A1124-10mg | Amyloid Beta-Peptide (1-40) (human) [131438-79-4] Clinisciences

Amyloid β-Peptide (1-40) (human), (C194H295N53O58S1), a peptide with the sequence H2N-DAEFRHDSGYEVHHQKLVFFAEDVGSNKGAIIGLMVGGVVIA-OH, MW= 4329.8. Amyloid beta (Aβ or Abeta) is a peptide of 36-43 amino acids that is processed from the Amyloid precursor protein. While best known as a component of amyloid plaques in association with Alzheimer's disease, evidence has been found that Aβ is a highly multifunctional peptide with significant non-pathological activity⁽¹⁾. Aβ is the main component of deposits found in the brains of patients with Alzheimer's disease. Brain Aβ is elevated in patients with sporadic Alzheimer’s disease. Aβ is the main constituent of brain parenchymal and vascular amyloid, it contributes to cerebrovascular lesions and is neurotoxic⁽²⁾. Aβ protein is generated by successive action of the β and γ secretases. The γ secretase, which produces the C-terminal end of the Aβ peptide, cleaves within the transmembrane region of APP and can generate a number of isoforms of 36-43 amino acid residues in length. The most common isoforms are Aβ₄₀ and Aβ₄₂; the longer form is typically produced by cleavage that occurs in the endoplasmic reticulum, while the shorter form is produced by cleavage in the trans-Golgi network⁽³⁾.

A1124_1

Figure1 structure of Amyloid β-Peptide (1-40) (human)

Ref:

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. "Monomeric amyloid-β inhibits microglial inflammatory activity in the brain via an APP/heterotrimeric G protein-mediated pathway." bioRxiv. July 26, 2023.
2. 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
3. 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
4. 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
5. 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
Solubility	insoluble in EtOH; ≥23.8 mg/mL in H2O; ≥43.28 mg/mL in DMSO
SDF	Download SDF
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]
Cell lines	CA1 pyramidal cells
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.
Reaction Conditions	200 nM, 20 min
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]
Animal models	Male Charles River Wistar rats
Dosage form	Intraperitoneal injection, 400 mg/kg
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%).
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] 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.