beta-Amyloid (1-42) human/high-purity/Peptide sales

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Introduction from Drug peptide supply about:beta-Amyloid (1-42) human

chemical formula of beta-Amyloid (1-42) human
English name beta-Amyloid (1-42) human
Chinese name BETA-淀粉样多肽1-42
CAS NO 107761-42-2
Peptide sequence Asp-Ala-Glu-Phe-Arg-His-Asp-Ser-Gly-Tyr-Glu-Val-His-His-Gln-Lys-Leu-Val-Phe-Phe-Ala-Glu-Asp-Val-Gly-Ser-Asn-Lys-Gly-Ala-Ile-Ile-Gly-Leu-Met-Val-Gly-Gly-Val-Val-Ile-Ala
Molecular formula C203H311N55O60S1
Molecular weight 4514.1
storage temperature 2-8℃
purity ≥98%
Package 1mg;5mg;10mg;50mg;100mg,1g or according to customer’s detail requirement.
Product English synonyms AmyloidβREFDUPL:Beta-Amyloid(1-42),sodiumsalt;Β-AMYLOIDPEPTIDE(1-42),RAT

Introduction of β-Amyloid (1-42)(human)

This peptide is well suited to the quantitative determination of A 42 peptide. Alzheimer’s disease (AD) is characterized by the presence of extracellular plaques and intracellular neurofibrillary tangles (NFTs) in the brain. The major protein component of these plaques is beta amyloid peptide (A), a 40- to 43- amino-acid peptide cleaved from amyloid precursor protein by secretase (BACE) and a putative (gamma) secretase. Increased release of the ‘longer forms’ of A peptide, A 42 and A 43, which have a greater tendency to aggregate than A 40, occurs in individuals expressing certain genetic mutations, expressing certain ApoE alleles or may other, still undiscovered factors.

Mechanism of β-amyloid peptide Aβ1-42 peptide

Numerous mutations identified in the gene encoding beta-amyloid precursor protein (βAPP) are associated with early-onset familial Alzheimer’s disease. Studies have also shown that mutations in the genes encoding presenilin 1 and presenilin 2 alter the processing of βAPP, resulting in increased extracellular concentrations of the amyloid β peptide Aβ1-42 (43) relative to Aβ1-40. Biophysical and biochemical experiments have shown that Aβ1-42(43) can act as a catalyst for the aggregation and deposition of β-amyloid peptide (Aβ), which has neurotoxic effects associated with senile plaque formation. Additionally, antibodies recognizing Aβ1-42 showed increased long-form peptides in presenilin and βAPP mutants, while other studies used Aβ-specific antibodies to prevent Aβ fibrillar aggregation in vitro. Amino acid sequence verified by amino acid analysis or sequencing. This product is supplied in a non-neurotoxic form prior to the pre-incubation step. The emergence of toxicity has recently been shown to correlate with the degree of beta-sheet structure. For neurotoxicity studies and substrate cleavage assays.


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