Quick summary
Amylin (IAPP) is a 37-amino acid pancreatic hormone co-secreted with insulin that slows gastric emptying and suppresses glucagon. It is the basis for pramlintide (FDA-approved) and cagrilintide (~25% weight loss in trials).
Overview
Amylin (IAPP) is a 37-amino acid peptide hormone co-secreted with insulin from pancreatic beta cells in approximately a 100:1 ratio (insulin:amylin). It plays a critical role in postprandial glycemic control by slowing gastric emptying, suppressing glucagon, and promoting satiety. Amylin is the structural template for pramlintide (Symlin, FDA-approved) and the next-generation analog cagrilintide.
Mechanism of action
Amylin activates amylin receptors (AMY1–3), which are heterodimers of calcitonin receptors (CTR) and receptor activity-modifying proteins (RAMPs 1–3). In the area postrema and nucleus accumbens, amylin signaling reduces food intake and slows gastric motility. It suppresses postprandial glucagon secretion in a glucose-dependent manner. Pathological aggregation of IAPP into amyloid fibrils in beta cell islets is implicated in type 2 diabetes progression via inflammasome activation, ER stress, and membrane disruption.
Dosing protocols
| Purpose | Route | Dosage | Frequency | Notes |
|---|---|---|---|---|
| research (animal models) | subcutaneous | 1–10 nmol/kg | per study protocol |
Dosing information is for educational purposes only. Consult a qualified healthcare professional before using any peptide.
Research summary
Pramlintide (synthetic amylin analog) is FDA-approved as an adjunct to insulin in T1D and T2D, reducing postprandial glucose excursions by ~40 mg/dL and body weight by 1–2 kg. Cagrilintide (Novo Nordisk long-acting amylin analog) combined with semaglutide (CagriSema) produced ~25% weight loss in Phase 2 trials (SCALE) and is advancing to Phase 3. IAPP amyloid research is central to understanding beta cell failure in T2D.[1][2][3][4][5]
Evidence grading
Each claimed benefit is graded by the strength of available evidence. Grades reflect study quality, not effect size.
Strong = multiple RCTs · Moderate = limited trials or observational · Preliminary = animal or in vitro only · Insufficient = anecdotal or no published data
Side effects
Side effects vary by individual. This is not an exhaustive list. Report unusual symptoms to a healthcare professional.
Common stacks
Peptides commonly paired with Amylin for synergistic effects.
Legal status
Native amylin (IAPP) is available for research use only. Pramlintide (Symlin) is FDA-approved by prescription. Cagrilintide is investigational (Phase 3). Pure IAPP peptide is not approved for human administration.
Sourcing & access
Research compound
Amylin is classified as a research compound. Regulatory status varies by jurisdiction. Always verify current legal status and source from vendors providing third-party certificates of analysis (COA).
Frequently asked questions
Amylin, also called Islet Amyloid Polypeptide (IAPP), is a 37-amino acid peptide hormone co-secreted with insulin from pancreatic beta cells. It plays a critical role in postprandial glycemic control by slowing gastric emptying, suppressing glucagon, and promoting satiety.
Amylin activates amylin receptors (AMY1-3), which are heterodimers of calcitonin receptors and receptor activity-modifying proteins (RAMPs). In the area postrema and nucleus accumbens, amylin signaling reduces food intake and slows gastric motility while suppressing postprandial glucagon secretion.
Pramlintide, a synthetic amylin analog, is FDA-approved and has a well-characterized safety profile. Common side effects include nausea, hypoglycemia risk when combined with insulin, and injection site reactions. Native amylin peptide has not been evaluated in human clinical trials.
Cagrilintide, a long-acting amylin analog by Novo Nordisk, combined with semaglutide (CagriSema) produced approximately 25% weight loss in Phase 2 trials. Amylin's satiety-promoting and gastric-slowing effects make it a key target for next-generation obesity treatments.
Pathological aggregation of IAPP into amyloid fibrils in pancreatic islets is implicated in type 2 diabetes progression. These aggregates cause beta cell death through inflammasome activation, ER stress, and membrane disruption, making IAPP amyloid research central to understanding T2D.
Research references
- Islet amyloid polypeptide: structure, function, and pathophysiologyReview
- Pramlintide as an adjunct to insulin therapy improves long-term glycemic and weight control in patients with type 2 diabetes: a 1-year randomized controlled trialClinicalTrials.gov
- Progressive reduction in body weight after treatment with the amylin analog pramlintide in obese subjects: a phase 2, randomized, placebo-controlled, dose-escalation studyClinicalTrials.gov
- Effect of pramlintide on satiety and food intake in obese subjects and subjects with type 2 diabetesPubMed
- Islet amyloid polypeptide, islet amyloid, and diabetes mellitusReview