Cagrilintide Research, Specifications & Scientific Information

Introduction

Cagrilintide is the compound in this family that is not an incretin analogue at all. Where semaglutide, tirzepatide and retatrutide are all built around receptors in the glucagon–secretin family, cagrilintide is an analogue of amylin — the pancreatic hormone co-secreted with insulin — and it acts at a different receptor family entirely ^[1]. That is why it is usually described alongside those compounds rather than against them: the interest is in what happens when two unrelated mechanisms are engaged at once.

Its design problem was also unlike theirs. Native amylin has a strong propensity to form amyloid fibrils, which the development paper names as the central obstacle to turning it into a drug; the earlier analogue pramlintide solved aggregation but not duration, and required three injections a day ^[3]. Cagrilintide is the lipidated analogue that came out of that work, stable enough to handle and long-acting enough for a weekly interval.

This page is a reference record. It sets out what has been published about cagrilintide's structure, its receptor pharmacology and its clinical literature, with every source resolved against PubMed, Crossref or ClinicalTrials.gov at the time the page was built. It describes research. It does not describe use in people or animals, and it carries no guidance of any kind on handling the material.

What Is Cagrilintide?

Cagrilintide is an investigational, lipidated 37-residue peptide analogue of human amylin, developed by Novo Nordisk under the code NNC0174-0833 and described in the medicinal chemistry literature in 2021 ^[3]. It is not an approved medicine in the United States and has not been approved by the U.S. Food and Drug Administration for any indication.

Most of its clinical record is not about cagrilintide alone. The compound has been carried through phase 3 principally as a fixed co-administration with semaglutide, referred to in the literature as CagriSema, and the single-agent data stop at phase 2 ^{[4, 6]}. That asymmetry matters when reading the evidence: the trials with the largest populations and the longest follow-up were not studying this molecule on its own.

Two names for the same material circulate — cagrilintide, and the development code NNC0174-0833, which is how the earlier registered trials describe it.

Cagrilintide Specifications

The 37-residue string above is the backbone recorded for cagrilintide in the FDA/NCATS Global Substance Registration System under UNII AO43BIF1U8, written in single-letter code. Two features of the real molecule are not visible in it. First, the two cysteine residues near the N-terminus form an intramolecular disulfide bridge, which the register carries separately as a cyclic disulfide in the substance's systematic name; the peptide is therefore not a linear chain. Second, the molecule is lipidated — the published account describes it as a stable, lipidated long-acting amylin analogue, and the systematic name recorded against the same registry entry places a twenty-carbon diacid on the N-terminal lysine through a gamma-glutamyl linker. The design constraint the paper names is unusual for this class: native amylin has a strong propensity to form amyloid fibrils, so the analogue had to be stabilised against aggregation as well as against clearance. The molecular formula and mass shown here are those carried by PubChem compound identifier 171397054 for the complete lipidated molecule. The supplier catalog record for this material carries no formula, mass or CAS number; the values here come from public registers, and the certificate of analysis supplied with a laboratory order is the record for a given lot.

Values that a public register does not carry are shown as not publicly characterised rather than estimated. Identifiers are reference values; the certificate of analysis supplied with a laboratory order is the record for a given lot.

How Does Cagrilintide Work?

Amylin is a 37-residue hormone secreted by pancreatic beta cells alongside insulin. Its receptors are not dedicated proteins in the way the GLP-1 receptor is. They are formed when the calcitonin receptor — itself a class B1 G protein-coupled receptor — associates with one of the receptor activity-modifying proteins, and the resulting complexes have pharmacology that neither component has alone ^[1].

That construction is the reason amylin pharmacology is harder to describe in a sentence than incretin pharmacology. There is no single amylin receptor; there is a family of complexes whose relative distribution differs by tissue, and selectivity between them and the calcitonin receptor is a real design variable rather than a formality.

Functionally, the clinical literature describes amylin as a pancreatic hormone that induces satiety, and that is the property the analogue was developed around ^[4]. What cagrilintide adds to native amylin is not a new mechanism but stability and duration: lipidation gives it a plasma half-life reported in the range of 159 to 195 hours in early clinical study ^[2].

