| Identification | Back Directory | [Name]
AMYLOID BETA-PROTEIN (HUMAN, 25-35) TRIFLUOROACETATE | [CAS]
131602-53-4 | [Synonyms]
Aβ25-35
GSNKGAIIGLM
BETA-AMYLOID
-Amyloid(25-35)
β-Amyloid (25-35)
BETA-AMYLOID (25-35)
β-Amyloid (25-35) TFA
25-35) TRIFLUOROACETATE
β-Amyloid peptide(25-35)
AMyloid b-Protein (25-35)
β-Amyloid (25-35) (human)
AMyloid beta (25-35) huMan
1: PN: US20030114510 SEQID
AMYLOID BETA-PROTEIN (HUMAN
Amyloid beta-peptide(25-35)
AMYLOID BETA-PROTEIN (25-35)
BETA-AMYLOID, FRAGMENT 25-35
M.W. 1060.27 C45H81N13O14S
Amyloidb-Peptide(25-35)(human)
amyloid β-protein fragment 25-35
amyloid B-protein fragment 25-35
Amyloid β-Protein Fragment 25-35
biotinylated?，Biotin-GSNKGAIIGLM
Amyloid β-peptide (25-35) (human)
Human beta-amyloid peptide(25-35)
AMyloid β-peptide (25-35) (huMan)
AMYLOID BETA-PROTEIN FRAGMENT 25-35
BETA-AMYLOID PEPTIDE [25-35], HUMAN
AMYLOID BETA-PEPTIDE (25-35) (HUMAN)
AMyloid β-peptide (25-35) (huMan)TFA
GLY-SER-ASN-LYS-GLY-ALA-ILE-ILE-GLY-LEU-MET
AMYLOID-BETA PROTEIN (25-35), HUMAN, MOUSE, RAT
Amyloid β-Protein (25-35) trifluoroacetate salt
H-GLY-SER-ASN-LYS-GLY-ALA-ILE-ILE-GLY-LEU-MET-OH
Amyloid beta-Protein Fragment 25-35 >=97% (HPLC)
Amyloid beta-Protein (25-35) trifluoroacetate salt
AMYLOID BETA-PROTEIN (HUMAN, 25-35) TRIFLUOROACETATE
GLY-SER-ASN-LYS-GLY-ALA-ILE-ILE-GLY-LEU-MET TRIFLUOROACETATE
AMYLOID BETA-PROTEIN (HUMAN, 25-35) TRIFLUOROACETATE USP/EP/BP
GSNKGAIIGLM(131602 53 4(free base)),GSNKGAIIGLM(131602534(free base))
β-amyloid peptide,Abeta,inhibit,Inhibitor,Amyloid-β,βAmyloid (2535),β Amyloid (25 35)
AC-ASN-TRP-CYS-LYS-ARG-GLY-ARG-LYS-GLN-CYS-LYS-THR-HIS-PRO-HIS-NH2: AC-NWCKRGRKQCKTHPH-NH2
Glycyl-L-seryl-L-asparaginyl-L-lysylglycyl-L-alanyl-L-isoleucyl-L-isoleucylglycyl-L-leucyl-L-methionine
L-Methionine,glycyl-L-seryl-L-asparaginyl-L-lysylglycyl-L-alanyl-L-isoleucyl-L-isoleucylglycyl-L-leucyl- | [Molecular Formula]
C45H81N13O14S | [MDL Number]
MFCD04113709 | [MOL File]
131602-53-4.mol | [Molecular Weight]
1060.27 |
| Chemical Properties | Back Directory | [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 | [form ]
Lyophilized. | [pka]
3.24±0.10(Predicted) | [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 | [SMILES]
CCC(C)C(NC(=O)C(NC(=O)C(C)NC(=O)CNC(=O)C(CCCCN)NC(=O)C(CC(N)=O)NC(=O)C(CO)NC(=O)CN)C(C)CC)C(=O)NCC(=O)NC(CC(C)C)C(=O)NC(CCSC)C(O)=O |
| Hazard Information | Back Directory | [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 |
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Sigma-Aldrich
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