MicroVue™ C3a Plus EIA

The MicroVue C3a Plus Enzyme Immunoassay is for the measurement of C3a in plasma and serum.


Product Specifications

Citations 66
Specimen

Serum/EDTA Plasma 10 μL

LLOQ 0.023 ng/mL
ULOQ 2.531 ng/mL
Assay Time 2.5 hours
Cross Reactivity

African Green Monkey, Cynomolgous monkey, Rhesus monkey

Ordering Information

For Research Use Only in the United States. Not for use in diagnostic procedures.
Catalog Number A031
Catalog Number (CE) A032
Size 96 wells/test
Price (USD) $745.00
Price (EURO) 660,00 €

Contact us

US Phone+1 (858) 552 1100
EU Phone+353 (91) 412 474
US Emailcontact-us@quidelortho.com
EU Emailcontact-emea@quidelortho.com

Specifications

Description

The MicroVue C3a Plus Enzyme Immunoassay is for the measurement of C3a in plasma and serum.

Size 96 wells/test
Form

96 well plate with 12 eight-well strips in a resealable foil pouch

Specimen Serum/EDTA Plasma 10 μL
Limit of Detection (LOD) 0.012 ng/mL
Lower Limit of Quantitation (LLOQ) 0.023 ng/mL
Upper Limit of Quantitation (ULOQ) 2.531 ng/mL
Intra Assay 4.5–5.3%
Inter Assay 5.9–19.6%
Standards 5
Controls 2
Sample Values

Serum 71.0–589.2 ng/mL, EDTA Plasma 33.8–268.1 ng/mL

Assay Time 2.5 hours
Cross Reactivity

African Green Monkey, Cynomolgous monkey, Rhesus monkey

Storage

Store the unopened kit at 2°C to 8°C. Refer to Product Insert for additional storage details.

Background

Under normal conditions, activation of the classical, alternative, or lectin complement pathways results in the formation of a C3 convertase multi-molecular enzyme capable of cleaving C3 to C3a and C3b. C3a is a low molecular weight (approximately 9kD) protein fragment of 77 amino acids. C3a is rapidly metabolized by the serum enzyme carboxypeptidase N to a more stable, 76 amino acid form, C3a des-Arg. For convenience, both forms will be referred to as “C3a” for purposes of this documentation. The MicroVue C3a Plus assay, a rapid, highly specific and quantitative procedure for measuring C3a levels, is designed for investigations into the role or status of complement pathway activation in numerous research settings, and for monitoring the generation of C3a in vivo or in vitro. C3a has been shown to increase vascular permeability, to be spasmogenic and chemotactic, and to induce the release of pharmacologically active mediators from a number of cell types. The role of C3a in the pathogenesis of inflammatory reactions seen in gram-negative bacterial sepsis, trauma, ischemic heart disease, cerebral ischemia, post dialysis syndrome and several autoimmune diseases (including rheumatoid arthritis, lupus erythematosus, and acute glomerulonephritis) is well documented.