Cagrilintide Mechanism of Action

In vitro research

The receptor pharmacology cagrilintide operates within is set out in the reference literature on amylin: receptors assembled from the calcitonin receptor and receptor activity-modifying proteins, belonging to the class B1 G protein-coupled receptor family and signalling separately from the incretin receptors that the compounds it is co-administered with engage ^[1].

The compound-specific characterisation is a medicinal chemistry account rather than a receptor-profiling paper. It reports the development of a stable, lipidated long-acting amylin analogue and the structure-activity work that selected this molecule from among its alternatives ^[3]. Quantitative receptor potency figures for cagrilintide at each amylin receptor subtype are not stated in that abstract and are not reproduced here.

Analytical characterisation of supplied material is a separate exercise from receptor pharmacology. For a peptide carrying an intramolecular disulfide and a lipid chain, identity confirmation relies on liquid chromatography with mass spectrometric detection against a reference standard, and purity on chromatographic separation.

What Is Cagrilintide Being Researched For?

Registered clinical research involving cagrilintide has covered:

• Obesity and overweight, single agent — a phase 2 trial ranging over five administered amounts with both a placebo and an active comparator ^[4].
• Obesity and overweight, in combination with semaglutide — a phase 1b pharmacokinetic study ^[2] followed by a phase 3a programme ^[6].
• Type 2 diabetes — a three-arm phase 2 trial comparing the combination against each of its components ^[5], and a phase 3a trial of the combination ^[7].

Each of those is research into a pharmaceutical product candidate, conducted by its sponsor under a registered protocol. None of it is research into, or evidence about, research-grade material supplied for laboratory use.

Human Research on Cagrilintide

Human clinical research

Results from pharmaceutical clinical trials describe the investigational material and populations used in those studies and should not be interpreted as establishing the effects of research-grade materials offered for laboratory use.

Phase 1b in combination with semaglutide

Population. 96 participants aged 18–55 with a body-mass index of 27.0–39.9 kg/m² and otherwise healthy, recruited at a single centre in the United States; 95 were exposed. Mean age 40.6 years (SD 9.2); 59% men; 54% Black or African American ^{[2, 8]}.

Endpoint and duration. Primary endpoint the number of treatment-emergent adverse events from baseline to end of follow-up. Six sequential overlapping cohorts, co-escalated with semaglutide 2.4 mg over 16 weeks, four weeks at target, five weeks of follow-up, with no lifestyle intervention ^[2].

Result. Exposure was proportional to the amount of cagrilintide administered and did not affect semaglutide exposure or elimination. Cagrilintide half-life was 159–195 hours with a median time to maximum concentration of 24–72 hours; semaglutide half-life in the same participants was 145–165 hours. At week 20, mean percentage body-mass reductions were 15.7% (1.2 mg) and 17.1% (2.4 mg) against 9.8% for pooled placebo, estimated treatment differences of −6.0% (95% CI −9.9 to −2.0) and −7.4% (95% CI −11.2 to −3.5); the 4.5 mg group reached 15.4% against 8.0% for matched placebo, difference −7.4% (95% CI −12.8 to −2.1) ^[2].

Adverse events. 566 adverse events in 92 participants, of which 207 (37%) were gastrointestinal disorders. Most were mild to moderate, and the proportion of participants with at least one adverse event was similar across groups ^[2].

Limitations. A phase 1b safety and pharmacokinetic study of 95 people at one site, with body-mass change as an exploratory endpoint only. Every participant received semaglutide, so nothing here separates the contribution of cagrilintide.

Phase 2 as a single agent, across a range of administered amounts

Population. 906 adults without diabetes, with a body-mass index of at least 30 kg/m² or at least 27 kg/m² with hypertension or dyslipidaemia, at 57 sites in ten countries: 706 assigned to cagrilintide 0.3–4.5 mg, 99 to liraglutide 3.0 mg, 101 to placebo ^{[4, 9]}.

