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Ac-KLVFF-NH2 is the N-terminal and C-terminal modified form of the amyloid-beta (16-20) inhibitor peptid KLVFF. The modification leads to higher stability against peptidases.
The KLVFF peptide is one of several inhibitors of amyloid-beta aggregation that have been published. Many of them are fragments and modified peptides derived from the native amyloid-beta sequence. Others were identified by phage display approaches. An overview about peptides that target amyloid-beta is described by Stains et al. (2007) ChemMedChem 2, 1674-1692.
The characteristic of Alzheimer disease is the accumulation of amyloid plaques in the brain. The major components of these plaques are 39-42 residue-long amyloid-ß-peptides, which form insoluble fibrils via self-assembly. The amyloid-ß-peptides are fragments of the broadly distributed, membrane-bound amyloid precursor protein APP, encoded on chromosome 21. They are formed from the proteolytic cleavage of APP by ß- and g-secretases. Cleavage occurs after residue 40 or after residue 42. Even slightly increased amounts of amyloid-ß1-42 are described to be sufficient to cause Alzheimer's disease.
P2255 - Amyloid-beta (16-20) - KLVFF >
P2304 - Amyloid-beta (10-20) - YEVHHQKLVFF >
P2249 - Amyloid-beta (1-40) human - DAEFRHDSGYEVHHQKLVFFAEDVGSNKGAIIGLMVGGVV >
P2250 - Amyloid-beta (1-40) human - DAEFRHDSGYEVHHQKLVFFAEDVGSNKGAIIGLMVGGVV - HCl salt peptide >
P2247 - Amyloid-beta (1-40) rat - DAEFGHDSGFEVRHQKLVFFAEDVGSNKGAIIGLMVGGVV >
P2248 - Amyloid-beta (1-40) rat - DAEFGHDSGFEVRHQKLVFFAEDVGSNKGAIIGLMVGGVV - HCl salt peptide >
P2303 - Amyloid-beta (1-42) human - DAEFRHDSGYEVHHQKLVFFAEDVGSNKGAIIGLMVGGVVIA >
Sequence: Ac-KLVFF-NH2 (N-terminal acetylated and N-terminal amidated)
Purity: >70% / >95% (HPLC)
Appearance: lyophilized, white powder
Sicherheits Hinweise / Safety
Klassifizierungen / Classificationeclass-Nr: 34-16-04-90
Dokumente - Protokolle - Downloads
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