Exalpha Biologicals, Inc.

Accelerating the Pace of Discovery
Exalpha Biologicals, Inc.

beta-Amyloid (Abeta) [1-16]

  • Product Code: X1886M
  • Size: 100 µg
  • Price (USD): $397

Cat #

X1886M		 Quantity:      

Product Name

beta- Amyloid (Abeta) [1-16]









Product Type

Monoclonal Antibody




Western Blot, Immunoprecipitation, Immunohistochemistry,


Protein A/G Chromatography


100 µg

Price (USD)



Beta-amyloid peptides are lipophilic metal chelators with metal-reducing activity. They bind transient metals such as copper, zinc and iron. and in vitro, can reduce Cu(2+) and Fe(3+) to Cu(+) and Fe(2+), respectively. Beta-amyloid peptides bind to lipoproteins and apolipoproteins E and J in the CSF and to HDL particles in plasma, inhibiting metal-catalyzed oxidation of lipoproteins. Promotes both tau aggregation and TPK II-mediated phosphorylation. Interaction with overexpressed HADH2 leads to oxidative stress and neurotoxicity.1 The gamma-CTF peptides as well as the caspase-cleaved peptides, including C31, are potent enhancers of neuronal apoptosis


Synthetic peptide corresponding to amino acids 1-16 of A? (?-amyloid) peptide.

Positive Control

Expressed in all fetal tissues examined with highest levels in brain, kidney, heart and spleen. Weak expression in liver. In adult brain, highest expression found in the frontal lobe of the cortex and in the anterior perisylvian cortex-opercular gyri. Moderate expression in the cerebellar cortex, the posterior perisylvian cortex-opercular gyri and the temporal associated cortex. Weak expression found in the striate, extra-striate and motor cortices.


In PBS without preservatives or carrier proteins

Customer Storage

Product should be stored at -20ºC. Aliquot to avoid freeze/thaw cycles

Target Molecular Weight

86.9 kDa

Database Links:



1. Kim, K.S. et al. (1988) Production and characterization of monoclonal antibodies reactive to synthetic cerebrovascular amyloid peptide. Neurosci. Res. Commun. 2: 121-131. 2. Kim, K.S. et al. (1990) Detection and quantitation of amyloid B-peptide with two monoclonal antibodies. Neurosci. Res. Commun. 7:113-123. 3. Kitaguchi, T. et al. (1990) Beta-protein immunoreactivity in brains of patients with neuronal ceroid lipofuscinosis: ultrastructural and biochemical demonstration. Neurosci. Lett. 112(2-3):155-160. 4. Melchor, J.E. and W.E. van Nostrand (2000) Fibrillar amyloid ?-protein mediates the pathologic accumulation of its secreted precursor in human cerebrovascular smooth muscle cells. J. Biol. Chem. 275(13):9782-9791 (cites the use of this antibody in Western blotting performed under non-reducing conditions). 5. Koldamova, R.P. et al. (2001) Apolipoprotein A-I directly interacts with amyloid precursor protein and inhibits A beta aggregation and toxicity. Biochemistry 40(12):3553-3560 (cites the use of this antibody in Western blotting performed under reducing conditions [mercaptoethanol]). 6. Kusiak, J.W. et al. (2001) Expression of mutant amyloid precursor proteins decreases adhesion and delays differentiation of Hep-1 cells. Brain Res. 896:146-152 (cites the use of this antibody in immunoprecipitation in a system for the detection of sAPP?). 7. Chishti, M.A. et al. (2001) Early-onset amyloid deposition and cognitive deficits in transgenic mice expressing a double mutant form of amyloid precursor protein 695. J. Biol. Chem. 276(24):21562-21570 (cites the use of this antibody in immunohistochemistry). 8. Lefterov, I.M. et al. (2000) Human bleomycin hydrolase regulates the secretion of amyloid precursor protein. FASEB J. 14:1837-1847.