Endpoint and duration. Primary endpoint the percentage change in body mass from baseline to week 26, under both a trial-product and a treatment-policy estimand. Twenty-six weeks of treatment including up to six weeks of escalation, then six weeks of follow-up without treatment ^[4].

Result. Under the trial-product estimand, mean percentage reductions across the cagrilintide groups were 6.0% to 10.8% (6.4–11.5 kg) against 3.0% (3.3 kg) for placebo, estimated treatment differences of 3.0% to 7.8%, p < 0.001. Against the active comparator, cagrilintide 4.5 mg reached 10.8% (11.5 kg) against 9.0% (9.6 kg) for liraglutide 3.0 mg, an estimated treatment difference of 1.8%, p = 0.03 ^[4].

Adverse events. Gastrointestinal disorders and administration-site reactions were most frequent. Gastrointestinal events occurred in 41–63% of cagrilintide participants against 32% on placebo, principally nausea at 20–47% against 18%. Permanent discontinuation occurred in 73 participants (10%), similarly across groups, mostly for adverse events (30, 4%) ^[4].

Limitations. Twenty-six weeks; a design intended to characterise the relationship between the amount administered and the response, rather than a confirmatory one; participants and investigators were masked to active versus pooled placebo but not between different active treatments, and the comparator margin against liraglutide was narrow.

Phase 2 in type 2 diabetes — the three-arm comparison

Population. 92 adults with type 2 diabetes and a body-mass index of 27 kg/m² or higher, on metformin with or without an SGLT2 inhibitor, at 17 sites in the United States. Mean age 58 years (SD 9); 64% male ^{[5, 10]}.

Endpoint and duration. Primary endpoint the change from baseline in glycated haemoglobin at 32 weeks. Randomised 1:1:1 to the combination, semaglutide alone, or cagrilintide alone, all escalated to 2.4 mg once weekly ^[5].

Result. Mean HbA1c change to week 32 was −2.2 percentage points for the combination, −1.8 for semaglutide alone and −0.9 for cagrilintide alone. The combination was superior to cagrilintide alone (estimated treatment difference −1.3 percentage points, 95% CI −1.7 to −0.8, p < 0.0001) but not to semaglutide alone (−0.4 percentage points, 95% CI −0.8 to 0.0, p = 0.075). Mean change in body mass was −15.6%, −5.1% and −8.1% respectively, the combination being greater than either single agent, p < 0.0001 for both. Continuous-glucose-monitoring time in range moved from 45.9%, 32.6% and 56.9% at baseline to 88.9%, 76.2% and 71.7% at week 32 ^[5].

Adverse events. Reported by 68%, 71% and 80% of the three groups. Mild or moderate gastrointestinal events were most common. No level 2 or 3 hypoglycaemia and no fatal adverse events ^[5].

Limitations. Ninety-two participants across three arms — roughly thirty per group — over 32 weeks, at sites in one country. This is nonetheless the most informative published trial about cagrilintide as a single agent, because it is the only one with a monotherapy arm set beside both the combination and the comparator.

Preclinical Research on Cagrilintide

In vitro research

The preclinical record published under cagrilintide's own name is thinner than for the incretin compounds it is studied alongside, and is best described for what it is: a medicinal chemistry development account rather than an in vivo pharmacology programme.

That account frames the problem in terms of physical chemistry. A hallmark of amylin is its high propensity toward the formation of amyloid fibrils, which the authors describe as making it a challenging drug design effort; the commercially available analogue pramlintide addressed that but has a short half-life and requires three daily injections. The paper reports the development of a stable, lipidated long-acting analogue and some of the structure-activity work that selected it for clinical development ^[3].

No published rodent efficacy study is cited on this page, because none was located that reports cagrilintide by name with figures that could be verified against a register. The absence is stated rather than filled: the compound's evidence base begins, in the indexed literature, at the medicinal chemistry and then moves directly into human study.

Other Areas of Cagrilintide Research

Human clinical research

Results from pharmaceutical clinical trials describe the investigational material and populations used in those studies and should not be interpreted as establishing the effects of research-grade materials offered for laboratory use.

