IAPP (islet amyloid polypeptide), also known as amylin, is a glucoregulatory peptide hormone critical for energy homeostasis. It selectively inhibits insulin-stimulated glucose utilization and glycogen deposition in muscle through amylin receptor (AMYR) complexes while leaving adipocyte glucose metabolism unaffected 1. IAPP plays a metabolic role in postprandial glucose regulation by delaying gastric emptying and suppressing hyperglucagonemia 2. In type 2 diabetes, pathological IAPP accumulation becomes problematic. Human IAPP forms cytotoxic oligomers and amyloid fibrils in pancreatic islets, with toxicity primarily associated with early-phase oligomeric intermediates rather than mature fibrils 3. Both intracellular misfolding—triggered by protein synthesis defects, unfolded protein response failure, or degradation pathway overload—and extracellular amyloid-membrane interactions drive β-cell apoptosis 3, 4. Metabolic stress from insulin resistance and hyperglycemia exacerbates IAPP production and aggregation propensity 4. IAPP also functions as an islet autoantigen in type 1 diabetes, with autoreactive T cells targeting IAPP-derived epitopes, and IAPP aggregates act as pro-inflammatory stimuli 2. The peptide's therapeutic potential has been explored through IAPP analogues like pramlintide and novel inhibitors including silybins and graphene quantum dots, which prevent aggregation and protect β-cells from toxicity 5, 6.