< 0.5% cross-reactivity observed with available related molecules.< 50% cross-species reactivity observed with species tested.
No significant interference observed with available related molecules.
The Quantikine Human Acetylcholinesterase/ACHE Immunoassay is a 4.5 hour solid phase ELISA designed to measure ACHE levels in cell culture supernates, tissue lysates, serum, and plasma. It contains CHO cell-expressed recombinant human ACHE and antibodies raised against the recombinant protein. Results obtained for naturally occurring human ACHE showed linear curves that were parallel to the standard curves obtained using the Quantikine Human ACHE Immunoassay standards. These results indicate that this kit can be used to determine relative mass values for natural human ACHE.
Intra-Assay Precision (Precision within an assay) Three samples of known concentration were tested twenty times on one plate to assess intra-assay precision.
Inter-Assay Precision (Precision between assays) Three samples of known concentration were tested in twenty separate assays to assess inter-assay precision. Assays were performed by at least three technicians using two lots of components.
The recovery of human ACHE spiked to levels throughout the range of the assay in various matrices was evaluated.
Average % Recovery
Cell Culture Media (n=4)
Cell Lysis Buffer (n=4)
EDTA Plasma (n=4)
Heparin Plasma (n=4)
To assess the linearity of the assay, samples containing and/or spiked with high concentrations of human ACHE were diluted with Calibrator Diluent to produce samples with values within the dynamic range of the assay.
Preparation and Storage
Store the unopened product at 2 - 8 °C. Do not use past expiration date.
The classical role of ACHE is to terminate cholinergic neurotransmission by hydrolysis of acetylcholine (ACH). ACHE is thought to be involved in the pathology of Alzheimer's disease (AD) by accelerating the assembly of Abeta peptides into fibrillar species through forming complexes with Abeta via the peripheral anionic site on ACHE. ACHE inhibitors have been used to delay symptoms of AD patients by virtue of their ability to enhance ACH availability, as well as reduce amyloidogenesis and subsequent neurotoxicity. Its involvement in the cholinergic anti-inflammatory pathway connects ACHE with a possible marker of low-grade systemic inflammation in obesity, hypertension, coronary heart disease, and AD. Alternative splicing produces three isoforms: an amphipathic form that exists as both monomeric and mutimeric forms, a soluble-monomeric form lacking the cysteine residue near the C-terminus, and a GPI-anchored dimeric form found in the membranes of erythrocytes. The recombinant mouse ACHE (rmACHE) was expressed as the amphipathic form that consists of soluble monomer and mutimeric forms.