Amyloid β-peptide (42-1) (human)

Pricing Availability Delivery Time Qty
Cat.No. 3391 - Amyloid b-peptide (42-1) (human) | Ala-Ile-Val-Val-Gly-Gly-Val-Met-Leu-Gly-Ile-Ile-Ala-Gly-Lys-Asn-Ser-Gly-Val-Asp-Glu-Ala-Phe-Phe-Val-Leu-Lys-Gln-His-His-Val-Glu-Tyr-Gly-Ser-Asp-His-Arg-Phe-Glu-Ala-Asp | CAS No. 317366-82-8
Description: Inactive control peptide for amyloid β-peptide (1-42) (Cat. No. 1428)
Datasheet
Citations (1)
Reviews
Literature

Biological Activity

Inactive control peptide for amyloid β-peptide (1-42), the predominant form of amyloid β-peptide found in the brains of patients with Alzheimer's disease.

Active Analog also available.

Technical Data

M. Wt 4514.08
Formula C203H311N55O60S
Sequence AIVVGGVMLGIIAGKNSGVDEAFFVLKQHHVEYGSDHRFEAD
Storage Store at -20°C
CAS Number 317366-82-8
PubChem ID 16132430
InChI Key PLOPBXQQPZYQFA-AXPWDRQUSA-N
Smiles [H]N[C@@H](C)C(=O)N[C@@H]([C@@H](C)CC)C(=O)N[C@@H](C(C)C)C(=O)N[C@@H](C(C)C)C(=O)NCC(=O)NCC(=O)N[C@@H](C(C)C)C(=O)N[C@@H](CCSC)C(=O)N[C@@H](CC(C)C)C(=O)NCC(=O)N[C@@H]([C@@H](C)CC)C(=O)N[C@@H]([C@@H](C)CC)C(=O)N[C@@H](C)C(=O)NCC(=O)N[C@@H](CCCCN)C(=O)N[C@@H](CC(N)=O)C(=O)N[C@@H](CO)C(=O)NCC(=O)N[C@@H](C(C)C)C(=O)N[C@@H](CC(O)=O)C(=O)N[C@@H](CCC(O)=O)C(=O)N[C@@H](C)C(=O)N[C@@H](CC1=CC=CC=C1)C(=O)N[C@@H](CC1=CC=CC=C1)C(=O)N[C@@H](C(C)C)C(=O)N[C@@H](CC(C)C)C(=O)N[C@@H](CCCCN)C(=O)N[C@@H](CCC(N)=O)C(=O)N[C@@H](CC1=CNC=N1)C(=O)N[C@@H](CC1=CNC=N1)C(=O)N[C@@H](C(C)C)C(=O)N[C@@H](CCC(O)=O)C(=O)N[C@@H](CC1=CC=C(O)C=C1)C(=O)NCC(=O)N[C@@H](CO)C(=O)N[C@@H](CC(O)=O)C(=O)N[C@@H](CC1=CNC=N1)C(=O)N[C@@H](CCCNC(N)=N)C(=O)N[C@@H](CC1=CC=CC=C1)C(=O)N[C@@H](CCC(O)=O)C(=O)N[C@@H](C)C(=O)N[C@@H](CC(O)=O)C(O)=O

The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis.

All Tocris products are intended for laboratory research use only.

Solubility Data

SolubilitySoluble to 0.50 mg/ml in water

Preparing Stock Solutions

The following data is based on the product molecular weight 4514.08. Batch specific molecular weights may vary from batch to batch due to solvent of hydration, which will affect the solvent volumes required to prepare stock solutions.

Concentration / Solvent Volume / Mass 1 mg 5 mg 10 mg
1 mM 0.22 mL 1.11 mL 2.22 mL
5 mM 0.04 mL 0.22 mL 0.44 mL
10 mM 0.02 mL 0.11 mL 0.22 mL
50 mM 0 mL 0.02 mL 0.04 mL

Molarity Calculator

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*When preparing stock solutions always use the batch-specific molecular weight of the product found on the vial label and SDS / CoA (available online).

Reconstitution Calculator

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Dilution Calculator

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Product Datasheets

Certificate of Analysis / Product Datasheet
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Safety Datasheet

References

References are publications that support the products' biological activity.

Walsh et al (2002) Amyloid-beta peotide is toxic to neurons in vivo via indirect mechanisms. Neurobiol.Dis. 10 20 PMID: 12079400

Xiong et al (2007) Mitochondrial respiratory inhibition and oxidative stress elevate β-secretase (BACE1) proteins and activity in vivo in the rat retina. Exp.Brain Res. 181 435 PMID: 17429617

Boyd-Kimball et al (2005) Proteomic identification of proteins oxidized by Aβ(1-42) in synaptosomes: Implications for Alzheimer's disease. Brain Res. 1004 206 PMID: 15885219


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1 Citation for Amyloid β-peptide (42-1) (human)

Citations are publications that use Tocris products. Selected citations for Amyloid β-peptide (42-1) (human) include:

Esposito et al (2011) Cannabidiol reduces Aβ-induced neuroinflammation and promotes hippocampal neurogenesis through PPARγ involvement. PLoS One 6 e28668 PMID: 22163051


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Literature in this Area

Tocris offers the following scientific literature in this area to showcase our products. We invite you to request* or download your copy today!

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Neurodegeneration

Neurodegeneration Product Guide

A collection of over 275 products for neurodegeneration research, the guide includes research tools for the study of:

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Alzheimer's

Alzheimer's Poster

Alzheimer's disease (AD) is a degenerative brain disease and the most common cause of dementia, affecting approximately 47 million people worldwide. Updated in 2015, this poster summarizes the structural and functional changes observed in the progression of this neurodegenerative disease, as well as classic AD drug targets.