Type 2 diabetes mellitus is a chronic hyperglycaemic disorder caused by defective action and secretion of insulin. It is characterized by a progressive decline in pancreatic β-cell function and mass and the occurrence of insoluble amyloid deposits within the islets of Langerhans. These amyloid deposits comprise predominantly of fibrillar aggregates of the 37-amino acid human amylin (hA) monomer, also known as islet amyloid polypeptide (IAPP), which is co-secreted with insulin from pancreatic islet β-cells via the regulated secretory pathway. hA has a propensity to aggregate in vitro into fibrillar structures through the self-association of monomers that is largely mediated by an amyloidogenic region spanning amino acids 20-29 (reviewed in ref. 8).