Cagrilintide (AM833) is a synthetic, acylated long-acting peptide developed by Novo Nordisk as an amylin analogue — an agonist of the amylin (islet-amyloid-polypeptide) receptors rather than a member of the incretin family. Where GLP-1 compounds such as Semaglutide act through incretin biology, Cagrilintide engages a separate, complementary satiety pathway centred on the brainstem. That distinction is precisely why it is studied as the companion to Semaglutide in the CagriSema research programme, one of the most closely watched weight-management combinations in metabolic science.
Cagrilintide (AM833) is a long-acting amylin analogue — an amylin/islet-amyloid-polypeptide receptor agonist, not an incretin — developed by Novo Nordisk and studied on a once-weekly research schedule. Its defining role is as the companion to Semaglutide 2.4 mg in the combination known as CagriSema. In a Phase 1b combination trial (The Lancet, 2021) cagrilintide plus semaglutide produced roughly 15.7% (1.2 mg) to 17.1% (2.4 mg) weight loss over 20 weeks versus about 9.8% for semaglutide alone; Phase 2 monotherapy dose-finding reported dose-dependent weight loss up to ~10.8% at 4.5 mg over 26 weeks. CagriSema advanced to the Phase 3 REDEFINE obesity programme, with results reported in 2025. It has a ~7–8-day half-life, is supplied as a lyophilised powder reconstituted with bacteriostatic water, and remains an investigational compound for in vitro research use only — not approved for human use. Research-grade Cagrilintide is available from RS Bio Labs in two strengths at ≥99% purity; see the buy Cagrilintide UK page.
Cagrilintide, known by its developer code AM833, is a synthetic long-acting analogue of amylin (islet amyloid polypeptide, IAPP) engineered by Novo Nordisk. Amylin is a 37-amino-acid neuroendocrine hormone co-secreted with insulin from pancreatic β-cells that regulates postprandial glucagon, slows gastric emptying and promotes satiety. Cagrilintide is an amylin receptor agonist — and this is the single most important thing to understand about it: it belongs to a different pharmacological class from the incretins. It is not a GLP-1, GIP or glucagon agonist. It acts through the amylin/calcitonin-receptor system rather than the incretin axis.
That class distinction is not a technicality; it is the whole point of the compound's research programme. Because amylin engages satiety circuits that only partially overlap with those recruited by GLP-1, cagrilintide is studied not as a rival to the incretins but as a partner to them. Its most prominent application is the combination with Semaglutide 2.4 mg — the fixed-dose research combination branded CagriSema — which pairs amylin agonism with GLP-1 agonism in a single once-weekly regimen. The hypothesis is that two mechanisms acting on complementary pathways deliver additive, and possibly synergistic, weight-management effects.
As of 2026 Cagrilintide is an investigational compound; the CagriSema combination reached Phase 3 in the REDEFINE obesity programme and it is not approved by any regulator. RS Bio Labs supplies it strictly as a research reagent for in vitro laboratory work. Researchers looking to buy Cagrilintide in the UK can obtain it in two strengths, each third-party HPLC tested to ≥99% purity.
Cagrilintide emerged from Novo Nordisk's long-running work on amylin pharmacology. The scientific lineage runs from native amylin — a hormone that, like native GLP-1, is rapidly cleared and prone to aggregation — through the first-generation short-acting analogue pramlintide, to the acylated, plasma-stable, long-acting analogue that became AM833.
Native human amylin is a poor drug candidate: it has a very short circulating half-life and an intrinsic tendency to form amyloid fibrils. Pramlintide, a soluble non-aggregating analogue, solved the aggregation problem but retained a short duration of action requiring multiple daily doses. Cagrilintide's engineering objective was a once-weekly amylin analogue — achieved through a C20 fatty-diacid acylation strategy conceptually similar to the one Novo Nordisk used to make semaglutide long-acting, which promotes reversible albumin binding and greatly extends the half-life.
The compound's clinical debut came in the Phase 1b combination trial reported in The Lancet in 2021 (Enebo and colleagues), which studied concomitant administration of multiple doses of cagrilintide with semaglutide 2.4 mg for weight management. That study established both the tolerability of the combination and the additive-effect signal that drove the subsequent programme. Monotherapy dose-finding followed, and the CagriSema combination advanced into the Phase 3 REDEFINE programme in obesity, with results reported in 2025.
