Beta-Amyloid (3-16)

Aβ(3-16) is an N-terminally truncated amyloid-beta fragment containing the histidine-rich metal-binding region. Removing the first two residues changes the Cu2+ coordination environment, making this peptide useful for mechanistic studies of metal binding and oxidation chemistry.

• amyloid-beta aggregation research
• Alzheimer's disease research
• structure-function studies
• sequence-fragment controls

N-terminal truncation and fragment boundaries can substantially change solubility, metal binding and aggregation behavior. This exact sequence should therefore be treated as a distinct research reagent rather than substituted with full-length Aβ.

1. N-Terminal Deletions Modify the Cu2+ Binding Site in Amyloid-β