Evidence Grade C — Moderate human evidence. 74 published studies, 47 human. 42 registered clinical trials.
Medically reviewed by a licensed medical professional
Cagrilintide is a long-acting amylin analogue from Novo Nordisk — targeting a different satiety pathway than GLP-1 drugs like semaglutide. While it produces meaningful weight loss on its own (about 12%), its primary strategic value is as the amylin component of CagriSema, a combination with semaglutide designed to achieve greater weight loss than either drug alone.
Cagrilintide is also known by these brand and alternate names:
74 published studies: 47 human, 3 animal, 5 in-vitro, 39 reviews
Cagrilintide is in Phase III development (not yet approved). In a Phase II trial (706 patients), cagrilintide 4.5 mg achieved 10.8% weight loss, outperforming the active comparator liraglutide 3.0 mg (9.0%). Phase III results (REDEFINE-1) showed 11.8% weight loss as monotherapy.
Cagrilintide's primary strategic significance is as the amylin component of CagriSema (#162). As a standalone agent, its weight loss is less than currently available GLP-1 agonists like semaglutide. Its value lies in the complementary mechanism that produces additive effects when combined with semaglutide.
Cagrilintide activates amylin receptors in the brain, promoting satiety through a pathway that is complementary to but distinct from GLP-1. While GLP-1 drugs primarily affect appetite and gastric emptying, amylin signalling acts on both the homeostatic (energy balance) and hedonic (reward-based) feeding centres. This dual-centre suppression of food intake may explain the additive weight loss observed when amylin is combined with GLP-1 agonists.
In a Phase II trial of 706 patients, the highest dose of cagrilintide achieved 10.8% weight loss, outperforming the active comparator liraglutide (9.0%). Phase III monotherapy results (REDEFINE-1) showed 11.8% weight loss — meaningful but less than currently available GLP-1 treatments like semaglutide. Cagrilintide's true potential lies in combination. By targeting the amylin pathway alongside GLP-1, it adds a complementary mechanism that amplifies weight loss beyond what either pathway achieves alone. The Phase III monotherapy programme (RENEW) was initiated in late 2025. Injection-site reactions occur in about 17% of patients. No regulatory filing for cagrilintide as a standalone treatment has been made, and approval is unlikely before 2028.
PeptideTrace tracks 42 registered clinical trials for Cagrilintide sourced from ClinicalTrials.gov.
A Research Study to Compare Two Different Versions of Injectable CagriSema in People With Type 2 Diabetes
A Research Study to See How Much CagriSema Lowers Blood Sugar and Body Weight Compared to Placebo in Children and Adolescents With Type 2 Diabetes
A Research Study to Compare Different Versions of Injectable CagriSema and Placebo in People With Excess Body Weight
Evaluation of the Tolerability of Cagrilintide in Participants Not Tolerating GLP-1-RA Therapies Due to Gastrointestinal Adverse Events
A Research Study to Look at How Two Different Doses of CagriSema and One Dose of Semaglutide Help People Living With Obesity With or Without Type 2 Diabetes Lose Weight
Cagrilintide (AM833/NN0174) is a long-acting acylated human amylin analog peptide developed by Novo Nordisk for obesity treatment. The 37-amino-acid peptide has a molecular weight of approximately 4,409 Da and molecular formula C194H312N54O59S2. A C20 fatty diacid moiety linked via gamma-glutamic acid enables reversible albumin binding, producing a half-life of 159-195 hours (approximately 7 days) suitable for once-weekly subcutaneous injection. CAS number: 1415456-99-3. Cagrilintide represents Novo Nordisk's amylin-based approach to obesity pharmacotherapy, serving both as a standalone candidate and as one half of the CagriSema combination therapy.
Cagrilintide is a nonselective agonist of amylin receptors AMY1R (CTR+RAMP1) and AMY3R (CTR+RAMP3), as well as the calcitonin receptor (CTR), with binding IC50 values of 170 pM at human AMY3R and 223 pM at human CTR. The compound suppresses appetite through dual action on both homeostatic hypothalamic pathways and hedonic reward center circuits in the brain. Additional pharmacological effects include slowing of gastric emptying and suppression of postprandial glucagon secretion, contributing to improved glycemic control alongside weight reduction.
In the Phase 2 dose-finding trial (Lau et al., Lancet 2021; NCT03856047; N=706), cagrilintide 4.5 mg achieved -10.8% weight loss versus -3.0% with placebo (estimated treatment difference -7.8 percentage points; P<0.001), outperforming the active comparator liraglutide 3.0 mg which produced -9.0% weight loss. In the REDEFINE-1 Phase 3 trial monotherapy arm (N=302), cagrilintide 2.4 mg delivered -11.8% weight loss at 68 weeks (trial product estimand) compared with -2.3% for placebo. Novo Nordisk has initiated the dedicated RENEW Phase 3 monotherapy program. Key safety signals include gastrointestinal events (nausea, constipation) and injection-site reactions affecting approximately 17% of participants in the REDEFINE-1 monotherapy arm.
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Danuglipron's original twice-daily formulation achieved 8–13% weight loss in Phase IIb but with treatment discontinuation rates exceeding 50%, with nausea affecting up to 73% of patients. Pfizer discontinued the twice-daily formulation and is developing a once-daily modified-release version. Danuglipron is not a peptide. Its development trajectory illustrates that even effective weight loss compounds can fail commercially if tolerability is inadequate. The reformulation effort aims to reduce peak drug concentrations that likely drive the gastrointestinal side effects.
Setmelanotide is marketed as Imcivree (Rhythm Pharmaceuticals; approved November 2020 for POMC, PCSK1, or LEPR deficiency; June 2022 for Bardet-Biedl syndrome; December 2024 expanded to patients aged 2 years and older). Genetic testing confirming an eligible mutation is required before treatment. In patients with POMC or PCSK1 deficiency, approximately 80% achieved at least 10% weight loss in clinical trials. In Bardet-Biedl syndrome, 32.3% achieved the same threshold. The most common side effects are injection-site reactions and skin darkening (due to the melanocortin pathway's connection to pigmentation). Setmelanotide exemplifies precision medicine — it is highly effective in the specific genetic populations it targets but is not indicated for common obesity.
CT-388 is in Phase II/III development (not yet approved). Phase II results (469 patients, 48 weeks) showed 22.5% placebo-adjusted weight loss at the highest dose, with low discontinuation rates due to adverse events (5.9%). Phase III trials are underway. The combination of high efficacy and low discontinuation rates in Phase II is notable — many obesity drugs achieve high weight loss but suffer from tolerability-driven dropouts. Roche's $2.7 billion acquisition of the developer signals significant confidence in the programme.
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