Amyloid Beta-Peptide (1-40) (human)
Amyloid beta-Peptide (1-40) (human) (CAS 131438-79-4) is a polypeptide with the sequence H2N-DAEFRHDSGYEVHHQKLVFFAE-DVGSNKGAIIGLMVGGVVIA-OH and a molecular weight of 4329.8. Amyloid beta-protein (Aβ or Abeta) is a 36-43-amino-acid polypeptide produced by sequential beta- and gamma-secretase processing of the amyloid precursor protein and is the major component of Alzheimer's disease-associated amyloid plaques; in the brains of sporadic Alzheimer's disease patients, elevated Aβ levels cause cerebrovascular pathology and neurotoxicity [2]. Gamma-secretase cleaves within the transmembrane domain of APP to generate the C-terminus of the Abeta peptide, producing multiple isoforms 36-43 amino acids in length, of which Abeta40 and Aβ42 are the most common; longer Aβ forms are generated by cleavage in the endoplasmic reticulum and shorter Aβ forms in the trans-Golgi network [3]. Abeta is also a multifunctional peptide with non-pathological activities [1].
Amyloid beta-Peptide (1-40) is commonly used to establish Alzheimer's disease (AD) animal models, and intracerebral injection induces amyloid deposition and learning and memory dysfunction.
References
1. Lahiri DK, Maloney B (September 2010). "Beyond the signaling effect role of amyloid–β42 on the processing of AβPP, and its clinical implications". Exp. Neurol. 225 (1): 51–4.
2. Hardy J, Duff K, Hardy KG, Perez-Tur J, Hutton M (September 1998). "Genetic dissection of Alzheimer's disease and related dementias: amyloid and its relationship to tau". Nat. Neurosci. 1 (5): 355–8.
3. Hartmann T, Bieger SC, Brühl B, Tienari PJ, Ida N, Allsop D, Roberts GW, Masters CL, Dotti CG, Unsicker K, Beyreuther K (September 1997). "Distinct sites of intracellular production for Alzheimer's disease A beta40/42 amyloid peptides". Nat. Med. 3 (9): 1016–20.
- 1. Hyo Jun Kwon, Devi Santhosh, et al. "A novel monomeric amyloid β-activated signaling pathway regulates brain development via inhibition of microglia." Elife. 2024 Dec 5:13:RP100446. PMID: 39635981
- 2. Nathalia Simea Münch, Subir Das, et al. "Unveiling the effect of CaCl 2 on amyloid β aggregation via supercritical angle Raman and fluorescence spectroscopy and microscopy." Phys Chem Chem Phys. 2024 Oct 23;26(41):26266-26276. PMID: 39371012
- 3. Si-Hai Wu, Junjie Ma, et al. "Ratiometric Imaging Detection of Amyloid-β Fibrils by a Dual-Emissive Tris-Heteroleptic Ruthenium Complex." Inorg Chem. 2024 Sep 30;63(39):17983-17992. PMID: 39287976
- 4. Hyo Jun Kwon, Devi Santhosh, et al. "Monomeric amyloid-β inhibits microglial inflammatory activity in the brain via an APP/heterotrimeric G protein-mediated pathway." bioRxiv. July 26, 2023
- 5. Sijia Hao, Yayu Yang, et al. "Glycosides and Their Corresponding Small Molecules Inhibit Aggregation and Alleviate Cytotoxicity of Aβ40." ACS Chem Neurosci. 2022 Mar 16;13(6):766-775. PMID: 35230090
- 6. Sijia Hao, Xia Li, et al. "Hydroxycinnamic Acid from Corncob and Its Structural Analogues Inhibit Aβ40 Fibrillation and Attenuate Aβ40-Induced Cytotoxicit." J. Agric. Food Chem. 2020,July 23, 2020 PMID: 32700906
- 7. Hao S, Li X, et al. "CLVFFA-functionalized gold nanoclusters inhibit Aβ40 fibrillation, fibrils prolongation and disaggregate mature fibrils." ACS Chem Neurosci. 2019 Oct 22 PMID: 31637909
- 8. Hald ES, Timm CD, et al. "Amyloid Beta Influences Vascular Smooth Muscle Contractility and Mechanoadaptation." J Biomech Eng. 2016 Nov 1;138(11) PMID: 27590124
| Physical Appearance | A solid |
| Storage | Desiccate at -20°C |
| M.Wt | 4329.86 |
| Cas No. | 131438-79-4 |
| Formula | C194H295N53O58S |
| Synonyms | Asp-Ala-Glu-Phe-Arg-His-Asp-Ser-Gly-Tyr-Glu-Val-His-His-Gln-Lys-Leu-Val-Phe-Phe-Ala-Glu-Asp-Val-Gly-Ser-Asn-Lys-Gly-Ala-Ile-Ile-Gly-Leu-Met-Val-Gly-Gly-Val-Val; β-Amyloid (1-40) |
| Solubility | insoluble in EtOH; ≥23.8 mg/mL in H2O; ≥43.28 mg/mL in DMSO |
| 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 |
CA1 pyramidal cells |
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Preparation method |
The solubility of this peptide in sterile water is >10 mM. Stock solution should be splited and stored at -80°C for several months. |
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Reaction Conditions |
200 nM, 20 min |
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Applications |
Aβ (1-40) reversibly increased IBa evoked at +20 mV. This increase was observed for 6 of 11 cells and reached 1.74 ± 0.06. The activation curve showed that Aβ (1-40) caused an apparent voltage-dependent increase in IBa, with an enhancement of IBa at the test potentials between 0 and +30 mV. |
| 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 (-30%) was detected one week after the injection of Aβ (1-40). 30 days after the Aβ (1-40) peptide injection, the decrease in Ach release was still statistically significant (-38%). K+-stimulated ACh release was similarly affected by the treatment. Aβ (1-40) treatment induced a significant decrease in the stimulated release on day 14 after lesioning (-43%). |
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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] Rovira C, Arbez N, Mariani J. Aβ (25-35) and Aβ (1-40) act on different calcium channels in CA1 hippocampal neurons. Biochemical and biophysical research communications, 2002, 296 (5): 1317-1321. [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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| Description | Aβ40 is a peptide processed from the amyloid precursor protein (APP). | |||||
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Quality Control & MSDS
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Chemical structure

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