Amyloid Beta-peptide (25-35) (human)
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
Figure2. Formula of Amyloid β-Peptide (25-35) (human)
C45H81N13O14S
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
| Physical Appearance | A solid |
| Storage | Desiccate at -20°C |
| M.Wt | 1060.27 |
| Cas No. | 131602-53-4 |
| Formula | C45H81N13O14S |
| Synonyms | Gly-Ser-Asn-Lys-Gly-Ala-Ile-Ile-Gly-Leu-Met |
| Solubility | insoluble in EtOH; insoluble in H2O; ≥106 mg/mL in DMSO |
| Chemical Name | Amyloid Beta-peptide (25-35) (human) |
| SDF | Download SDF |
| 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 |
| Shipping Condition | Small Molecules with Blue Ice, Modified Nucleotides with Dry Ice. |
| General tips | We do not recommend long-term storage for the solution, please use it up soon. |
| Cell experiment: [1] | |
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Cell lines |
Embryonic rat hippocampal cells |
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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. |
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Reaction Conditions |
20 μM, 6 hours |
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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] | |
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Animal models |
Male Charles River Wistar rats |
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Dosage form |
Intraperitoneal injection, 400 mg/kg |
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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%). |
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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. |
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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. |
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