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Cagrilintide

Long-Acting Amylin Analog · CagriSema Component · Appetite Reduction

A long-acting analog of the pancreatic hormone amylin (co-secreted with insulin from beta cells). Cagrilintide reduces appetite, slows gastric emptying, and suppresses glucagon — complementary to GLP-1 agonism. Combined with semaglutide as CagriSema, the combination achieved up to 25% weight loss in trials.

Amylin receptor agonist
Long-acting weekly dosing
CagriSema + semaglutide
25% weight loss (combo)
Novo Nordisk developer
By PeptideBond Editorial Team·Sources: PubMed, FDA.gov, published clinical trials·Last updated: March 2026
Educational only — not medical advice.Disclaimer
Category
Amylin Analog
Route
SC injection (weekly)
Receptor
AMY1/AMY3 (amylin + calcitonin)
Developer
Novo Nordisk
Evidence
Phase III (CagriSema)

What Is Cagrilintide?

Cagrilintide is a long-acting acylated analog of amylin, a 37-amino-acid peptide hormone that is co-secreted with insulin from pancreatic beta cells after meals. Amylin's natural functions — slowing gastric emptying, suppressing glucagon, and promoting satiety — complement GLP-1's effects through distinct receptor pathways.

The most exciting development is CagriSema — the fixed-dose combination of cagrilintide + semaglutide in a single weekly injection. In the REDEFINE clinical program, CagriSema achieved approximately 25% weight loss — rivaling surgery and potentially superior to any current single-agent therapy.

Core Concept
Cagrilintide activates amylin receptors (AMY1 and AMY3, which are heterodimers of the calcitonin receptor with RAMP1 or RAMP3). These receptors are found in the area postrema and nucleus tractus solitarius — brainstem regions that control satiety and gastric function. By activating a DIFFERENT set of brain satiety circuits than GLP-1 (which primarily acts in the hypothalamus), cagrilintide provides additive appetite suppression when combined with semaglutide. The acylation (fatty acid conjugation) extends its half-life for once-weekly dosing.

Cagrilintide is a long-acting analog of amylin, a peptide hormone co-secreted with insulin by pancreatic β-cells after meals. Amylin complements insulin's glucose-lowering effects by slowing gastric emptying, suppressing postprandial glucagon secretion, and promoting satiety. The only previously approved amylin analog — pramlintide (Symlin) — required injection before every meal due to its short half-life. Cagrilintide's structural modifications enable once-weekly dosing, making it practical for the first time.

The most significant development for cagrilintide is its combination with semaglutide as CagriSema — Novo Nordisk's next-generation obesity treatment. Phase III trials of CagriSema have shown weight loss exceeding 20%, approaching or matching tirzepatide's results. The rationale is compelling: combining amylin receptor agonism (satiety, gastric slowing) with GLP-1 receptor agonism (appetite suppression, insulin secretion) creates a dual-pathway approach through entirely different receptor systems than tirzepatide's GLP-1/GIP mechanism.

If approved, CagriSema would give Novo Nordisk a product to compete directly with Eli Lilly's tirzepatide and potentially retatrutide, maintaining competitive positioning in the rapidly evolving obesity drug market.

>Structure & Sequence

Cagrilintide
(acylated amylin analog — modified 37aa sequence)
MW: ~4,000 Da · 37 (modified) residues
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Mechanism of Action

Cagrilintide works through amylin receptors in the brainstem, while semaglutide works through GLP-1 receptors in the hypothalamus. Because these are anatomically and pharmacologically distinct satiety pathways, combining them produces additive (possibly synergistic) weight loss. This is the same principle that makes combination drug therapy effective in other diseases — targeting multiple points in a pathway produces greater effects than maxing out a single target.

CagriSema Dual Mechanism
Cagrilintide
activates AMY1/AMY3 receptors
Brainstem
satiety signaling (area postrema)
+ Semaglutide
activates GLP-1R
Hypothalamus
appetite suppression (arcuate nucleus)
Two pathways
additive effect
Result
25% weight loss (combination)

Key Mechanisms

PathwayEffectSignificance
Amylin receptor agonismActivates AMY1/AMY3 in area postremaDistinct satiety pathway from GLP-1
Gastric slowingReduces gastric emptying rateProlongs satiety and reduces postprandial glucose spikes
Glucagon suppressionReduces inappropriate postprandial glucagonComplements GLP-1-mediated glucagon suppression
Additive with GLP-1Different brain targets = additive appetite reductionCagriSema achieves greater weight loss than either agent alone
AcylationFatty acid conjugation for albumin bindingExtends half-life for once-weekly injection

Evidence Base

StudyDesignFindingsLevel
REDEFINE 1Phase III, n=3,417, 68 weeksCagriSema 2.4mg: ~25% mean body weight loss. Superior to semaglutide 2.4mg alone (~16%).Level I
REDEFINE 2Phase III, T2DSuperior HbA1c reduction and weight loss vs semaglutide alone in T2D patientsLevel I
Cagrilintide monotherapyPhase IICagrilintide alone produced ~10-11% weight loss at highest dose over 26 weeksLevel II
CagriSema vs surgeryIndirect comparison25% weight loss approaches outcomes of sleeve gastrectomy (~25-30%)Indirect

Safety & Side Effects

GI side effects: Nausea, vomiting, and diarrhea are the most common adverse effects, consistent with amylin receptor agonism's effect on gastric motility. When combined with semaglutide (CagriSema), GI side effects may be amplified, though Phase III data suggests the combination is generally well-tolerated with gradual dose escalation.

Hypoglycemia: Amylin analogs can increase hypoglycemia risk when used with insulin. This is less of a concern with cagrilintide alone or in CagriSema for obesity (where patients are not typically on insulin), but is relevant for the Type 2 diabetes indication.

Injection site reactions: Mild injection site reactions reported in clinical trials. No significant systemic safety concerns identified in Phase III data to date.

Regulatory Status

JurisdictionStatus
FDANot yet approved. NDA submitted 2025 for CagriSema. Decision expected 2025-2026.
Novo NordiskDeveloper. Would be next-generation successor to Wegovy.
Market impactIf approved, CagriSema could become the most effective obesity medication available

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