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A specimen of the Metabolic drawer Drawer A · Metabolic

Amycretin

Investigational

A novel single-molecule dual GLP-1/amylin receptor agonist developed by Novo Nordisk. Unlike CagriSema (a fixed-dose combination), amycretin is a unified peptide that activates both pathways. Phase 1 trials showed superior weight loss signals versus semaglutide, with both oral and subcutaneous formulations in development.

NNC0487-0111 · Oral Amycretin · Subcutaneous Amycretin

Research evidence
Moderate

8 human studies

Preclinical
33%
Clinical
67%

Based on 12 cited sources

Evidence Score62/100
Emerging / moderate
Research Depth70/100
Mechanism80/100
Plausibility89/100
Global Coverage27/100
Community Experience18/100
Effectiveness82/100

clinically demonstrated · low confidence

Demonstrated effect magnitude — not a recommendation or safety claim.

ResearchDepth: two placebo-controlled phase 1/1b-2a Lancet RCTs (oral PMID:40550229, SC PMID:40550231), total human N <300, no SR yet. Mechanism: well-characterized dual GLP-1R + amylin-receptor agonism with mapped hypothalamic/area-postrema pathways and SC dose-response. Plausibility: full mechanism-to-weight-loss chain, coherent with incretin biology, strong same-class analogy (semaglutide, CagriSema). GlobalCoverage: single-sponsor, single US site, not yet independently replicated, advancing to phase 3. CommunityExperience: investigational, negligible real-world use outside trials. Effectiveness basis clinical: SC amycretin ~24% weight loss (placebo-subtracted ~23pp) far exceeds obesity MCID; confidence low (early small phase 1/2 data, one sponsor).

Scored May 2026 How we rate →
~
Evidence Level
moderate
Not approved for human use by any regulatory agency
Limited human clinical trial data
Consult a healthcare provider before use
Not FDA Approved WADA Prohibited
Identity
SCALE · 1:1 N-TERMINUS C-TERMINUS Not disclosed
Also Known As
NNC0487-0111 • Oral Amycretin • Subcutaneous Amycretin
Class
Dual GLP-1/Amylin agonist (acylated peptide)
Length
0 amino acids
Mol. weight
Not disclosed
Sequence
Proprietary (not publicly disclosed)
Molecular Structure
Hydrophobic
Polar
Positive
Negative

The proposed mechanisms of amycretin are based on Phase 1 clinical data and extensive preclinical validation of the dual GLP-1/amylin pathway approach.

How It Works (Simplified)

Amycretin is a single molecule designed to activate two appetite-control systems simultaneously:

GLP-1 Activation

Activates GLP-1 receptors in hypothalamus for appetite suppression and pancreas for glucose-dependent insulin release, like semaglutide.

Amylin Activation

Activates amylin receptors in brainstem (area postrema) providing a second, independent satiety signal through different neural circuits.

Leptin Sensitization

Amylin pathway restores responsiveness to leptin in obesity, a mechanism not achieved by GLP-1 agonists alone.

Engineered for oral delivery using absorption enhancer technology, enabling once-daily pill format versus weekly injections.

Key Research: Roth JD et al. (2008) demonstrated amylin restores leptin sensitivity in obesity. PMID:18458326

Important Limitations

  • Peer-reviewed efficacy data are limited to early-phase trials (phase 1 oral and phase 1b/2a subcutaneous, both published in The Lancet in 2025); phase 3 outcome data are not yet available
  • A large phase 3 program (AMAZE) and phase 2/3 type 2 diabetes trials are registered and underway, but their results have not yet been published
  • Subcutaneous phase 1b/2a trial had a high participant withdrawal rate, which limits interpretation of the bodyweight findings
  • Long-term safety beyond 36 weeks not established
  • Head-to-head comparisons with semaglutide/tirzepatide are indirect only
  • Molecular structure and sequence not publicly available
i. GLP-1 Pathway · Hypothalamic Satiety
AmycretinGLP-1R activationPOMC/CART neuronsSatiety signalNPY/AgRP inhibitionReduced hungerPancreatic beta cellsInsulin secretion
ii. Amylin Pathway · Brainstem Satiety
AmycretinAMY1/AMY3 receptorsArea postrema activationMeal terminationLeptin sensitizationEnhanced satiety
Mechanism GLP-1 receptor activation in hypothalamus and pancreas
Established 8 direct studies
Benefit shown to reduce body weight and improve glycemic control
Evidence Level
Moderate
4 Human
2 Animal
2 In Vitro
Mechanism Amylin receptor activation in area postrema/brainstem
Established 6 direct studies
Benefit appears to enhance satiety through independent neural pathway
Evidence Level
Moderate
2 Human
3 Animal
1 In Vitro
Mechanism Delayed gastric emptying via dual pathway activation
Supported 4 direct studies
Benefit may prolong post-meal satiety and reduce food intake
Evidence Level
Low
2 Human
2 Animal
Mechanism Glucose-dependent insulin secretion enhancement
Established 5 direct studies
Benefit shown to improve glycemic control with low hypoglycemia risk
Evidence Level
Moderate
3 Human
2 Animal
Mechanism Confidence
Established
Supported
Emerging
Evidence Level
High
Moderate
Low
Very Low
Phase 01 1
Week 1-4

