the intermediate-affinity IL-2R, and therefore drives the expansion of CD56bright natural killer (NK) cells. Furthermore, there appears to be a direct correlation between CD56bright NK cell expansion and DAC HYP efficacy in reducing relapses and MRI evidence of disease activity in patients with RMS in phase II and phase III double-blind, placebo- and active comparator-controlled trials. Therapeutic efficacy was maintained during open-label extension studies. However, treatment was associated with an increased risk of rare adverse events, including cutaneous inflammation, autoimmune hepatitis, central nervous system Drug Reaction with Eosinophilia Systemic Symptoms (DRESS) syndrome, and autoimmune Glial Fibrillary Acidic Protein (GFAP) alpha immunoglobulin-associated encephalitis. As a result, DAC HYP was removed from clinical use in 2018. The lingering importance of DAC is that its use led to a deeper understanding of the underappreciated role of innate immunity in the potential treatment of autoimmune disease.