REDEFINE 1 — phase 3a in overweight or obesity. 3,417 adults without diabetes, with a body-mass index of 30 or higher or 27 or higher with at least one obesity-related complication, randomised 21:3:3:7 to the cagrilintide–semaglutide combination (2,108), semaglutide alone (302), cagrilintide alone (302) or placebo (705), with lifestyle intervention in all groups, for 68 weeks. Coprimary endpoints were the relative change in body mass and a reduction of 5% or more against placebo. Estimated mean percentage change in body mass to week 68 was −20.4% with the combination against −3.0% with placebo, an estimated difference of −17.3 percentage points (95% CI −18.1 to −16.6, P < 0.001). Gastrointestinal adverse events affected 79.6% of the combination group against 39.9% of the placebo group, mainly transient and mild to moderate ^{[6, 12]}.

REDEFINE 2 — phase 3a with type 2 diabetes. 1,206 adults with type 2 diabetes, a body-mass index of 27 or more and glycated haemoglobin of 7 to 10%, in twelve countries, randomised 3:1 to the combination (904) or placebo (302) for 68 weeks. Estimated mean change in body mass to week 68 was −13.7% against −3.4%, an estimated difference of −10.4 percentage points (95% CI −11.2 to −9.5, P < 0.001). Glycated haemoglobin of 6.5% or less was reached by 73.5% against 15.9%. Gastrointestinal adverse events were reported by 72.5% against 34.4% ^{[7, 11]}.

Both trials studied the combination against placebo. The single-agent arms in REDEFINE 1 exist, but the comparison this page can report from the primary publication is the one the trial was designed around, which is the combination against placebo. Nothing above separates what cagrilintide contributes from what semaglutide contributes; the phase 2 trial in type 2 diabetes described in the previous section is the study that attempted that separation, and it did so in ninety-two people.

Current Research Status

Status as of September 22, 2026. This block is rendered from maintained fields, not from prose, so it cannot go stale in one place and stay current in another.

Cagrilintide vs Related Compounds

The distinction between cagrilintide and the compounds it is usually set beside is the receptor family, and nothing else stated here.

Receptor family

Cagrilintide acts at amylin receptors — calcitonin receptor complexes with receptor activity-modifying proteins ^[1]. Semaglutide, tirzepatide and retatrutide act at incretin and glucagon-family receptors. These are different branches of the class B1 receptor family.

Earlier amylin analogue

Pramlintide is the amylin analogue that preceded cagrilintide and is commercially available as an adjunct to insulin therapy. Its limitation was duration, not stability ^[3].

Why they are combined rather than compared

Because the mechanisms are independent, cagrilintide and semaglutide have been studied co-administered rather than head to head, and most of the phase 3 record describes the pair ^{[6, 7]}.

Regulatory position

Cagrilintide is investigational, alone and in combination. Semaglutide and tirzepatide are active ingredients of approved pharmaceutical products. Approval is specific to a finished product and an indication and does not extend across a pharmacological class.

No comparison of effect between these compounds is made on this page in its own voice. Where trials compared them, their populations, endpoints and limitations are given above, and the results belong to the papers that report them.

Chemical & Molecular Characteristics

Cagrilintide is a lipidated, disulfide-bridged 37-residue peptide. The backbone recorded in the FDA/NCATS Global Substance Registration System under UNII AO43BIF1U8 is KCNTATCATQRLAEFLRHSSNNFGPILPPTNVGSNTP.

Three points qualify that string, and two of them are unusual for this library.

The peptide is cyclic, not linear. The two cysteine residues near the N-terminus form an intramolecular disulfide bridge, recorded in the substance's systematic name as a cyclic disulfide. A single-letter string cannot show a bridge, so the sequence above under-describes the molecule's topology as well as its chemistry.

The lipid is not in the letters. The published description is of a stable, lipidated long-acting analogue ^[3], and the systematic name recorded against the same registry entry places a twenty-carbon diacid on the N-terminal lysine through a gamma-glutamyl linker. That modification is what converts an aggregation-prone hormone with a short half-life into a molecule with a plasma half-life measured in days ^[2].