Based on GLP-1/amylin class effects: Initial appetite suppression and reduced food intake. GI side effects (nausea, reduced appetite) most common during this period. Weight loss begins, typically 2-4% in first month.

Phase 02 2
Week 4-12

Oral phase 1 data: weight reduction observed over the 12-week multiple-ascending-dose period as dose escalation completes. GI tolerability typically improves after initial weeks.

Phase 03 3
Week 12-24

Continued weight loss trajectory. In the subcutaneous phase 1b/2a trial, weight loss continued beyond week 12. Metabolic improvements (if diabetic) would be expected based on class effects.

Phase 04 4
Week 24-36

Subcutaneous phase 1b/2a trial reported bodyweight reductions of up to ~24% vs placebo at week 36 (60 mg arm). Weight loss may begin plateauing at higher doses. Long-term tolerance and adherence not yet characterized.

Research-based observations

This timeline reflects observations from published clinical and preclinical studies. Individual responses may vary significantly. This is not a guarantee of effects or a dosing schedule. Consult qualified healthcare providers for personalized guidance.

Good Signs (4 indicators)
Amycretin is in development by Novo Nordisk (not available through compounding)
Clinical trials through registered sites only
No legitimate source for amycretin outside clinical trials
Novo Nordisk has not licensed manufacturing to any third party
Warning Signs (3 indicators)
Any claim to sell amycretin is suspect (still investigational)
Sources claiming 'research chemical' amycretin should be avoided
No COA can be valid for a proprietary investigational compound
Bad Signs (4 indicators)
Any product claiming to be amycretin available for purchase
Underground lab or 'research peptide' marketing
Claims of early access or leaked compound
Any non-clinical-trial source is fraudulent
Positive quality indicator
Requires evaluation
Potential quality issue

For Research Evaluation Only

These quality indicators are general guidelines based on typical peptide characteristics. Professional laboratory testing (HPLC, mass spectrometry) provides definitive quality verification. This checklist is for initial visual evaluation only.

Synergistic
Compatible
Caution
Avoid

Both are GLP-1 receptor agonists. Combining would result in overlapping mechanisms with potential for additive GI side effects. Not intended for concurrent use.

Both target GLP-1 receptor with additional mechanisms. Concurrent use would provide overlapping GLP-1 activity. Not recommended for combination.

Both are GLP-1 receptor agonists. Overlapping mechanisms would not provide additive benefit and may increase adverse event risk.

CagriSema contains both GLP-1 and amylin agonist components. Amycretin duplicates this dual mechanism in a single molecule. Combination would be redundant and potentially unsafe.

Amycretin already incorporates amylin receptor agonism. Adding cagrilintide would duplicate the amylin pathway with no expected additional benefit.

Research Note: Interaction data is based on published literature, mechanistic understanding, and theoretical considerations. Most peptide combinations lack direct clinical study. This information is for educational purposes only and does not constitute medical advice. Always consult qualified healthcare providers.

This dossier synthesizes available evidence from peer-reviewed literature, regulatory documents, and clinical trial registries. Evidence strength ratings follow a modified GRADE approach.

For complete methodology details, see our Methodology page.

Important Disclaimer

This dossier is for educational purposes only and does not constitute medical advice. Always consult a qualified healthcare provider before making health decisions.

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