Key facts
- Amylin is a 37-amino-acid peptide hormone made by pancreatic beta cells and released together with insulin after meals.[1][2]
- It slows gastric emptying, suppresses glucagon after meals and ends meals sooner by signalling fullness through the area postrema in the brainstem.[2][4]
- Amylin receptors are the calcitonin receptor paired with RAMP1, RAMP2 or RAMP3 (AMY1, AMY2, AMY3).[5]
- Native human amylin clumps into amyloid fibrils, so drugs use modified analogues: pramlintide (approved 2005), cagrilintide, petrelintide and eloralintide.[6][2]
What Is Amylin?
Amylin is a 37-amino-acid peptide hormone made by the beta cells of the pancreas, stored with insulin and released with it in response to food.[1][2]
It is also called islet amyloid polypeptide (IAPP), and it is one of the main products of the pancreatic beta cells.[3] Amylin acts mainly as a glucose-regulating hormone and a regulator of energy balance, working largely through areas of the brain outside the blood-brain barrier.[1]
What Does Amylin Do?
Amylin does three main things after a meal: it slows gastric emptying, suppresses glucagon release, and reduces food intake by increasing satiety.[2]
- Slows gastric emptying. Food leaves the stomach more slowly, without changing how much is absorbed overall.[2]
- Suppresses glucagon after meals. Insulin alone does not normalise this, and lower glucagon means less glucose released by the liver.[2]
- Ends meals sooner. Amylin controls meal size by triggering satiation, mainly through direct action on the area postrema in the brainstem.[4]
- Works with leptin. Amylin makes the brain more sensitive to leptin, the long-term satiety hormone.[4]
Amylin Receptors: AMY1, AMY2 and AMY3
Amylin receptors form when the calcitonin receptor pairs with one of three receptor activity-modifying proteins: RAMP1 makes AMY1, RAMP2 makes AMY2 and RAMP3 makes AMY3.[5]
This is why selectivity matters. Cagrilintide is described as acting on amylin and calcitonin receptors with similar potency. Eloralintide was designed for AMY1 and is about 12-fold more potent there than at the calcitonin receptor alone.[9][8] See eloralintide vs cagrilintide.
Why Amylin Drugs Use Analogues, Not Amylin Itself
Native human amylin rapidly clumps into amyloid fibrils that are toxic to beta cells, which limits its use as a drug, so medicines use modified amylin analogues.[6]
- Islet amyloid made of aggregated amylin is linked to beta-cell loss in type 2 diabetes.[3]
- Pramlintide swaps three amino acids for proline (positions 25, 28 and 29) to reduce clumping, but it needs an acidic pH of about 4.0 to stay in solution.[2][6]
- Newer analogues such as petrelintide are designed to stay stable at neutral pH, so they can be combined with other peptides.[7]
- Eloralintide adds a fatty acid that binds albumin, giving a half-life of about two weeks.[8]
Amylin Analogues and Agonists Compared
Pramlintide is the only approved amylin analogue (FDA, 2005, for diabetes), while cagrilintide, petrelintide, eloralintide and amycretin are long-acting amylin-based drugs in development for obesity.[2]
| Drug | Developer | Type | Dosing | Status (Nov 2026) | Best reported weight result |
|---|---|---|---|---|---|
| Pramlintide (Symlin) | AstraZeneca (label holder) | Amylin analogue | Before each main meal | Approved 2005, diabetes only | -0.8 to -1.6 kg in label trials[2] |
| Eloralintide | Eli Lilly | Selective amylin agonist | Once weekly | Phase 3 (ENLIGHTEN) | -20.1% at 48 wk, 9 mg[10] |
| Cagrilintide | Novo Nordisk | Amylin and calcitonin agonist | Once weekly | With semaglutide (CagriSema) filed Dec 2025[15] | -10.8% at 26 wk alone[11] |
| Petrelintide | Zealand Pharma and Roche | Amylin analogue | Once weekly | Phase 3 (ZUPREME-3 to 5) | -10.7% at 42 wk[12] |
| Amycretin (zenagamtide) | Novo Nordisk | GLP-1 and amylin agonist in one molecule | Weekly injection or daily pill | Phase 3 (AMAZE) | -24.3% at 36 wk, 60 mg injection[13] |
Read the full profiles: what is eloralintide and amycretin (zenagamtide).
