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CagrilintideClinical evidence

Long-acting amylin analog

A long-acting analog of amylin, the satiety hormone co-secreted with insulin, researched for obesity both alone and combined with semaglutide (CagriSema).

📋 Regulatory status

Investigational — phase 3. Not approved as a standalone medicine.

Also known as: AM833

⚙️ How it works

Cagrilintide mimics amylin and acts as an agonist at brain amylin receptors AMY1 and AMY3 — calcitonin-receptor cores paired with receptor-activity-modifying proteins — in the hindbrain and hypothalamus. Through these it engages both homeostatic and reward-related appetite circuits, reducing food intake. It also slows gastric emptying and promotes satiety, a pathway distinct from GLP-1 signalling, which is why the two add together rather than overlap. Acylation extends its half-life enough for once-weekly use.

🔬 What the research found

In the phase 3 REDEFINE programme, cagrilintide alone produced roughly 11.8% body-weight reduction at 68 weeks versus about 2.5% on placebo. Combined with semaglutide (CagriSema), mean reduction reached about 20.4% at 68 weeks, beating semaglutide alone (~14.9%) and cagrilintide alone (~11.5%) — evidence of a genuinely additive dual-pathway effect. Mechanistic work confirmed brain amylin receptors AMY1 and AMY3 mediate the weight effect.

We report both positive and negative trial results. For exact study protocols, read the sources — we cite them rather than repackage them.

🎯 What it's studied to help

Bars reflect the strength & volume of research evidence for each use — not a guarantee of results.

Amylin-receptor agonism suppresses appetite and slows gastric emptying, producing double-digit weight loss in phase 3 trials.
Slows gastric emptying and alters satiety signalling — which underlies both its efficacy and its GI side effects.

⚠️ Side effects reported in studies

Predominantly gastrointestinal, as with the amylin and incretin class — nausea, vomiting and constipation — usually mild to moderate and most frequent during dose escalation in trials. Injection-site reactions were also reported.

🔗 Often researched alongside

Semaglutide — additive: amylin-receptor satiety plus GLP-1 signalling suppress appetite more than either alone (the CagriSema rationale). Tirzepatide — discussed comparatively as a rival multi-pathway approach.

Mechanistic context only — we don't publish combinations, amounts or protocols.

⚖️ How it compares

Closest to pramlintide, the first-generation amylin analog, but acylation gives cagrilintide a far longer half-life. Versus semaglutide it works through amylin rather than incretin receptors — a different pathway, which is exactly why the combination outperforms either.

❓ Frequently asked

Is it a GLP-1 drug?

No. It is an amylin analog acting on amylin receptors — a separate satiety pathway that can add to GLP-1 effects.

What is CagriSema?

A fixed combination of cagrilintide and semaglutide, studied for greater weight loss than either component alone.

Is it approved?

Not as of the latest available data — it remains investigational in phase 3.

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⚠️ Educational research information only — not medical advice. Many peptides are sold strictly for laboratory research and are not approved treatments. The evidence scores reflect research interest and strength, not efficacy or safety for any individual. Always consult a qualified professional.