RESEARCH MONOGRAPH · KDC-MN-294

Cagrilintide

May 9, 2026 Kodiac biolabs Research Revised May 30, 2026 3 min read

Our opinion on this compound

71/100

Long-acting amylin analog that's the most under-discussed half of the CagriSema story, genuinely interesting solo too

Cagrilintide is Novo Nordisk's long-acting amylin analog and honestly it's probably the most undercovered piece of metabolic pharmacology this decade. Everyone's talking about CagriSema (the cagrilintide-plus-semaglutide combination in phase 3 for obesity), but the cagrilintide-alone phase 2 data are quietly impressive in their own right. Around 10 percent body weight reduction over 26 weeks at the high dose, in a population on top of standard care, and that's monotherapy.

The molecule is amylin with substitutions that produce a once-weekly pharmacokinetic profile (C7 fatty acid attachment for albumin binding, similar conceptual approach to semaglutide's C18 diacid), plus modifications that increase potency at the amylin receptor subtypes. So you're getting the gastric emptying delay, the glucagon suppression, and the central satiety effect of the amylin pathway, but with weekly dosing instead of pre-meal pramlintide injections.

What's interesting is the additive effect with GLP-1 agonism. The phase 2 CagriSema data showed 17 percent weight loss at 32 weeks, which exceeds what either component does monotherapy and is approaching the territory tirzepatide and retatrutide occupy. The mechanism rationale is that amylin and GLP-1 hit overlapping but distinct satiety pathways, and the combination engages more of the brain weight-regulation circuitry than either alone.

What we like: phase 2 data is strong, mechanism is clean, and the receptor pharmacology of the amylin/GLP-1 combo is more interesting than the simple additive story suggests. The phase 3 (REDEFINE program) is going to be the deciding read.

What we dont love is that cagrilintide is genuinely under-discussed outside of the combination context. The monotherapy efficacy is real and the side effect profile (nausea, mostly) is class-typical without being meaningfully worse than the GLP-1s.

Sourcing for research-grade cagrilintide is tightening up. It's a peptide with a fatty acid sidechain that requires some non-trivial synthesis, and the QC needs to confirm the acyl modification cleanly. HPLC plus mass spec is mandatory, not optional. Research-grade material from competent peptide suppliers is around but the variance is wider than for the simpler peptides.

Evidence: 68
Mechanism: 85
Reliability: 72
Safety: 65
Sourcing: 60
Value: 60
Signal: 78
Staying power: 80

Plain-language summary Intrigue 75 / 100

Cagrilintide is a long-acting amylin analog from Novo Nordisk, built by attaching a fatty-acid chain to a modified amylin so it binds plasma albumin and circulates for about a week (versus less than an hour for native amylin). It uses the same long-acting trick as semaglutide. The strategic value is that combining cagrilintide with semaglutide hits both the GLP-1 and amylin systems, and phase 2 trials of the combination (CagriSema) showed weight loss exceeding semaglutide alone, approaching tirzepatide territory. Phase 3 trials are ongoing. The amylin axis is a credible second front in obesity treatment alongside the incretins. Not stocked by Kodiac. This monograph is provided for research and educational reference.

Intrigue 0–100 blends mechanism novelty, evidence strength, and translational potential. Kodiac editorial, not peer-reviewed.

Long-acting amylin analog

A long-acting amylin analog with attached fatty acid for albumin binding; under development as an obesity treatment in combination with semaglutide.

Abstract

Cagrilintide (CAS 1415456-37-9; modified amylin analog with C18 fatty acid attached at lysine for albumin binding; molecular weight approximately 4870 Da) is a long-acting amylin receptor agonist developed by Novo Nordisk for obesity. The compound is structurally derived from pramlintide with addition of a C18 fatty acid linker for albumin binding (the same long-acting strategy as semaglutide), extending plasma half-life from less than 1 hour for amylin to approximately 7 days for cagrilintide. Phase 1 and 2 trials in obesity demonstrated dose-dependent weight loss; in combination with semaglutide (the CagriSema combination), phase 2 trials showed up to 17 percent body weight loss at 32 weeks, approaching the magnitude of bariatric surgery. Phase 3 trials (REDEFINE program) are ongoing. Plasma half-life supports subcutaneous dosing. Used as the prototype long-acting amylin agonist in metabolic research.

Mechanism of action

Long-acting amylin receptor agonist with albumin-binding fatty acid extension. Mechanistic effects identical to pramlintide with extended duration.

Reported research dose ranges

Investigational; phase 2 doses 0.3 to 4.5 mg subcutaneous (often combined with semaglutide).

References

Lau DCW, et al. cagrilintide for weight management in people with overweight and obesity. Lancet 2021.
Enebo LB, et al. Safety, tolerability, pharmacokinetics, and pharmacodynamics of concomitant administration of multiple doses of cagrilintide with semaglutide 2.4 mg for weight management. Lancet 2021.
Knudsen LB, et al. The discovery and development of liraglutide and semaglutide. Front Endocrinol 2019.

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KDC-MN-294

The full reference document is provided strictly for research use only. It reports research dose ranges from the published literature, not instructions for use in humans or animals.

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Cagrilintide

Abstract

Mechanism of action

Reported research dose ranges

References

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Abstract

Mechanism of action

Reported research dose ranges

References

Read the full monograph

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