Type 2 diabetes mellitus is characterized as a chronic hyperglycemic disorder caused by defective action and/or secretion of insulin leading to vascular complications that are ultimately responsible for morbidity and mortality. The deficiency in insulin secretion in diabetic patients is associated with a reduction in β-cell mass.

A feature of the β-cell islets in Type 2 diabetes is the presence of insoluble amyloid deposits. Islet amyloid is comprised mostly of fibrillar aggregates of a unique protein known as amylin. This protein is co-secreted with insulin and is involved in the regulation of glucose homeostasis. Research from the Protemix laboratory has shown that amylin aggregates cause β-cell death through apoptosis (programmed β-cell death), suggesting that the biological processes evoked by the amylin aggregation can mediate β-cell failure in the pathogenesis of type 2 diabetes.

The oversecretion of amylin and/or alteration of amylin peptide processing can lead to the production of amylin aggregates and the subsequent loss of islet β-cells. Protemix is currently investigating the use of orally active small molecules to suppress formation of these cytotoxic amylin as a means of preventing the destruction of islet β-cells, and thus preserving normal glucose regulation and slowing diabetes progression in Type 2 diabetes. This research also has a wider relevance for the treatment of amyloid-mediated diseases such as Alzheimer's and Huntington Disease.