Amyloid beta-peptide (25-35)

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Amyloid beta-peptide (25-35)
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Amyloid beta-peptide(25-35), the fragment Aβ(25-35) of the Alzheimer's amyloid β-peptide, is functionally required for the neurotrophic and neurotoxic effects associated with Alzheimer's disease.

Peptide Inhibitors
Catalog number
CAS number
Molecular Formula
Molecular Weight
Amyloid beta-peptide (25-35)
Size Price Stock Quantity
10 mg $299 In stock
(2S)-2-[[(2S)-2-[[2-[[(2S,3S)-2-[[(2S,3S)-2-[[(2S)-2-[[2-[[(2S)-6-amino-2-[[(2S)-4-amino-2-[[(2S)-2-[(2-aminoacetyl)amino]-3-hydroxypropanoyl]amino]-4-oxobutanoyl]amino]hexanoyl]amino]acetyl]amino]propanoyl]amino]-3-methylpentanoyl]amino]-3-methylpentanoyl]amino]acetyl]amino]-4-methylpentanoyl]amino]-4-methylsulfanylbutanoic acid
H-Gly-Ser-Asn-Lys-Gly-Ala-Ile-Ile-Gly-Leu-Met-OH; glycyl-L-seryl-L-asparagyl-L-lysyl-glycyl-L-alanyl-L-isoleucyl-L-isoleucyl-glycyl-L-leucyl-L-methionine; Amyloid β-Protein (25-35); Amyloid-Protein (25-35)
1.249 g/cm3
Boiling Point
1517.336°C at 760 mmHg
Store at -20°C
Soluble in DMSO, Water
InChI Key
Canonical SMILES
1.Alzheimer's amyloid-beta peptide inhibits sodium/calcium exchange measured in rat and human brain plasma membrane vesicles.
Wu A;Derrico CA;Hatem L;Colvin RA Neuroscience. 1997 Oct;80(3):675-84.
Na+/Ca2+ exchange activity was measured by monitoring vesicular Ca2+ content after incubation in buffers containing 45Ca2+. When Na+-loaded vesicles were placed into Na+-free buffer, vesicular Ca2+ content increased rapidly and reached a plateau after two to three minutes. Only preaggregated amyloid-beta1-40 (Abeta1-40) and Abeta25-35 reduced vesicular Ca2+ content. Both peptides produced a maximal reduction in Ca2+ content of approximately 50%. The peptides reduced Ca2+ content with similar potency and half maximal effects were seen at less than 10 microM for Abeta25-35. Calcium-loaded vesicles mediate a rapid Ca2+/Ca2+ exchange, which also was inhibited by aggregated Abeta25-35. Aggregated Abeta25-35 did not affect the passive Ca2+ permeability of the vesicles. Aggregated Abeta25-35 reduced Ca2+ content in plasma membrane vesicles isolated from normal and Alzheimer's disease frontal cortex with less potency but the same efficacy as seen in rat brain. Aggregated Abeta25-35 did not produce nonspecific effects on vesicle morphology such as clumping or loss of intact vesicles. When placed in the buffer used to measure Ca2+ content, Congo Red at molar ratios of less than one blocked the inhibitory effect of preaggregated Abeta25-35.
2.Neuroprotection by hypothalamic peptide proline-rich peptide-1 in Abeta25-35 model of Alzheimer's disease.
Galoyan AA;Sarkissian JS;Chavushyan VA;Meliksetyan IB;Avagyan ZE;Poghosyan MV;Vahradyan HG;Mkrtchian HH;Abrahamyan DO Alzheimers Dement. 2008 Sep;4(5):332-44. doi: 10.1016/j.jalz.2007.10.019.
BACKGROUND: ;This work sought to determine the effects of hypothalamic proline-rich peptide (PRP)-1 in a rat model of Alzheimer's disease.;METHODS: ;Complex histochemical, electrophysiologic, and behavioral analyses were performed on intact or diseased Wistar rats (n = 28). Pathologic conditions were induced by bilateral intracerebroventricular injection of amyloid peptide Abeta25-35. The diseased rats received systemic administration of PRP-1 or placebo control.;RESULTS: ;Abeta25-35 caused cellular neurodegeneration with marked glial reaction in the hippocampal complex and almost full destruction of the dentate fascia, which was not observed in conditions of PRP-1 administration after Abeta25-35 injection. Hippocampal neurons of intact animals responded to high-frequency (tetanic) stimulation of entorhinal cortex of ipsilateral cerebral hemisphere by tetanic and posttetanic potentiation of a different intensity and duration, which was accompanied by posttetanic depression. Abeta25-35 led to significant changes in the level and pattern of hippocampal neuronal activity, indicating the absence of both tetanic and posttetanic activity. Poststimulus activity manifestations rarely occurred and rapidly decreased after repeated trials.
3.Protective effect of Polygonum multiflorum Thunb on amyloid beta-peptide 25-35 induced cognitive deficits in mice.
Um MY;Choi WH;Aan JY;Kim SR;Ha TY J Ethnopharmacol. 2006 Mar 8;104(1-2):144-8. Epub 2005 Oct 10.
Amyloid beta protein (Abeta) may be neurotoxic during the progression of Alzheimer's disease by eliciting oxidative stress. This study was designed to determine the effect of Polygonum multiflorum Thunb water extract (PWE) on Abeta25-35-induced cognitive deficits and oxidative stress in mice. Mice were fed experimental diets comprising either 0.5 or 1% PWE for 4 weeks, and then received a single intracerebroventricular (i.c.v.) injection of Abeta25-35 (10 microg/mouse). Behavioral changes in the mice were evaluated using passive avoidance and water-maze tests. The consumption of PWE significantly ameliorated the cognitive deficits caused by i.c.v. injection of Abeta25-35. The Abeta25-35 treatment accelerated the lipid peroxidation, and PWE attenuated the Abeta-induced increase in brain levels of thiobarbituric acid reactive substances. There was an increase in glutathione peroxidase activity in PWE-treated groups. The acetylcholinesterase activity in the brain and serum was lower in PWE supplemented groups than in the only Abeta-injected group. These findings suggest that PWE exerts a preventive effect against cognitive deficits induced by Abeta25-35 accumulation in Alzheimer's disease, and that this effect is mediated by the antioxidant properties of PWE.

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