Amyloid Beta-peptide (25-35) (human)
Amyloid Beta-peptide (25-35) (human) (CAS: 131602-53-4) represents a neurotoxic fragment derived from the human β-amyloid peptide. This 11-amino acid segment possesses high aggregation propensity, conferring pronounced toxic effects on neuronal cells relative to longer amyloid sequences. Mechanistically, the peptide promotes neurodegeneration, memory impairment, and cognitive dysfunction, as evidenced by animal models displaying impaired spatial learning and memory following intracerebroventricular administration. This peptide segment appears naturally in Alzheimer's disease (AD) patient brains, especially within neurons of the subiculum and entorhinal cortex, as well as in muscle tissues from individuals with inclusion body myositis. As a result, Aβ(25-35) serves as an extensively utilized research tool in Alzheimer's pathology studies.
| 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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