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货号
KDJ48702
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描述
PRINCIPLE OF THE ASSAY This assay employs the quantitative competitive enzyme immunoassay technique. Recombinant Human SOST has been pre-coated onto a microplate. Standards or samples are premixed with biotin-labeled antibody and then pipetted into the wells. Romosozumab in the sample competitively binds to the pre-coated protein with biotin-labeled Romosozumab. 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 Romosozumab bound in the initial step. The color development is stopped and the intensity of the color is measured.
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应用
Used for the quantitative determination of Romosozumab concentration in serum and plasma. -
检测方法
Colorimetric -
样本类型
Plasma, Serum -
实验类型
Quantitative -
检测范围
125 - 8,000 ng/mL -
灵敏度
42.86 ng/mL -
精准度
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)
3744.0
1019.7
242.5
3473.3
830.7
169.8
Standard deviation
265.8
111.3
26.3
388.9
99.2
30.7
CV (%)
7.1
10.9
10.8
11.2
11.9
18.1
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回收率
80-120% -
运输
2-8 ℃ -
稳定性和存储
When the kit was stored at the recommended temperature for 6 months, the signal intensity decreased by less than 20%. For unopened kits, if you want to prolong the storage time, please store the Standard, Detection A, Detection B and Microplate at - 20℃, the rest reagents should be store at 4℃. -
别名
785A070802, AMG 785, CDP-7851, romosozumab-aqqg, sclerostin Ab, CAS: 909395-70-6
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背景
Romosozumab, a specific inhibitor of sclerostin, is a unique approach to therapy for postmenopausal osteoporosis and related disorders. The elucidation of sclerostin deficiency as the molecular defect of syndromes of high bone mass with normal quality, and the pivotal role of sclerostin as a mediator of osteoblastic activity and bone formation, provided the platform for the evaluation of inhibitors of sclerostin to activate bone formation.
