Cagrilintide vs Semaglutide
Cagrilintide (Long-acting amylin receptor agonist (amylin analog)) and Semaglutide (GLP-1 receptor agonist) are documented as co-studied in the PeptiDex library. This page puts the two entries side by side on class, molecular weight, half-life, origin, mechanism and studied research areas — every value taken from the entry it belongs to.
Why these two are co-studied
Cross-referenced for research context — not a usage or combination recommendation.
At a glance
| Attribute | Cagrilintide | Semaglutide |
|---|---|---|
| Compound class | Long-acting amylin receptor agonist (amylin analog) | GLP-1 receptor agonist |
| Research category | GLP-1 Family | GLP-1 Family |
| Length (amino acids) | Not documented | 31 amino acids |
| Molecular weight | ~3731 g/mol | 4113.6 g/mol |
| Half-life | ~7 days | ~7 days |
| Origin | An investigational long-acting amylin analog developed by Novo Nordisk, studied both alone and in combination with semaglutide. It has been evaluated in clinical trials in the 2020s. | Developed by Novo Nordisk as a long-acting analog of the human incretin hormone GLP-1, building on the earlier once-daily liraglutide. It received first regulatory approvals in 2017 (injectable) and 2019 (oral). |
“Not documented” means the PeptiDex entry records no value for that field. Nothing on this page is estimated, and no figure is carried over from one compound to the other.
How Cagrilintide works
Cagrilintide is a modified, long-acting analog of the pancreatic hormone amylin that acts as an agonist at amylin and calcitonin receptors. Amylin signaling promotes satiety, slows gastric emptying, and reduces food intake through central and peripheral pathways distinct from the incretin (GLP-1) system. Structural modifications and acylation extend its half-life to support once-weekly administration.
How Semaglutide works
Semaglutide is a structurally modified analog of native glucagon-like peptide-1 (GLP-1) that binds and activates the GLP-1 receptor. Receptor activation enhances glucose-dependent insulin secretion, suppresses glucagon release, slows gastric emptying, and acts on central appetite-regulating pathways to reduce food intake. Its backbone modifications and a C18 fatty-acid (diacid) side chain promote albumin binding and resistance to DPP-4 degradation, giving it a prolonged duration of action.
Mechanistic descriptions reflect published research-literature understanding and are quoted from each compound's own entry. Much peptide research is preclinical (in-vitro or animal-model); mechanism in humans may differ and is not established for many compounds.
Where each one appears in the literature
The research contexts each entry documents. Listing a research area is not a claim of efficacy or a therapeutic indication, and the two lists are not scored against each other.
Described in identical terms for both
Cagrilintide
Semaglutide
What sets each apart
Cagrilintide
Cagrilintide is an amylin analog, not a GLP-1 or GIP agonist, so it acts through a different appetite-regulating pathway and is often studied in combination with incretin agents.
Semaglutide
Unlike dual or triple agonists, semaglutide is a selective GLP-1 receptor agonist. Its once-weekly dosing and availability in an oral form distinguish it from the older once-daily liraglutide.
Frequently asked questions
What is cagrilintide's half-life and dosing frequency?
Cagrilintide has a reported half-life of roughly 7-8 days (about 160-195 hours), thanks to lipid-modification-based half-life extension, which supports once-weekly administration in the literature. Its weekly kinetics make it a convenient partner for the weekly GLP-1 agonist semaglutide. Steady state is reached over several weeks of weekly dosing.
How does cagrilintide differ from a GLP-1 agonist like semaglutide?
Cagrilintide works through the amylin/calcitonin receptor system, whereas semaglutide works through the GLP-1 receptor. Because the pathways are distinct, the two are studied together for potentially additive effects — the basis of the CagriSema combination. Cagrilintide alone is less extensively characterized than semaglutide.
What is cagrilintide and what receptor class does it act on?
Cagrilintide (AM833) is a long-acting amylin analogue — it acts as an agonist at amylin and calcitonin receptors rather than the GLP-1 receptor. In research it is studied for satiety signaling, slowed gastric emptying, and body-weight effects, and it is the amylin half of the CagriSema combination. Its mechanism is complementary to, not overlapping with, GLP-1 agonists.
What is semaglutide and what receptor does it target?
Semaglutide is a long-acting GLP-1 (glucagon-like peptide-1) receptor agonist derived from the native GLP-1 peptide with amino-acid substitutions and a C18 fatty-diacid chain that binds albumin to extend its half-life. In research it is studied as a reference GLP-1 agonist in models of glucose regulation, appetite/food intake, and body-weight change. It is the mono-agonist against which many newer multi-receptor compounds are benchmarked.
What does semaglutide's long half-life mean for research design?
Semaglutide has a reported plasma half-life of roughly 7 days (about 155-184 hours), which is why once-weekly administration is used in the published literature. Steady-state concentrations are typically reached after about 4-5 weeks at a given dose level, so study designs generally include a multi-week dose-escalation before any maintenance-phase readout. This slow kinetics also means washout after discontinuation spans several weeks.
How is semaglutide dose-escalated in the research literature?
Published protocols use a stepwise weekly escalation, commonly 0.25 mg, then 0.5, 1.0, 1.7, and up to 2.4 mg once weekly, with each step typically held about 4 weeks. Escalation is used in the literature to reduce gastrointestinal tolerability issues rather than starting at the top dose. These are reference figures for research context only, not dosing guidance for humans.
Answers are the ones published on each compound's own PeptiDex entry. They are educational summaries of research-literature context and are not medical advice.