107761-42-2
Chemical Structure
β-Amyloid (1-42), human
Synonym(s): Amyloid β-peptide (1-42) (human)
- CAS No.: 107761-42-2
- Formula:C203H311N55O60S
- Molecular Weight:4514.04
SMILES: O=C(N[C@@H](C)C(N[C@@H](CCC(O)=O)C(N[C@@H](CC1=CC=CC=C1)C(N[C@@H](CCCNC(N)=N)C(N[C@@H](CC2=CNC=N2)C(N[C@@H](CC(O)=O)C(N[C@@H](CO)C(NCC(N[C@@H](CC3=CC=C(C=C3)O)C(N[C@@H](CCC(O)=O)C(N[C@@H](C(C)C)C(N[C@@H](CC4=CNC=N4)C(N[C@@H](CC5=CNC=N5)C(N[C@@H](CCC(N)=O)C(N[C@@H](CCCCN)C(N[C@@H](CC(C)C)C(N[C@@H](C(C)C)C(N[C@@H](CC6=CC=CC=C6)C(N[C@@H](CC7=CC=CC=C7)C(N[C@@H](C)C(N[C@@H](CCC(O)=O)C(N[C@@H](CC(O)=O)C(N[C@@H](C(C)C)C(NCC(N[C@@H](CO)C(N[C@@H](CC(N)=O)C(N[C@@H](CCCCN)C(NCC(N[C@@H](C)C(N[C@@H]([C@@H](C)CC)C(N[C@@H]([C@@H](C)CC)C(NCC(N[C@@H](CC(C)C)C(N[C@@H](CCSC)C(N[C@@H](C(C)C)C(NCC(NCC(N[C@@H](C(C)C)C(N[C@@H](C(C)C)C(N[C@@H]([C@@H](C)CC)C(N[C@@H](C)C(O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)[C@H](CC(O)=O)N
Biological Activity: 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[1][1][2][3][4][5][6][7].
| Cat. No. | Product Name | Purity | Description | Pricing | |||||||||||||||||||
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β-Amyloid (1-42), human | 99.69% | 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. | ||||||||||||||||||||
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β-Amyloid (1-42), human, HFIP-treated | 98.41% | β-Amyloid (1-42), human, HFIP-treated, a 42-amino acid peptide that has been treated with HFIP from β-Amyloid (1-42), human (HY-P1363A), 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, HFIP-treated remaining as a monomer exhibits antioxidant and neuroprotective effects. β-Amyloid (1-42), human, HFIP-treated, after being 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. | ||||||||||||||||||||
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β-Amyloid-15N (1-42), human TFA | β-Amyloid-15N (1-42), human (TFA) is the 15N-labledβ-Amyloid (1-42) (TFA). β-Amyloid (1-42), human TFA (Amyloid β-Peptide (1-42) (human) TFA) is a 42-amino acid peptide which plays a key role in the pathogenesis of Alzheimer disease. | |||||||||||||||||||||
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[U-13C,15N]-Aβ(1-42) | [U-13C,15N]-Aβ(1-42) is the 13C- and 15N-labeled Aβ(1-42). Abnormal levels and aggregation of beta-amyloid (Aβ) in the brain are considered key factors in the pathogenesis of Alzheimer's disease (AD). This isotope can be used in NMR studies of disease mechanisms and in mass spectrometry analysis. | |||||||||||||||||||||
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[U-15N]-Aβ(1-42) | [U-15N]-Aβ(1-42) is the 15N-labeled Aβ(1-42). Abnormal levels and aggregation of beta-amyloid (Aβ) in the brain are considered key factors in the pathogenesis of Alzheimer's disease (AD). This isotope can be used in NMR studies of disease mechanisms and in mass spectrometry analysis. | |||||||||||||||||||||
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- [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. [Content Brief]
- [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. [Content Brief]
- [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. [Content Brief]
- [4]. Porzoor A, et al. Pretreatment of chemically-synthesized Aβ42 affects its biological activity in yeast. Prion. 2014;8(6):404-10. [Content Brief]
- [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. [Content Brief]
- [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. [Content Brief]
- [7]. 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]