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Amyloid β-Peptide (1-40) (human)

Catalog #: 1191
1 Citation Datasheet / COA / SDS
Catalog # Availability Size / Price Qty
1191/1
Amyloid β-Peptide (1-40) (human)
1 Image
Description: Amyloid β-protein fragment

Purity: ≥95%

Product Details
Citations (1)
Reviews
Biological Activity Technical Data Background Product Datasheets Calculators

Biological Activity

Amyloid β-Peptide (1-40) (human) is a peptide found in plaques in the brains of patients with Alzheimer's disease. Shown to have both neurotrophic and neurotoxic effects.

Technical Data

M.Wt:
4329.86
Formula:
C194H295N53O58S
Sequence:
DAEFRHDSGYEVHHQKLVFFAEDVGSNKGAIIGLMVGGVV
Solubility:
Soluble to 1 mg/ml in water
Purity:
≥95%
Storage:
Store at -20°C
CAS No:
131438-79-4

The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis.
Tocris products are intended for laboratory research use only, unless stated otherwise.

Background References

  1. A? accumulation causes MVB enlargement and is modelled by dominant negative VPS4A
    K Willén, JR Edgar, T Hasegawa, N Tanaka, CE Futter, GK Gouras
    Mol Neurodegener, 2017;12(1):61.
  2. Beta-amyloid(1-40) effects on behavior and memory.
    Cleary et al.
    Brain Res., 1995;682:69
  3. Beta-amyloid(1-40)-induced neurodegeneration in the rat hippocampal neurons of the CA1 subfield.
    Miguel-Hidalgo and Cacabelos
    Acta Neuropathol., 1998;95:455
  4. β-Amyloid protein induces platelet aggregation and supports platelet adhesion.
    Kowalska and Badellino
    Biochem.Biophys.Res.Commun., 1994;205:1829
  5. Neurotrophic and neurotoxic effects of amyloid β protein: reversal by tachykinin neuropeptides.
    Yankner et al.
    Science, 1990;250:279

Product Datasheets

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Citation for Amyloid β-Peptide (1-40) (human)

The citations listed below are publications that use Tocris products. Selected citations for Amyloid β-Peptide (1-40) (human) include:

1 Citation: Showing 1 - 1

  1. Stimulation of endothelin B receptors by IRL-1620 decreases the progression of Alzheimer's disease.
    Authors: Briyal Et al.
    Neuroscience  2015;301:1

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