An investigational long-acting, lipidated analog of the pancreatic hormone amylin, developed by Novo Nordisk. It has been studied in phase 2 and phase 3 human trials, alone and alongside semaglutide, and in mouse receptor studies.
Cagrilintide was engineered from the amylin sequence with a fatty-acid side chain so it lasts longer in circulation than earlier amylin analogs such as pramlintide [1]. It activates amylin receptors, which are calcitonin receptors paired with RAMP proteins, and also the calcitonin receptor itself [1][2]. In mice lacking RAMP1 and RAMP3, cagrilintide's measured effects on food intake and body weight were largely absent, and fewer area-postrema neurons were activated, pointing to brain amylin receptors 1 and 3 as the main site of action in that model [2].
| Study | Model | Reported result | Source |
|---|---|---|---|
| Phase 2 dose-finding trial [3] | Human 706 adults, randomized, double-blind, placebo- and active-controlled, 26 weeks plus follow-up | Primary endpoint: percentage change in body weight at week 26. Published | Peer-reviewed Lancet 2021 |
| REDEFINE 1, phase 3a [4] | Human 3,417 adults, randomized, double-blind; included a cagrilintide-alone arm (n=302) alongside combination, semaglutide and placebo arms, 68 weeks | Coprimary endpoints: change in body weight and proportion reaching 5% or more weight reduction (combination vs placebo). Published | Peer-reviewed NEJM 2025 |
| Amylin receptor knockout study [2] | Mouse Wild-type vs RAMP1/3 double-knockout mice; high-fat-diet model, 3 weeks | Wild-type: day-1 food intake 1.2 g vs 2.7 g vehicle; body weight down 3.4 g. Knockouts: no change in food intake; 57% fewer area-postrema neurons activated | Peer-reviewed eBioMedicine 2025 |
Human trials are listed for research context only; outcomes are reported in the linked publications. Animal and lab results do not establish effects in humans.
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