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A specimen of the Metabolic drawer Drawer A · Metabolic

AOD-9604

Research Only

A modified fragment of human growth hormone (amino acids 176-191 with N-terminal tyrosine) studied for fat loss. Clinical development discontinued after Phase 2b/3 trials failed to show efficacy in 536 subjects. Now prohibited by WADA and excluded from FDA compounding.

Anti-Obesity Drug 9604 · Tyr-hGH Fragment 177-191 · hGH Fragment 176-191

Research evidence
Low

6 human studies

Preclinical
40%
Clinical
30%

Based on 20 cited sources

Evidence Score62/100
Emerging / moderate
Research Depth69/100
Mechanism81/100
Plausibility53/100
Global Coverage36/100
Community Experience62/100
Effectiveness22/100

clinically demonstrated · low confidence

Demonstrated effect magnitude — not a recommendation or safety claim.

Research depth: two multicenter RCTs (Phase 2a positive, pivotal Phase 2b/3 OPTIONS n=536 null), >800 human subjects, direct obesity outcome. Mechanism: well-characterized in rodents — beta-3-AR KO mice abolish the effect, cAMP/PKA to HSL lipolysis chain mapped. Plausibility: chain breaks at human translation; beta-3-AR human relevance contested and pivotal trial failed. Global coverage: ~20 studies, largely one research cluster, WADA-listed, no approval. Community: >7 years of clinic use with mixed, modest reports. Effectiveness basis clinical — early-phase human signals did not replicate; OPTIONS showed no significant difference, below obesity MCID.

Scored May 2026 How we rate →
!
Evidence Level
low
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 16 AA · 1,817.12 Da
Also Known As
Anti-Obesity Drug 9604 • Tyr-hGH Fragment 177-191 • hGH Fragment 176-191
Class
Hexadecapeptide
Length
16 amino acids
Mol. weight
1,817.12 Da
Sequence
YLRIVQCRSVEGSCGF
Molecular Structure
Y
L
R
I
V
Q
C
R
S
V
E
G
S
C
G
F
Hydrophobic
Polar
Positive
Negative

AOD-9604 is a modified fragment of human growth hormone representing amino acids 176-191 with an N-terminal tyrosine substitution. Unlike full-length GH, it does not bind the GH receptor and does not increase IGF-1. All proposed mechanisms are based primarily on animal and in vitro studies; the peptide failed human efficacy trials.

How It Works (Simplified)

AOD-9604 was designed to capture GH’s fat-burning effects without its side effects:

Beta-3 Activation

Binds to beta-3 adrenergic receptors on fat cells, signaling them to release stored fat for energy use.

Lipolysis Trigger

Activates hormone-sensitive lipase through cAMP/PKA cascade, breaking down triglycerides into free fatty acids.

Adipose Targeting

Preferentially accumulates in fat tissue, theoretically concentrating effects where fat is stored.

No GH Side Effects

Does not bind GH receptor, avoiding IGF-1 elevation and diabetogenic effects seen with full growth hormone.

Key Research: Heffernan et al. (2001) showed that beta-3-AR knockout mice fail to lose weight on chronic AOD-9604 treatment and that the peptide upregulates beta-3-AR expression, implicating this receptor in its lipolytic mechanism. PMID:11713213

