Peptide comparison
Cagrilintide vs Semaglutide
Cagrilintide and Semaglutide are both research peptides. This side-by-side compares their mechanism, typical research dosing, half-life, routes and safety so you can see how they differ. For research use only.
Reviewed by the Helica Labs research team · Last updated August 5, 2026
| Cagrilintide | Semaglutide | |
|---|---|---|
| Category | Metabolic | Metabolic |
| Overview | A long-acting acylated amylin analogue under clinical development by Novo Nordisk, studied primarily in combination with semaglutide for obesity; research use only. | GLP-1 receptor agonist with strong human-trial evidence for weight loss, glycemic control, and cardiovascular risk reduction. |
| How it works | Amylin is a 37-amino-acid peptide co-secreted with insulin by pancreatic beta-cells in response to meals. It acts primarily through amylin receptors (AMY1–3, heterodimers of the calcitonin receptor and receptor activity-modifying proteins RAMP1–3) in the area postrema and nucleus accumbens of the brain to promote satiety and reduce food intake. Native amylin also slows gastric emptying, suppresses post-prandial glucagon secretion, and modulates the dopaminergic reward circuitry involved in food motivation. Cagrilintide was designed to recapitulate these actions with sustained receptor engagement. Its fatty-diacid acylation confers reversible albumin binding that dramatically reduces renal clearance and peptidase degradation, extending the half-life from minutes (native amylin) to approximately seven days. In preclinical and clinical data, cagrilintide reduces caloric intake, lowers body weight through fat mass reduction, and suppresses glucagon — actions that are mechanistically complementary rather than redundant to GLP-1 receptor agonists such as semaglutide, which act through a distinct receptor system and have stronger effects on gastric emptying. This complementarity is the pharmacological rationale for the CagriSema combination. Human receptor-binding and signalling data are consistent with the proposed amylin-receptor mechanism, though the full characterisation of downstream neural pathways in humans remains an active area of research. | Semaglutide selectively activates the GLP-1 receptor, mimicking the incretin hormone GLP-1. It enhances glucose-dependent insulin secretion and suppresses glucagon release (lowering blood glucose with low intrinsic hypoglycemia risk), slows gastric emptying, and acts on appetite-regulating centers in the hindbrain and hypothalamus to increase satiety and reduce food intake. The glucose-dependent nature of its insulinotropic effect means insulin is stimulated mainly when blood glucose is elevated. Its long duration of action is driven by albumin binding and resistance to enzymatic degradation rather than by a different receptor target. |
| Half-life | Approximately 184 ± 7.4 hours (~7.7 days) at the 2.4 mg dose in human pharmacokinetic studies; range across doses approximately 159–195 hours. Time to maximum concentration (Tmax) is approximately 24 hours after subcutaneous injection. Steady-state is reached after approximately 4–5 weekly doses. This is markedly longer than native amylin (~15 minutes) or pramlintide (~50 minutes), attributable to albumin-binding via the fatty-diacid acylation. | ~1 week (~160 hours) |
| Dosing reference | Studied in clinical trials at weekly subcutaneous doses of 0.16 mg, 0.3 mg, 0.6 mg, 1.2 mg, 2.4 mg, and 4.5 mg, with dose escalation schedules. Phase 3 CagriSema trials pair cagrilintide 2.4 mg with semaglutide 2.4 mg in a once-weekly fixed-ratio injection. These doses are investigational; cagrilintide has no approved therapeutic dosing. | For type 2 diabetes (Ozempic), subcutaneous dosing typically starts at 0.25 mg once weekly for 4 weeks (a non-therapeutic initiation dose), increasing to 0.5 mg/week, then up to 1 mg or 2 mg/week as needed and tolerated. For chronic weight management (Wegovy), a stepwise 16-week escalation is used: 0.25 mg, 0.5 mg, 1 mg, 1.7 mg, then a 2.4 mg/week maintenance dose. Slow titration is emphasized to limit gastrointestinal side effects; rapid escalation has been linked to severe GI complications including gastroparesis. |
| Routes | subcutaneous | subcutaneous, oral |
| Safety & side effects | In Phase 1 and Phase 2 clinical trials, the most common adverse events were gastrointestinal: nausea, vomiting, diarrhoea, and constipation, consistent with the amylin mechanism of gastric-emptying slowing. These were typically mild-to-moderate and occurred most frequently during dose escalation. No serious unexpected safety signals have been publicly reported through Phase 2 data, though Phase 3 follow-up is ongoing. Theoretical and class-related risks include: injection-site reactions, hypoglycaemia when combined with insulin or sulfonylureas (amylin receptor agonism suppresses glucagon counter-regulation), and the potential for prolonged nausea or vomiting in sensitive individuals. Long-term safety data beyond 68 weeks of Phase 3 exposure are not yet available. As with all novel investigational compounds, the full safety and tolerability profile will not be established until Phase 3 data are complete and regulatory review is conducted. Cagrilintide is not an approved drug. Material sold outside of trials is unregulated and not subject to pharmaceutical quality controls. It is not permitted in competitive sport under WADA's S0 category (non-approved substances). This information is for research reference only. | Most common side effects are gastrointestinal: nausea, vomiting, diarrhea, constipation, and abdominal pain, usually mild-to-moderate and most pronounced during dose escalation. More serious but less common risks include acute pancreatitis, gallbladder disease (cholelithiasis/cholecystitis), and, with rapid dose escalation, gastroparesis. Hypoglycemia risk rises when combined with insulin or sulfonylureas. In rodents semaglutide caused dose-dependent thyroid C-cell tumors; human relevance is considered low, but it is contraindicated in those with personal/family history of medullary thyroid carcinoma or MEN 2, and in pregnancy. Worsening diabetic retinopathy was noted in SUSTAIN-6. Rapid weight loss may contribute to lean-mass loss. Use only under medical supervision; gray-market product carries purity and dosing-accuracy risks. |
For research use only. Not for human consumption. Always verify against current literature.
Frequently asked questions
- What is the difference between Cagrilintide and Semaglutide?
- Cagrilintide is categorised as a Metabolic research peptide, while Semaglutide is categorised as Metabolic. This page sets their mechanism, research dosing, half-life and routes side by side so you can compare them. Both are supplied strictly for laboratory research use only.
- What are the half-lives of Cagrilintide and Semaglutide?
- The reported half-life of Cagrilintide is Approximately 184 ± 7.4 hours (~7.7 days) at the 2.4 mg dose in human pharmacokinetic studies; range across doses approximately 159–195 hours. Time to maximum concentration (Tmax) is approximately 24 hours after subcutaneous injection. Steady-state is reached after approximately 4–5 weekly doses. This is markedly longer than native amylin (~15 minutes) or pramlintide (~50 minutes), attributable to albumin-binding via the fatty-diacid acylation., while Semaglutide is ~1 week (~160 hours). These figures are drawn from the research literature and are provided for reference only, not as dosing guidance.
- How are Cagrilintide and Semaglutide administered in research?
- In the literature, Cagrilintide is studied via subcutaneous, while Semaglutide is studied via subcutaneous, oral. This is reference information about the compounds for laboratory research only — not directions for use.
- Can Cagrilintide or Semaglutide be used in humans?
- No. Both Cagrilintide and Semaglutide are sold strictly as research chemicals for laboratory research use only. They are not medicines, are not for human or veterinary consumption, and nothing on this page is medical or dosing advice.