The registers, not the catalog, are the source here. The supplier catalog record for this material carries no CAS number, no molecular formula and no molecular weight. The values published on this page — CAS 1415456-99-3, formula C194H312N54O59S2, mass approximately 4,409 g/mol — come from PubChem compound identifier 171397054 and the substance register, and are reference values for the compound rather than measurements of any particular lot. The CAS number validates against the CAS check-digit algorithm.

Analytical Specifications

Analytical figures are lot-specific. Fields the catalog does not carry for the current lot are omitted rather than filled with a typical value. The certificate of analysis and the safety data sheet for the exact lot supplied are provided with a laboratory order; no purity figure on this page is a substitute for that document.

Frequently Asked Questions

Scientific References

1. Hay DL, Chen S, Lutz TA, et al.. Amylin: Pharmacology, Physiology, and Clinical Potential Pharmacological reviews; 2015. PMID 26071095 doi:10.1124/pr.115.010629
2. Enebo LB, Berthelsen KK, Kankam M, et al.. Safety, tolerability, pharmacokinetics, and pharmacodynamics of concomitant administration of multiple doses of cagrilintide with semaglutide 2·4 mg for weight management: a randomised, controlled, phase 1b trial Lancet (London, England); 2021. PMID 33894838 doi:10.1016/S0140-6736(21)00845-X
3. Kruse T, Hansen JL, Dahl K, et al.. Development of Cagrilintide, a Long-Acting Amylin Analogue Journal of medicinal chemistry; 2021. PMID 34288673 doi:10.1021/acs.jmedchem.1c00565
4. Lau DCW, Erichsen L, Francisco AM, et al.. Once-weekly cagrilintide for weight management in people with overweight and obesity: a multicentre, randomised, double-blind, placebo-controlled and active-controlled, dose-finding phase 2 trial Lancet (London, England); 2021. PMID 34798060 doi:10.1016/S0140-6736(21)01751-7
5. Frias JP, Deenadayalan S, Erichsen L, et al.. Efficacy and safety of co-administered once-weekly cagrilintide 2·4 mg with once-weekly semaglutide 2·4 mg in type 2 diabetes: a multicentre, randomised, double-blind, active-controlled, phase 2 trial Lancet (London, England); 2023. PMID 37364590 doi:10.1016/S0140-6736(23)01163-7
6. Garvey WT, Blüher M, Osorto Contreras CK, et al.. Coadministered Cagrilintide and Semaglutide in Adults with Overweight or Obesity The New England journal of medicine; 2025. PMID 40544433 doi:10.1056/NEJMoa2502081
7. Davies MJ, Bajaj HS, Broholm C, et al.. Cagrilintide-Semaglutide in Adults with Overweight or Obesity and Type 2 Diabetes The New England journal of medicine; 2025. PMID 40544432 doi:10.1056/NEJMoa2502082
8. A Research Study of How NNC0174-0833 Taken With Semaglutide Works in People Who Are Overweight or Obese 2018. NCT03600480
9. Research Study Investigating How Well NNC0174-0833 Works in People Suffering From Overweight or Obesity. 2019. NCT03856047
10. Research Study to Look at How Well Cagrilintide Together With Semaglutide Works in People With Type 2 Diabetes 2021. NCT04982575
11. A Research Study to See How Well CagriSema Helps People With Type 2 Diabetes and Excess Body Weight Lose Weight 2023. NCT05394519
12. A Research Study to See How Well CagriSema Helps People With Excess Body Weight Lose Weight 2022. NCT05567796

Every identifier above is resolved against PubMed, Crossref or ClinicalTrials.gov at build time, and the title returned by the register is compared with the title stored here. A page does not publish if a reference fails to resolve.

Research-Use Information

For in vitro research use only. This material is a laboratory reagent. It is not a drug, food, dietary supplement, or cosmetic and is not for human or veterinary use, including ingestion, injection, or any other administration. No information on this page describes or implies any effect in humans or animals. Sold only to researchers under our Terms of Sale.

Related laboratory reagent: Cagrilintide specifications and lot documentation