Amylin (islet amyloid polypeptide, IAPP) is an endogenous 37-amino-acid peptide hormone (MW ~3903.3 g/mol) co-secreted with insulin from pancreatic beta cells in response to nutrient ingestion. It plays a key role in postprandial glucose regulation by slowing gastric emptying, suppressing glucagon secretion, and promoting satiety. Amylin is deficient in type 1 diabetes and relatively deficient in advanced type 2 diabetes. While amylin itself is not used as a drug due to its propensity to form amyloid fibrils, it is the basis for the approved analog pramlintide (Symlin) and the investigational long-acting analog cagrilintide.
Category: Metabolic / Endogenous Hormone. Evidence rating: B (meaningful human data).
Clinical status: Endogenous hormone. Not itself used as a drug. Serves as the basis for pramlintide (Symlin, FDA-approved) and cagrilintide (investigational).
Amylin is synthesized as an 89-amino-acid preprohormone in pancreatic beta cells and processed to its mature 37-amino-acid form with a C-terminal amide and an intramolecular disulfide bond between Cys-2 and Cys-7. It is co-packaged with insulin in secretory granules and released in a roughly 1:100…
Safety considerations: As an endogenous hormone, amylin itself is not administered therapeutically; Native human amylin readily aggregates into amyloid fibrils at physiological concentrations, making it unsuitable as a drug; Amyloid aggregates are cytotoxic to beta cells and contribute to disease progression in T2D.
Reviewed by the PeptideAtlas Editorial Team. Last reviewed: 2026-08-12.
Human amylin has a strong tendency to misfold into amyloid fibrils — the same type of protein aggregation seen in Alzheimer disease. At the concentrations needed for therapeutic dosing, human amylin rapidly forms insoluble, potentially toxic aggregates. Pramlintide was engineered with three proline substitutions to prevent this.
Amyloid deposits of aggregated amylin (IAPP) are found in the pancreatic islets of approximately 90% of T2D patients at autopsy. These deposits are thought to contribute to progressive beta cell loss. As beta cells are damaged, both insulin and amylin secretion decline, worsening glucose control.
Amylin and insulin are co-secreted from beta cells but have distinct functions. Insulin lowers blood glucose by promoting glucose uptake. Amylin complements insulin by slowing gastric emptying (delaying glucose absorption), suppressing glucagon (reducing hepatic glucose output), and promoting satiety (reducing food intake).
Pramlintide (Symlin) is an FDA-approved synthetic amylin analog. Cagrilintide is a next-generation long-acting amylin analog being developed by Novo Nordisk, studied both alone and in combination with semaglutide (CagriSema) for obesity and diabetes.