Cagrilintide is an agonist at the amylin receptors — heterodimeric complexes formed by the calcitonin receptor paired with receptor activity-modifying proteins (RAMP1, RAMP2 and RAMP3), giving the AMY₁, AMY₂ and AMY₃ subtypes. This is a fundamentally different receptor system from the class B incretin receptors targeted by GLP-1 and GIP compounds. The principal sites of action relevant to weight-management research lie in the brainstem — the area postrema and the dorsal vagal complex — where amylin signalling drives satiety and slows gastric emptying.
The combination thesis is the crux of the design. Amylin acts predominantly through the brainstem, whereas GLP-1 recruits additional hypothalamic and vagal satiety circuits; because the two pathways are only partially overlapping, agonising both simultaneously is expected to produce a larger appetite-suppressing effect than either alone. This is why cagrilintide is developed as the amylin arm of CagriSema rather than positioned against the incretins — it adds a mechanism the incretins do not supply. For a broader treatment of how the incretin classes differ from one another, see our guide to GLP-1 vs GIP vs glucagon agonists; cagrilintide sits outside all three of those, in the amylin class.
Cagrilintide's clinical evidence base centres on two themes: monotherapy dose-finding, and — far more prominently — the combination with semaglutide. The key readouts are summarised below, followed by the individual trial cards.
| Trial / population | Publication | n | Headline result |
|---|---|---|---|
| Phase 1b · Cagrilintide + Semaglutide 2.4 mg | The Lancet, 2021 | 285 | ~15.7% (1.2 mg) to ~17.1% (2.4 mg) at 20 wk vs ~9.8% semaglutide alone |
| Phase 2 · Cagrilintide monotherapy (dose-finding) | Dose-finding, 26 wk | 706 | Dose-dependent weight loss up to ~10.8% at 4.5 mg |
| Phase 2 · CagriSema vs components (T2D) | The Lancet, 2023 | — | CagriSema superior to semaglutide or cagrilintide alone |
| Phase 3 · REDEFINE (obesity) | Reported 2025 | — | Pivotal CagriSema obesity programme |
Cagrilintide's defining pharmacokinetic feature is its terminal half-life of approximately seven to eight days. This is a direct consequence of the molecule's C20 fatty-diacid acylation, which drives reversible binding to serum albumin. Albumin binding acts as a circulating reservoir, slows renal clearance, and shields the peptide from rapid proteolytic degradation — the same design principle used across Novo Nordisk's long-acting peptide portfolio, including semaglutide.
A ~7–8-day half-life supports a once-weekly research schedule and, crucially, matches the dosing cadence of the GLP-1 partner in CagriSema, allowing both components to be administered on the same weekly rhythm. As with any compound dosed at roughly one half-life intervals, plasma concentrations accumulate over successive administrations and approach steady state after about four to five half-lives — on the order of four to six weeks. This accumulation behaviour is why published protocols use gradual dose escalation: titrating upward over several weeks allows tolerance to the gastrointestinal effects to develop as concentrations rise.
| Parameter | Value (approx.) | Note |
|---|---|---|
| Terminal half-life | ~7–8 days | Fatty-acid/albumin driven |
| Research schedule | Once weekly | ~1 half-life dosing interval |
| Time to steady state | ~4–6 weeks | ~4–5 half-lives |
| Receptor system | Amylin / calcitonin (AMY₁₋₃) | Distinct from incretin receptors |
| Elimination | Proteolysis + renal | Slowed by albumin binding |
As a lyophilised (freeze-dried) powder, Cagrilintide is highly stable. Removing water from the formulation dramatically slows the chemical degradation pathways — hydrolysis, deamidation, oxidation and aggregation — that shorten a peptide's shelf life in solution. Amylin-family peptides are historically prone to aggregation, which is precisely why the acylated analogue was engineered for solubility and stability; sealed, protected from light and kept cool, lyophilised Cagrilintide retains its integrity over long periods.
