β-Amyloid (1-42), human (TFA)

β-Amyloid (1-42) (Amyloid β-peptide (1-42), human TFA, a 42-amino acid peptide that has not been treated with HFIP, is a brain-penetrant amyloid protein fragment, which can be used in research on Alzheimer's disease and Down’s syndrome. β-Amyloid (1-42), human TFA remaining as a monomer exhibits antioxidant and neuroprotective effects. β-Amyloid (1-42), human TFA, after being monomericized by HFIP and dissolved in DMSO to form the stock solution, on the one hand, can form soluble oligomers (AβOs) when incubated at 4 °C, which have synaptic toxicity and neurotoxicity; on the other hand, it can be incubated at 37 °C to form insoluble fibrils, with lower neurotoxicity, and participating in the oxidative damage process. Aβ42 oligomers bind to various neuronal surface receptors (such as PrPc, mGluR5, NMDA receptors, etc.), triggering oxidative stress, calcium homeostasis imbalance, and synaptic toxicity via activating downstream signaling pathways, leading to neuronal dysfunction and death[1][2][3][4][5][6][7].

Product Specifications

Product Name Alternative

Amyloid β-peptide (1-42) (human) TFA

UNSPSC

12352209

Target

Amyloid-β

Type

Peptides

Related Pathways

Neuronal Signaling

Applications

Neuroscience-Neurodegeneration

Field of Research

Neurological Disease

Assay Protocol

https://www.medchemexpress.com/Amyloid__beta_-Peptide__1-42__human.html

Purity

99.66

Solubility

DMSO : 33.33 mg/mL (ultrasonic) |H2O : 25 mg/mL (ultrasonic)

Smiles

O=C([C@@H](N)CC(O)=O)N[C@H](C(N[C@H](C(N[C@H](C(N[C@H](C(N[C@H](C(N[C@H](C(N[C@H](C(NCC(N[C@H](C(N[C@H](C(N[C@H](C(N[C@H](C(N[C@H](C(N[C@H](C(N[C@H](C(N[C@H](C(N[C@H](C(N[C@H](C(N[C@H](C(N[C@H](C(N[C@H](C(N[C@H](C(N[C@H](C(NCC(N[C@H](C(N[C@H](C(N[C@H](C(NCC(N[C@H](C(N[C@H](C(N[C@H](C(NCC(N[C@H](C(N[C@H](C(N[C@H](C(NCC(NCC(N[C@H](C(N[C@H](C(N[C@H](C(N[C@H](C(O)=O)C)=O)[C@H](CC)C)=O)C(C)C)=O)C(C)C)=O)=O)=O)C(C)C)=O)CCSC)=O)CC(C)C)=O)=O)[C@H](CC)C)=O)[C@H](CC)C)=O)C)=O)=O)CCCCN)=O)CC(N)=O)=O)CO)=O)=O)C(C)C)=O)CC(O)=O)=O)CCC(O)=O)=O)C)=O)CC1=CC=CC=C1)=O)CC2=CC=CC=C2)=O)C(C)C)=O)CC(C)C)=O)CCCCN)=O)CCC(N)=O)=O)CC3=CNC=N3)=O)CC4=CNC=N4)=O)C(C)C)=O)CCC(O)=O)=O)CC5=CC=C(O)C=C5)=O)=O)CO)=O)CC(O)=O)=O)CC6=CNC=N6)=O)CCCNC(N)=N)=O)CC7=CC=CC=C7)=O)CCC(O)=O)=O)C.O=C(O)C(F)(F)F

Molecular Formula

C205H312F3N55O62S

Molecular Weight

4628.06

References & Citations

[1]Solntseva EI, et al. Impact of amyloid-β peptide (1-42) on voltage-gated ion currents in molluscan neurons. Bull Exp Biol Med. 2011 Oct;151 (6) :671-4.|[2]Barucker C, et al. Nuclear translocation uncovers the amyloid peptide Aβ42 as a regulator of gene transcription. J Biol Chem. 2014 Jul 18;289 (29) :20182-91.|[3]Stefania Sabella, et al. Capillary electrophoresis studies on the aggregation process of beta-amyloid 1-42 and 1-40 peptides. Electrophoresis. 2004 Oct;25 (18-19) :3186-94.|[4]Porzoor A, et al. Pretreatment of chemically-synthesized Aβ42 affects its biological activity in yeast. Prion. 2014;8 (6) :404-10. |[5]Zou K, et al. A novel function of monomeric amyloid beta-protein serving as an antioxidant molecule against metal-induced oxidative damage. J Neurosci. 2002 Jun 15;22 (12) :4833-41.|[6]Peters C, et al. Alzheimer's Aβ interacts with cellular prion protein inducing neuronal membrane damage and synaptotoxicity. Neurobiol Aging. 2015 Mar;36 (3) :1369-77.|[7]Yao ZX, et al. Function of beta-amyloid in cholesterol transport: a lead to neurotoxicity. FASEB J. 2002 Oct;16 (12) :1677-9.|[8]Jancsó G, et al. Beta-amyloid (1-42) peptide impairs blood-brain barrier function after intracarotid infusion in rats. Neurosci Lett. 1998 Sep 4;253 (2) :139-41.|[9]Bourgade K, et al. β-Amyloid peptides display protective activity against the human Alzheimer's disease-associated herpes simplex virus-1. Biogerontology. 2015 Feb;16 (1) :85-98.|[10]Fu L, et al. Comparison of neurotoxicity of different aggregated forms of Aβ40, Aβ42 and Aβ43 in cell cultures. J Pept Sci. 2017 Mar;23 (3) :245-251.|[11]Wang H, et al. Amyloid-beta1-42 induces reactive oxygen species-mediated autophagic cell death in U87 and SH-SY5Y cells. J Alzheimers Dis. 2010;21 (2) :597-610.|[12]Fei X, et al. Degradation of FA reduces Aβ neurotoxicity and Alzheimer-related phenotypes. Mol Psychiatry. 2021 Oct;26 (10) :5578-5591.

Shipping Conditions

Blue Ice

Storage Conditions

-80°C, 2 years; -20°C, 1 year (Powder, sealed storage, away from moisture)

Scientific Category

Peptides

Clinical Information

No Development Reported

Citation 01

Aging. 2021 Jun 9;13 (11) :15569-15579.|Am J Physiol Cell Physiol. 2024 Jun 1;326 (6) :C1697-C1709.|Biomed Pharmacother. 2024 Jul 24:178:117199.|Brain Res. 2024 Aug 19:149173.|Cell Mol Biol (Noisy-le-grand) . 2024 Jan 31;70 (1) :200-206.|Cell Rep. 2025 Feb 23;44 (3) :115343.|Eur J Med Chem. 2022 Dec 15:244:114841.|Front Aging Neurosci. 2022 Apr 25;14:890134.|Int Immunopharmacol. 2025 Apr 28:157:114746.|Int J Nanomedicine. 2024 May 29:19:4977-4994.|Mol Med Rep. 2021 Apr;23 (4) :280.|University of Nottingham. 2023 Apr 13.|Yonsei Med J. 2019 Jul;60 (7) :640-650. |FASEB J. 2024 Sep;38 (17) :e23861.|J Neuroinflammation. 2024 Dec 23;21 (1) :327.|Mol Divers. 2025 Jul 13.