Important Limitations

  • Failed human trials - Phase 2b/3 with 536 subjects showed no significant weight loss vs placebo
  • Species translation failure - Beta-3 receptor biology differs significantly between rodents and humans
  • No FDA approval - Excluded from 503A compounding list in 2024
  • WADA prohibited - Banned in sport (Section S2.5)
  • All efficacy data is preclinical - Human pharmacokinetics may not support therapeutic effect
i. Beta-3 Adrenergic Receptor Pathway · Lipolysis
AOD-9604Beta-3-AR ActivationAdenylyl CyclasecAMP IncreasePKA ActivationHormone-Sensitive LipaseTriglyceridesFree Fatty Acids + Glycerol
ii. cAMP/PKA Pathway · Fat Oxidation
AOD-9604cAMP/PKA activationFatty acid oxidationEnergy release
Mechanism Beta-3 adrenergic receptor activation stimulating lipolysis
Supported 5 direct studies
Benefit suggested to reduce body fat in obese individuals
Evidence Level
Low
2 Human
4 Animal
3 In Vitro
Mechanism cAMP/PKA pathway activation increasing fatty acid oxidation
Supported 3 direct studies
Benefit may enhance fat metabolism without diabetogenic effects
Evidence Level
Low
1 Human
3 Animal
2 In Vitro
Mechanism Selective adipose tissue accumulation targeting fat cells
Emerging 2 direct studies
Benefit suggested to preferentially mobilize fat from obese adipocytes
Evidence Level
Very Low
3 Animal
2 In Vitro
Mechanism Confidence
Established
Supported
Emerging
Evidence Level
High
Moderate
Low
Very Low

Reported positives

  • Fat loss without affecting blood glucose levels reported
  • No impact on IGF-1 or growth hormone levels cited as safety advantage
  • Targeted abdominal fat reduction claimed
  • Well-tolerated with few reported side effects

Reported negatives

  • Fat loss effects modest and inconsistent in reports
  • Limited clinical evidence despite widespread marketing
  • Results inferior to GLP-1 agents for weight management
  • Product quality concerns from research suppliers

“Popular in weight loss clinics. Community views mixed — some report benefits, many find effects modest.”

Self-reported, unverified accounts — not clinical evidence and no substitute for the cited research. Anecdotes are prone to selection bias and placebo effects.

Phase 01 1
Week 1-4

Based on Phase 2a trial data: Some subjects showed initial fat mobilization. Animal studies indicate beta-3 receptor upregulation begins within first weeks. Clinical significance in humans unproven.

PMID:11673763
Phase 02 2
Week 4-12

Preclinical studies showed reduced body weight gain and increased fat oxidation in obese mice over chronic dosing. Any early human signal did not replicate in the larger Phase 2b/3 trial.

PMID:11673763
Phase 03 3
Week 12-24

Pivotal OPTIONS study (24 weeks, n=536) showed no significant difference from placebo at any dose tested. Effects observed in mice did not translate to humans.

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 (6 indicators)
White to off-white lyophilized powder
Dissolves completely in bacteriostatic water
Clear, colorless solution after reconstitution
Certificate of analysis (COA) showing >98% purity
Third-party HPLC and mass spectrometry verification
Proper vacuum seal on vial
Warning Signs (4 indicators)
Slightly off-white powder (may still be acceptable)
Slower dissolution time than expected
COA from manufacturer only without third-party verification
Purity listed between 95-98%
Bad Signs (6 indicators)
Yellow, brown, or discolored powder
Visible particles or cloudiness after reconstitution
Gel-like consistency or clumping
No COA or fraudulent-appearing documentation
Strong unusual odor
Compromised vial seal
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 target weight/fat loss through different mechanisms. Overlapping metabolic effects warrant monitoring. AOD-9604 failed clinical trials while semaglutide is FDA-approved.

Similar metabolic targets - combining with approved GLP-1/GIP agonists may have unpredictable effects. AOD-9604 lacks efficacy evidence.

Both derived from GH-related pathways - tesamorelin is GHRH analog, AOD-9604 is GH fragment. May have overlapping or competing effects on lipid metabolism.

CJC-1295 elevates full GH pathway while AOD-9604 is a non-functional GH fragment. Combining GH secretagogues with GH fragments may be redundant.

Ipamorelin stimulates endogenous GH release - adding AOD-9604 (failed GH fragment) alongside active GH secretagogues lacks rationale.

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.

20 Sources 6 Human 8 Preclinical

Full reference list available on request. All citations link to PubMed for verification.

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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