The Mercodia Ultrasensitive Mouse Insulin ELISA is based on highly specific monoclonal antibodies with insignificant or no cross-reactivity to C-peptide or proinsulin.
Read the Directions for Use
Mercodia Ultrasensitive Mouse Insulin ELISA provides a method for the quantitative determination of insulin in mouse serum, plasma or cell culture medium.
Format: 1 x 96 wells/10 x 96 wells
Samples: Serum, plasma, cell culture medium
Sample volume: 25 μL
Assay range: 0.025 - 1.5 μg/l
Detection limit: ≤ 0.025 μg/l
Incubation: (min) 120+15
The detection limit is ≤ 0.025 μg/L as determined with the
methodology described in ISO11843-Part 4.
Recovery upon addition is 76 - 94 % (85 %).
Recovery upon dilution is 110 - 132 % (123 %).
Each sample was analyzed in 4 replicates on 16 different
|Sample||Mean Value||Coefficient of variation|
|(μg/L)||within assay %||between assay %||total assay %|
Mercodia Mouse Insulin ELISA is a solid phase two-site enzyme
immunoassay based on the sandwich technique, in which two
monoclonal antibodies are directed against separate antigenic
determinants on the insulin molecule. Insulin in the sample reacts
with anti-insulin antibodies bound to microtitration wells and
peroxidase-conjugated anti-insulin antibodies in the solution.
Summary of protocol
The following cross-reactions have been tested:
|Human Insulin||195 %|
|Human proinsulin||82 %|
|Human C-pepitde||< 0.05 %|
|IGF-I||< 0.02 %|
|IGF-II||< 0.02 %|
|Rat insulin||146 %|
|Rat proinsulin||14 %|
|Rat C-peptide||< 0.001 %|
|Porcine insulin||628 %|
|Ovine insulin||256 %|
|Bovine insulin||110 %|
Jones, H, B, Reens, J (2014)
Islets of Langerhans from prohormone convertase-2 knockout mice show alpha-cell hyperplasia and tumorigenesis with elevated alpha-cell neogenesis
Favre, G, A, Lebrun, P (2014)
Constitutive activation of the renin-angiotensin system reduces visceral fat and improves glucose tolerance in mice
Saito, M, Kaneda, A, Sugiyama, T (2015)
Production of a mouse strain with impaired glucose tolerance by systemic heterozygous knockout of the glucokinase gene and its feasibility as a prediabetes model