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Amyloid Beta-peptide (25-35) (human) Functional domain of Aβ

Catalog No.A1039
Size Price Stock Qty
1mg
$56.00
In stock
5mg
$168.00
In stock
10mg
$280.00
In stock
25mg
$392.00
In stock

Tel: +1-832-696-8203

Email: [email protected]

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Sample solution is provided at 25 µL, 10mM.

Product Citations

1. Guo CC, Jiao CH, et al. "Silencing of LncRNA BDNF-AS attenuates Aβ(25-35)-induced neurotoxicity in PC12 cells by suppressing cell apoptosis and oxidative stress." Neurol Res. 2018 Jun 14:1-10. PMID:29902125

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Quality Control & MSDS

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Chemical structure

Amyloid Beta-peptide (25-35) (human)

Related Biological Data

Amyloid Beta-peptide (25-35) (human)
Aβ (25-35) treatment inhibited the cell survival rate in a dose-dependent manner.
Method:MTT assay; Cell Lines:SH-SY5Y cells; Concentrations:5-40 μM; Incubation Time:24 h.

Related Biological Data

CORM-3

Protocol

Cell experiment: [1]

Cell lines

Embryonic rat hippocampal cells

Preparation method

The solubility of this peptide in sterile water is >0.5mg/ml. Stock solution should be splited and stored at -80°C for several months.

Reaction Conditions

20 μM, 6 hours

Applications

To investigate the involvement of the tau phosphorylation kinases in Aβ (25–35)-induced tau phosphorylation, the level of each kinase was determined after Aβ (25–35) (20μM) exposure for various periods. GSK-3α did not show a significant change in response to Aβ (25–35), whereas MAP kinase decreased to ~ 60% of the control after 6h Aβ (25–35) exposure, when tau was phosphorylated maximally. TPK I/GSK-3βrapidly increased in response to Aβ (25–35), reaching a maximum (2.2-fold the control) at 6 h.

Animal experiment: [2]

Animal models

Male Charles River Wistar rats

Dosage form

Intraperitoneal injection, 400 mg/kg

Applications

A statistically significant decrease in basal ACh release (-28%) was detected one week after the injection of Aβ (25–35). The effect persisted for only two week. K+-stimulated ACh release was similarly affected by the treatment. Aβ (25–35) treatment induced a statistically significant decrease in the stimulated release on day 14 after lesioning (-45%).

Other notes

Please test the solubility of all compounds indoor, and the actual solubility may slightly differ with the theoretical value. This is caused by an experimental system error and it is normal.

References:

[1] Takashima A, Honda T, Yasutake K, et al. Activation of tau protein kinase I/glycogen synthase kinase-3 β by amyloid β peptide (25–35) enhances phosphorylation of tau in hippocampal neurons. Neuroscience research, 1998, 31(4): 317-323.

[2] Giovannelli L, Casamenti F, Scali C, et al. Differential effects of amyloid peptides β-(1–40) and β-(25–35) injections into the rat nucleus basalis. Neuroscience, 1995, 66(4): 781-792.

Amyloid Beta-peptide (25-35) (human) Dilution Calculator

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Chemical Properties

Cas No. 131602-53-4 SDF Download SDF
Synonyms Gly-Ser-Asn-Lys-Gly-Ala-Ile-Ile-Gly-Leu-Met
Chemical Name Amyloid Beta-peptide (25-35) (human)
Canonical SMILES CCC(C)C(C(=O)NC(C(C)CC)C(=O)NCC(=O)NC(CC(C)C)C(=O)NC(CCSC)C(=O)O)NC(=O)C(C)NC(=O)CNC(=O)C(CCCCN)NC(=O)C(CC(=O)N)NC(=O)C(CO)NC(=O)CN
Formula C45H81N13O14S M.Wt 1060.27
Solubility >106mg/ml in DMSO or soluble to 0.50 mg/ml in water Storage Desiccate at -20°C
Shipping Condition Evaluation sample solution : ship with blue ice.All other available size: ship with RT , or blue ice upon request
General tips For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.

Background

Met-Leu-Gly-Ile-Ile-Ala-Gly-Lys-Asn-Ser-Gly

Amyloid- β (Aβ) peptide is commonly found in human Alzheimer’s disease (AD) brain and is the main component of Alzheimer amyloid plaques. The predominant forms of Aβ in the human brain are Aβ (1-40) and Aβ (1-42).  However, the Aβ (25-35) fragment, which is physiologically present in elderly people, is the more toxic region and has recently been found to play a relevant role in AD due to its peculiar aggregation properties1.

Aβ (25-35) is regarded to be the functional domain of Aβ, responsible for its neurotoxic properties2-5.  It represents the actual biologically active region of Aβ6. Administration of Aβ (25-35) has been shown to lead to amnesia in mice, causing impairments of spatial working memory along with the degradation of passive avoidance reactions2-5.

In vivo, Aβ (25-35) is present in neurons of subiculum and entorhinal cortex of AD brains7.  It is also observed in Inclusion-Body Myositis (IBM) muscle8.

 

Figure1. Structure of Amyloid β-Peptide

 A1039_1

Figure2. Formula of Amyloid β-Peptide (25-35) (human)

C45H81N13O14S

 A1039_2

Ref:

1. Millucci L, Ghezzi L, Bernardini G, Santucci A (2010) Conformations and biological activities of amyloid beta peptide 25–35. Curr Protein Pept Sc 11: 54–67.

2. Stepanichev, M.Y.; Moiseeva, Y.V.; Lazareva, N.A.; Gulyaeva,N.V. Studies of the effects of fragment (25-35) of beta-amyloid peptide on the behavior of rats in a radial maze. Neurosci. Behav. Physiol., 2005, 35(5), 511-8.

3. Limón, I.D.; Díaz, A.; Mendieta. L.; Chamorro, G.; Espinosa, B.; Zenteno, E.; Guevara, J. Amyloid-beta(25-35) impairs memory and increases NO in the temporal cortex of rats. Neurosci. Res., 2009,63(2), 129-137.

4. Pike, C. J.; Burdick, D.; Walencewicz, A. J.; Glabe, C. G.; Cotman, C. W. Neurodegeneration induced by beta-amyloid peptides in vitro: the role of peptide assembly state. J. Neurosci., 1993, 13, 1676-1687.

5. Stepanichev, M.Yu; Lazareva N.A.; Onufriev, M.V.; Mitrokhina, O.S.; Moiseeva, Yu.V.; Gulyaeva, N.V. Effects of doses of fragment (25-35) of beta-amyloid peptide on behavior in rats. Neurosci. Behav. Physiol., 1998, 28(5), 564-6 .

6. D'Errico, G.; Vitiello, G.; Ortona, O.; Tedeschi, A.; Ramunno, A. and D'Ursi, A.M. Interaction between Alzheimer's A(25-35) peptide and phospholipid bilayers: The role of cholesterol. Biochimica. Biophys. Acta (BBA) – Biomembr., 2008, 1778, 2710-2716.

7. Kaneko, I.; Yamada, N.; Usui, Y.; Oda, T. Possible involvement of β -amyloids racemized at Ser residue in Alzheimer’s disease. Alzheimer’s Disease: Biology, Diagnose and Therapeutics. John Wiley & Sons: Chichester, 1997, pp. 519-528.

8. Kaneko, I.; Kubo, T.; Morimoto, K.; Kumagae, Y.; Miller, C.A. Ananimal model for Alzheimer’s disease using racemic