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AMYLOID BETA-PROTEIN (HUMAN, 25-35) TRIFLUOROACETATE

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AMYLOID BETA-PROTEIN (HUMAN, 25-35) TRIFLUOROACETATE Basic information

Product Name:
AMYLOID BETA-PROTEIN (HUMAN, 25-35) TRIFLUOROACETATE
Synonyms:
  • Amyloid beta-peptide(25-35)
  • AMYLOID BETA-PROTEIN (HUMAN, 25-35) TRIFLUOROACETATE
  • H-GLY-SER-ASN-LYS-GLY-ALA-ILE-ILE-GLY-LEU-MET-OH
  • AMYLOID BETA-PEPTIDE (25-35) (HUMAN)
  • AMYLOID BETA-PROTEIN FRAGMENT 25-35
  • AMYLOID BETA-PROTEIN (25-35)
  • AMYLOID-BETA PROTEIN (25-35), HUMAN, MOUSE, RAT
  • Amyloid beta-Protein (25-35) trifluoroacetate salt
CAS:
131602-53-4
MF:
C45H81N13O14S
MW:
1060.27
Product Categories:
  • proteins
  • Alzheimers and Neurodegenerative Disease Research
  • Amyloid beta Protein Fragments
  • Amyloid β Protein FragmentsNeuropeptides
  • Neurodegenerative Disease Peptides
  • β Amyloid Peptides
  • Peptide
  • Amyloid beta-peptide and related
  • Alzheimer
Mol File:
131602-53-4.mol
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AMYLOID BETA-PROTEIN (HUMAN, 25-35) TRIFLUOROACETATE Chemical Properties

Boiling point:
1517.3±65.0 °C(Predicted)
Density 
1.248±0.06 g/cm3(Predicted)
RTECS 
BU7435200
storage temp. 
-20°C
solubility 
insoluble in EtOH; insoluble in H2O; ≥106 mg/mL in DMSO
pka
3.24±0.10(Predicted)
form 
Lyophilized.
color 
Lyophilized White
Water Solubility 
Soluble in water.
Sequence
H-Gly-Ser-Asn-Lys-Gly-Ala-Ile-Ile-Gly-Leu-Met-OH
InChIKey
WIHBNMPFWRHGDF-SLVFWPMISA-N
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Safety Information

WGK Germany 
3
HS Code 
2930909899

MSDS

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AMYLOID BETA-PROTEIN (HUMAN, 25-35) TRIFLUOROACETATE Usage And Synthesis

Description

Beta-amyloid protein (Abeta), a major component of senile plaques of Alzheimer's disease (AD) in the brain, causes elevation of the intracellular free Ca2+ level and the production of robust free radicals. Beta-amyloid 25-35 induced apoptosis, characterized by decreased cell viability, neuronal DNA condensation, and fragmentation, is associated with an increase in intracellular free Ca2+ level, the accumulation of reactive oxygen species (ROS), and the activation of caspase-3. All of these effects induced by beta-amyloid 25-35 are reversed by genistein.

Uses

Amyloid β-Protein Fragment 25-35 has been used:

  • to induce neurotoxicity in cortical cultures
  • to induce Alzheimer′s disease in rat model
  • to induce apoptosis in mesenchymal stem cells (MSCs)

General Description

Amyloid β-Protein Fragment 25-35 (Aβ25-35) is derived from the amyloid-β protein.amyloid-β protein, which is mapped to human chromosome 21q21. Aβ25-35 lacks the N-terminal domain and the metal binding site and is majorly generated by proteolytic cleavage of Aβ(1?40) peptides. It has a β-sheet and β-turn structure.

Biological Activity

Amyloid β-peptide (25-35) (human) is a fragment of human amyloid β-peptide, functionally required for the neurotrophic and neurotoxic effects associated with Alzheimer's disease.

Biochem/physiol Actions

Amyloid β-Protein Fragment 25-35 (Aβ25-35) is involved in the pathogenesis of Alzheimer′s disease. Inhibitors of this transition may serve as a potential agent in managing Alzheimer′s disease. It is present in the subiculum and entorhinal cortex neurons of Alzheimer′s brain samples and inclusion-body myositis (IBM) muscle. It binds to receptors present in microglia and is capable of lipid membrane insertion. The functional domain sequence of Aβ comprising of sequence GSNKGAIIGLM elicits neurotrophic and neurotoxic effects. Aβ25-35 exhibits rapid aggregation and displays age dependant neurotoxicity.

Mechanism of action

Amyloid β (Aβ) peptide is a proven major contributing component of neuritic plaques of Alzheimer's disease (AD) . The formation of fibrillar deposits of Aβ peptide in brain is a key step in the pathogenesis of this disease, since the conversion of Aβ from soluble monomer to insoluble fibril is considered to cause the neuronal degeneration and clinical dementia in AD patients. Recent biophysical studies such as electron microscopy, solid-state NMR, Fourier transform infrared (FTIR), and electronic circular dichroism (ECD) spectra indicated that the Aβ fibrils exhibit a high β-sheet content. The conversion of normal Aβ peptides with water-soluble α-helical/random coil structures into the insoluble Aβ aggregates with an extensive β-sheet content is considered to be the predominant event in the onset of AD.

storage

-20°C

AMYLOID BETA-PROTEIN (HUMAN, 25-35) TRIFLUOROACETATESupplier

Hangzhou Peptidego Biotech Co.,Ltd. Gold
Tel
0571-87213919
Email
Eric@peptidego.com
3B Pharmachem (Wuhan) International Co.,Ltd.
Tel
821-50328103-801 18930552037
Email
3bsc@sina.com
BeiJing Hwrk Chemicals Limted
Tel
0757-86329057 18934348241
Email
sales4.gd@hwrkchemical.com
GL Biochem (Shanghai) Ltd
Tel
21-61263452 13641803416
Email
ymbetter@glbiochem.com
Nanjing Chemlin Chemical Co., Ltd
Tel
025-83697070
Email
info@chemlin.com.cn