β-Amyloid (1-42), human, Ala(13C3,15N) TFA
Based on 1 Customer Validation
β-Amyloid (1-42), human, Ala(13C3,15N) TFA is the 13C and 15N-labeled β-Amyloid (1-42), human (HY-P1363A). β-Amyloid (1-42) (Amyloid β-peptide (1-42)), human, 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 remaining as a monomer exhibits antioxidant and neuroprotective effects. β-Amyloid (1-42), human, 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.
For research use only. We do not sell to patients.
- Purity : 99.57%
- Formula: C20013C3H311N5415NO60S
- Molecular Weight:4518.01
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Storage:
Sealed storage, away from moisture.
Powder -80°C, 2 years , -20°C, 1 year* In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
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Biological Activity
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Chemical Information
- Purity & Documentation
- References
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Help & FAQs
Biological Activity
Description
In Vitro
Stable heavy isotopes of hydrogen, carbon, and other elements have been incorporated into drug molecules, largely as tracers for quantitation during the drug development process. Deuteration has gained attention because of its potential to affect the pharmacokinetic and metabolic profiles of drugs.
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
Application
1. This compound can be used as a tracer
2. This compound can be used as an internal standard for quantitative analysis by NMR, GC-MS, or LC-MS.
Chemical Information
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Appearance Solid
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Molecular Weight 4518.01
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Formula C20013C3H311N5415NO60S
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Color white
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Sequence
Asp-{Ala(13C3,15N)}-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-Ile-Ala
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Sequence Shortening
D-{Ala(13C3,15N)}-EFRHDSGYEVHHQKLVFFAEDVGSNKGAIIGLMVGGVVIA
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Sealed storage, away from moisture
Powder -80°C 2 years -20°C 1 year * In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)
Purity & Documentation
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Data Sheet (267 KB)
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SDS (252 KB)
- English - EN (252 KB)
- Français - FR (252 KB)
- Deutsch - DE (252 KB)
- Norwegian - NO (252 KB)
- Español - ES (252 KB)
- Swedish - SV (252 KB)
- Italian - IT (252 KB)
- Korean - KR (252 KB)
- Portuguese - PT (252 KB)
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Handling Instructions (2659 KB)
References
[1]. Porzoor A, et al. Pretreatment of chemically-synthesized Aβ42 affects its biological activity in yeast. Prion. 2014;8(6):404-10. [Content Brief]
[2]. 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. [Content Brief]
[3]. 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. [Content Brief]
[4]. Yao ZX, et al. Function of beta-amyloid in cholesterol transport: a lead to neurotoxicity. FASEB J. 2002 Oct;16(12):1677-9. [Content Brief]
[5]. 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. [Content Brief]
[6]. 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. [Content Brief]
[7]. 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. [Content Brief]
[8]. 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. [Content Brief]
[9]. Fei X, et al. Degradation of FA reduces Aβ neurotoxicity and Alzheimer-related phenotypes. Mol Psychiatry. 2021 Oct;26(10):5578-5591. [Content Brief]
[10]. 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. [Content Brief]
[11]. 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. [Content Brief]
[12]. 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. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
β-Amyloid (1-42), human, Ala(13C3,15N) TFA Related Classifications
HY-P1363S1 Related Classifications
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