Stability falls once the powder is reconstituted. In solution the peptide becomes susceptible to gradual hydrolysis and to physical stresses such as agitation (which can cause aggregation and foaming) and repeated freeze–thaw cycles (which mechanically damage peptide structure). Heat and light accelerate degradation in both states. In practical terms this means the lyophilised vial is the storage-stable form, and the reconstituted solution should be treated as a shorter-lived working stock — see Storage and Reconstitution below.
Correct storage preserves both the mass and the biological integrity of the compound. The guidance below reflects standard best practice for lyophilised research peptides.
| State | Temperature | Approx. shelf life | Notes |
|---|---|---|---|
| Lyophilised | −20 °C (freezer) | Months to years | Best long-term option; protect from light |
| Lyophilised | 2–8 °C (fridge) | Weeks to months | Fine for medium-term storage |
| Lyophilised | Room temperature | Days (transit) | Tolerates brief shipping periods |
| Reconstituted | 2–8 °C (fridge) | ~4–6 weeks | Bacteriostatic water aids stability; keep dark |
| Reconstituted | Frozen | Avoid | Freeze–thaw degrades the peptide |
Label reconstituted vials with the date of preparation, minimise exposure to light and heat, and avoid repeatedly warming and cooling a working stock. Allow refrigerated vials to return toward room temperature before handling to reduce condensation.
The following describes standard laboratory technique for preparing a research stock solution from a lyophilised vial. It is not guidance for human use of any kind.
Reconstitution simply means dissolving the freeze-dried powder into solution. The standard diluent for a multi-use research vial is bacteriostatic water (water with 0.9% benzyl alcohol, which suppresses microbial growth). You will also need a sterile syringe and alcohol wipes. Technique matters: wipe the vial stopper, draw the chosen volume of bacteriostatic water, and add it slowly down the inner glass wall rather than squirting it directly onto the powder. Let the peptide dissolve, swirl gently, and never shake — agitation causes foaming and can damage the peptide.
Concentration is simply the mass of peptide divided by the volume of water added. Adding more water gives a lower concentration:
| Vial | Bacteriostatic water added | Resulting concentration |
|---|---|---|
| 5 mg | 1 ml | 5 mg/ml |
| 5 mg | 2 ml | 2.5 mg/ml |
| 10 mg | 1 ml | 10 mg/ml |
| 10 mg | 2 ml | 5 mg/ml |
| 10 mg | 4 ml | 2.5 mg/ml |
Once reconstituted, store the vial refrigerated at 2–8 °C and use it within a few weeks (see Storage). Maintain sterility throughout and label the vial with the concentration and preparation date.
Cagrilintide is best understood by contrast with the incretin compounds it is studied alongside. It is an amylin analogue — a different pharmacological class from the GLP-1, GIP and glucagon agonists — and rather than competing with them it is developed as the amylin partner to Semaglutide in CagriSema. The table below places it against the most-studied incretin research peptides, with the amylin-versus-incretin distinction highlighted. For the mechanistic detail behind the incretin classes, see GLP-1 vs GIP vs glucagon.
| Compound | Receptor target | Class | Peak trial weight change | Half-life |
|---|---|---|---|---|
| Cagrilintide | Amylin / calcitonin | Amylin analogue | ~10.8% mono; ~17.1% with sema | ~7–8 days |
| CagriSema (Cagri + Sema) | Amylin + GLP-1 | Amylin + incretin | ~15.7–17.1% (Ph1b, 20 wk) | Weekly |
| Semaglutide | GLP-1 | Incretin (mono) | ~15% (Ph3, 68 wk) | ~7 days |
| Tirzepatide | GIP + GLP-1 | Incretin (dual) | ~22.5% (Ph3, 72 wk) | ~5 days |
| Retatrutide | GIP + GLP-1 + Glucagon | Incretin (triple) | ~24.2% (Ph2, 48 wk) | ~6 days |
The key takeaway is the class boundary: Semaglutide, Tirzepatide and Retatrutide are all incretin agonists that differ only in how many incretin receptors they engage, whereas Cagrilintide sits in the separate amylin class. That is exactly why it is combined with an incretin rather than compared against one — CagriSema stacks two mechanisms. To compare live pricing and strengths, see the buy Cagrilintide UK and Semaglutide pages.
The findings above are drawn from the following peer-reviewed publications and trial registrations. Links open on the publisher or registry site.