Amylin in Type 1 and Type 2 Diabetes
Type 1 diabetes is a state of both insulin and amylin deficiency, and amylin secretion after meals is also reduced in type 2 diabetes, which is why pramlintide is used alongside mealtime insulin.[14][2]
Pramlintide is injected before each major meal and carries a boxed warning for severe hypoglycaemia when used with insulin, usually within 3 hours of a dose. Its label calls for mealtime insulin to be cut by 50% when starting.[2]
Frequently Asked Questions
What is amylin?
Amylin is a 37-amino-acid hormone made by pancreatic beta cells and released with insulin after meals. It slows gastric emptying, suppresses glucagon and increases fullness.
What does amylin do in the body?
After a meal it slows how fast the stomach empties, lowers glucagon so the liver releases less glucose, and signals fullness through the area postrema in the brainstem.
What is an amylin agonist?
A drug that activates amylin receptors. Examples are pramlintide (approved for diabetes), and eloralintide, cagrilintide and petrelintide, which are in development for obesity.
Is amylin the same as GLP-1?
No. Amylin comes from pancreatic beta cells and acts on amylin receptors. GLP-1 comes from the gut and acts on the GLP-1 receptor. Some drugs, such as amycretin, target both.
Is there an approved amylin drug for weight loss?
Not as of November 2026. Pramlintide is approved only for diabetes. CagriSema, which includes the amylin analogue cagrilintide, was submitted to the FDA in December 2025.
Sources
- Hay DL, et al. Amylin: pharmacology, physiology, and clinical potential. Pharmacological Reviews 2015;67:564-600. DOI 10.1124/pr.115.010629
- FDA. SYMLIN (pramlintide acetate) prescribing information, revised 12/2019
- Westermark P, et al. Islet amyloid polypeptide, islet amyloid, and diabetes mellitus. Physiological Reviews 2011;91:795-826
- Lutz TA. Amylin and the control of eating. Neuropharmacology 2025;278:110587. DOI 10.1016/j.neuropharm.2025.110587
- Hay DL, et al. Update on the pharmacology of calcitonin/CGRP family receptors (IUPHAR Review 25). British Journal of Pharmacology 2018;175:3-17
- Wang H, et al. Rational design of non-amyloidogenic amylin analogues. Biochemistry 2014;53:5876-5884
- Roche media release, 5 Mar 2026: petrelintide phase 2 results
- Briere DA, et al. Discovery and first-in-human study of eloralintide. Molecular Metabolism 2025;102:102271. DOI 10.1016/j.molmet.2025.102271
- Bhattachar S, et al. Eloralintide 12-week multiple-dose phase 1. Diabetes, Obesity and Metabolism 2026;28(4):2651-2660. DOI 10.1111/dom.70439
- Eli Lilly press release, 6 Nov 2025: eloralintide phase 2 results
- Lau DCW, et al. Cagrilintide phase 2. The Lancet 2021;398:2160-2172. DOI 10.1016/S0140-6736(21)01751-7
- Garvey WT, et al. Petrelintide ZUPREME-1 phase 2. Lancet Diabetes & Endocrinology 2026;14:914-926
- Dahl K, et al. Amycretin phase 1b/2a. The Lancet 2025;406:149-162. DOI 10.1016/S0140-6736(25)01185-7
- Lebovitz HE. Adjunct therapy for type 1 diabetes mellitus. Nature Reviews Endocrinology 2010;6:326-334
- Novo Nordisk company announcement: CagriSema submitted to the US FDA, December 2025
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