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Cagrilintide

MARKETED

long-acting amylin/calcitonin receptor agonist (amylin analogue, once-weekly s.c.)

graded findings

effect domains

Evidence spread

High evidence 0Moderate evidence 5Low evidence 1Very low evidence 1

Cagrilintide is shown as a marketed evidence record where applicable. Findings describe observed research and regulatory records; they do not provide treatment advice.

Thin or bounded evidence here means uncertainty remains visible. It is not evidence that an effect has been ruled out.

Cagrilintide MARKETED

Weight change Decrease

Moderate evidence

Once-weekly cagrilintide monotherapy produced dose-dependent weight loss in adults with overweight/obesity; 4.5 mg gave ~10.8% (~11.5 kg) at 26 weeks vs ~3.0% placebo,...

Lau et al., Lancet 2021 (phase 2); Novo Nordisk REDEFINE 1, NEJM 2025 Source

Full findingOnce-weekly cagrilintide monotherapy produced dose-dependent weight loss in adults with overweight/obesity; 4.5 mg gave ~10.8% (~11.5 kg) at 26 weeks vs ~3.0% placebo, curves not plateaued. As a 2.4 mg monotherapy arm within REDEFINE 1 (68 wk, T2D-free), cagrilintide alone gave 11.5% mean weight reduction.

Populationphase 2: adults overweight/obesity, 0.3-4.5 mg, 26 wk, placebo-controlled; REDEFINE 1: cagrilintide 2.4 mg arm within 3,417 adults, 68 wk

Fundingindustry - Novo Nordisk

Scope limitsMechanism: amylin analogue at amylin/calcitonin receptors (AMY1-3), central satiety via area postrema/hypothalamus; reported to restore leptin sensitivity. Mostly developed as the cagrilintide component of CagriSema. Mechanistic paper PMC12270663 (AMY1/AMY3).

Comparatorsplacebo; liraglutide 3.0 mg (phase 2); semaglutide 2.4 mg (REDEFINE 1); CagriSema (REDEFINE 1)

Cagrilintide MARKETED

Weight change Decrease

Moderate evidence

Dose-dependent weight loss; 4.5 mg superior to liraglutide 3.0 mg over 26 wk

Lau DCW et al. Lancet 2021;398:2160-2172 Source

PopulationAdults overweight/obese without diabetes (n=706 cagrilintide), phase 2 dose-finding, 26 wk, RCT double-blind placebo+active controlled (NCT03856047)

Fundingindustry - Novo Nordisk

Comparatorsplacebo; liraglutide 3.0 mg

Thin or bounded evidence here means uncertainty remains visible. It is not evidence that an effect has been ruled out.

Cagrilintide MARKETED

Appetite and food intake Decrease

Moderate evidence

Once-weekly cagrilintide (0.3-4.5 mg, 26 wk) produced dose-dependent weight loss greater than placebo and greater than liraglutide 3.0 mg at the top dose in adults...

Lau DCW et al. Lancet 2021;398:2160-2172 Source

Full findingOnce-weekly cagrilintide (0.3-4.5 mg, 26 wk) produced dose-dependent weight loss greater than placebo and greater than liraglutide 3.0 mg at the top dose in adults with overweight/obesity without diabetes; amylin's mechanism is satiety induction via homeostatic and hedonic brain regions. Ad libitum energy intake was not the trial endpoint; weight loss is the downstream integral.

PopulationAdults with overweight/obesity without diabetes, n=706 cagrilintide, 26 weeks (NCT03856047)

Fundingindustry - Novo Nordisk

Scope limitsSponsor (Novo Nordisk); COI-flag. Newly added. Weight-as-proxy for appetite; no direct VAS/ad-libitum-intake endpoint. Amylin satiety mechanism per class. GI AEs (nausea 20-47% vs 18% placebo).

Comparatorsplacebo; liraglutide 3.0 mg

Cagrilintide MARKETED

Appetite and food intake Decrease

Very low evidence

A cross-species (rat/mouse/macaque/human) dorsal vagal complex atlas defined amylin-receptor (Calcr) neuronal mediators of cagrilintide's energy-balance effects:...

Ludwig MQ et al., Nat Metab 2026 (advance online) Source

Full findingA cross-species (rat/mouse/macaque/human) dorsal vagal complex atlas defined amylin-receptor (Calcr) neuronal mediators of cagrilintide's energy-balance effects: long-term cagrilintide upregulates prolactin-releasing hormone (Prlh) in conserved NTS Calcr/Prlh cells, and knocking down DVC Prlh abrogates cagrilintide's (but not semaglutide's) effect on food intake/body weight in rats — a mechanistic substrate for amylin-driven intake suppression.

PopulationRat (primary functional), with mouse/macaque/human transcriptomic mapping

Fundingacademic/independent analysis (manufacturer not study sponsor; per-study COI not individually audited)

Scope limitsanimal data; human relevance uncertain

Comparatorsvehicle; semaglutide (comparator agonist)

Thin or bounded evidence here means uncertainty remains visible. It is not evidence that an effect has been ruled out.

Cagrilintide MARKETED

Glycaemic control Decrease

Moderate evidence

As monotherapy in T2D, HbA1c reduction smaller than semaglutide or CagriSema

Frias JP et al. Lancet 2023;402:720-730 Source

PopulationT2D BMI ≥27 on metformin±SGLT2i (n=30 cagrilintide arm), phase 2, 32 wk, RCT (NCT04982575)

Fundingindustry-Novo Nordisk

Scope limitssmall sample (N~30)

Comparatorssemaglutide 2.4 mg; CagriSema

Thin or bounded evidence here means uncertainty remains visible. It is not evidence that an effect has been ruled out.

Cagrilintide MARKETED

Pharmacology and mechanism Not directional

Low evidence

Long-acting amylin analogue, once-weekly; half-life 159-195 h; PK dose-proportional and independent of co-dosed semaglutide

Enebo LB et al. Lancet 2021;397:1736-1748 Source

PopulationHealthy overweight (n=96), phase 1b co-administration with semaglutide 2.4 mg (NCT03600480)

Fundingindustry - Novo Nordisk (trial sponsor; inferred from registration trial)

Scope limitssmall sample (N~96)

Comparatorsplacebo

Thin or bounded evidence here means uncertainty remains visible. It is not evidence that an effect has been ruled out.

Cagrilintide MARKETED

Gastrointestinal tolerability Increase

Moderate evidence

GI disorders and injection-site reactions most frequent; more than placebo

Lau DCW et al. Lancet 2021;398:2160-2172 Source

PopulationOverweight/obese (n=706), phase 2, 26 wk

Fundingindustry - Novo Nordisk

Scope limitsGI burden lower than typical GLP-1 class — amylin tolerability narrative

Comparatorsplacebo; liraglutide 3.0 mg