Cagrilintide: Metabolic / Fat Loss research guide

Cagrilintide (AM833) is a long-acting, acylated analogue of the pancreatic hormone amylin. It is a non-selective agonist of the three amylin receptor subtypes (AMY1/2/3R) plus the calcitonin receptor, and acts on arcuate-nucleus appetite neurons to suppress hunger while delaying gastric emptying and lowering postprandial glucagon. A C20 fatty-diacid anchor binds serum albumin to extend its half-life to roughly eight days, supporting once-weekly research dosing.

GLP-1 agonists activate the GLP-1 receptor. Cagrilintide activates the amylin receptor family (AMY1/2/3R) plus the calcitonin receptor. The two pathways engage different appetite circuits, which is why combining them (as in CagriSema research) produces larger effects than either alone.

A Phase 2 dose-finding trial (Lancet 2021) reported dose-dependent body-weight reduction with cagrilintide monotherapy. In the Phase 3 REDEFINE 1 trial (NEJM 2025), the cagrilintide + semaglutide combination (CagriSema) reported a 20.4% mean reduction versus 3.0% placebo at 68 weeks on the treatment-policy estimand, with cagrilintide alone around 11.5% and semaglutide alone around 14.9%. These are descriptive clinical-trial findings, not outcomes promised for any use of this research-grade material.

They act through entirely different hormone systems: semaglutide is a GLP-1 receptor agonist, while cagrilintide is an amylin/calcitonin-receptor agonist. Their half-lives are similar (cagrilintide ~159–195 h, semaglutide ~145–165 h), both supporting once-weekly dosing. In the REDEFINE programme the two were studied together precisely because their satiety pathways are additive rather than redundant.

The most frequently reported events in published trials were gastrointestinal — nausea, vomiting, decreased appetite, constipation or diarrhoea — that were typically mild-to-moderate, escalation-related and transient, plus injection-site reactions. Gallbladder events have been noted in combination research. These are observations recorded in the clinical literature, not a safety profile for any human use of this research material.

Native human amylin forms amyloid fibrils that are toxic to pancreatic islet cells and make the peptide impractical for sustained research use. Substituting prolines at positions 25, 28, and 29 (borrowed from rat amylin, which does not aggregate) blocks the fibrillation pathway.

Keep the lyophilised powder at −20 °C in the freezer. Reconstitute with bacteriostatic water by directing it down the vial wall rather than onto the powder, then swirl gently — do not shake. After reconstitution, refrigerate at 1–6 °C and protect from light. Avoid repeated freeze-thaw cycles, which can damage the fatty-acid tail.

Cagrilintide is an investigational compound and is not an approved medicine on its own; the CagriSema combination remains in late-phase clinical development. The material supplied here is unapproved, research-grade laboratory material sold strictly for in-vitro and preclinical research use only — not for human use.

It depends on the peptide class. Cagrilintide is a long-acting amylin analogue studied for appetite and metabolic research, often alongside GLP-1 peptides. As with the GLP-1 class, the research literature on appetite-regulating peptides indicates the appetite effects depend on continued receptor stimulation, so they wane once administration stops and the compound clears; cagrilintide's long half-life means that clearance is gradual. These observations come from research and clinical studies — cagrilintide here is an unapproved research-grade peptide for laboratory research only and not for human use.

No, and no. This article is educational only. We do not provide dosing, medical recommendations, or health claims. Our products are sold strictly for laboratory research, not for personal use of any kind.

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