Public educational draft · 04 November 2026Clinical review pending →
AOD-9604 reference card with source-verified molecular imagery and original research-informed diagrams. Evidence levels and limitations are marked; full citations accompany the card on the website.

Visual summary only. The research findings, limitations and references accompany the card on this page.

The chemical drawing shows source-verified two-dimensional connectivity and stereochemistry, not an experimental three-dimensional conformation. The biological setting is an illustration. Original study diagrams summarize cited research without reproducing publication artwork or inventing quantitative results.

Verified chemical reference record

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Metabolic / incretin

AOD-9604

Experimental lipid-metabolism pathways

Oxidized reference peptide, free N and C termini
Molecular formula
C78H123N23O23S2
Molecular weight
1815.1 g/mol
Class
Disulfide-linked 16-residue peptide
Identity
YLRIVQCRSVEGSCGF

Research snapshot

AOD-9604 is a modified C-terminal growth-hormone fragment studied in lipid-metabolism models. Its experimental actions are not interchangeable with those of full-length human growth hormone.

Animal data / negative human trial

Identity & representation

Literature reference molecule. Catalog naming is not analytical confirmation of AXON contents, salt, purity or formulation. Tyr-hGH(177–191) fragment analogue; Cys7–Cys14 disulfide. Not intact growth hormone or an unspecified GH fragment.

Educational reference only. Not a dosing guide, treatment recommendation or product endorsement.

Oxidized 16-residue parent · Cys7–Cys14 disulfide[4]

View the chemical structure →

Sources checked: 2026-11-06. Identity and evidence limits are stated above. Independent specialist review is pending.

ClassDisulfide-linked 16-residue peptide

Target / pathwayExperimental lipid-metabolism pathways

Selected evidenceAnimal data / negative human trial

ScopeResearch summary; not a product or treatment assessment

What researchers study

AOD-9604 is a modified C-terminal growth-hormone fragment studied in lipid-metabolism models. Its experimental actions are not interchangeable with those of full-length human growth hormone.

  • Lipid oxidation and lipolysis in obese rodent models

  • Comparison with intact growth hormone in receptor assays

  • β3-adrenergic pathway involvement rather than assumed direct agonism

Mechanism in context

  1. Experimental exposure alters lipid-metabolism readouts
  2. Studies examine lipolysis and fat oxidation
  3. Rodent models measure weight gain and adipose outcomes

A specific clinically validated receptor pathway is not established here; selected experiments found no conventional hGH-receptor activation.

Simplified publication-grounded schematic, not a solved protein structure or proof of clinical benefit.

Selected evidence

A negative human OPTIONS trial is summarized in FDA’s 2024 review; its full primary peer-reviewed publication was not located. The selected PubMed studies are preclinical.

Metabolic studies of a synthetic lipolytic domain (AOD9604) of human growth hormone.[1]

Controlled preclinical experiment · Obese Zucker rats · 19 days

Observed: Treated rats gained less weight and had increased adipose lipolytic activity.

Limit: Reduced weight gain in rats is not demonstrated weight-loss efficacy in humans.

FDA AOD-9604-related bulk substances briefing document, November 2024, pages 21–22[5]

Randomized double-blind placebo-controlled OPTIONS trial, summarized by FDA · Adults with obesity · 24 weeks; primary weight endpoint at 12 weeks · Reported n: 502 · Enrolled: 536

Observed: The FDA review reports no significant weight-loss difference from placebo at the primary endpoint.

Limit: The primary methods/results publication was not located by FDA; the card cites the regulatory review of company disclosures.

Reference identity in detail

Sequences and form distinctions describe the cited reference substance, not a verified supplier preparation.

Read the sequence and form notes
Sequence
YLRIVQCRSVEGSCGF
Sequence notes
Tyr-hGH(177–191) fragment analogue; Cys7–Cys14 disulfide. Not intact growth hormone or an unspecified GH fragment.
Molecular formula
C78H123N23O23S2
Molecular weight (g/mol)
1815.1

Safety & evidence limits

  • Human weight-loss efficacy was not established in the FDA-reviewed OPTIONS trial; favorable rodent findings cannot substitute for that negative clinical result.

  • AOD-9604 is not full-length growth hormone; its receptor effects and molecular identity must remain distinct.

  • Oxidized disulfide and reduced thiol forms differ chemically; use the specified reference form and verified stereochemistry.

Practical identity notes

  • Tyr-hGH(177–191) fragment analogue; Cys7–Cys14 disulfide. Not intact growth hormone or an unspecified GH fragment.
  • Formula and mass apply only to the named reference form, excluding unspecified counterions, solvent and water.
  • Educational molecular reference • Selected studies, not a systematic review • No dosing guidance

The 10-second takeaway

A modified growth-hormone fragment with preclinical metabolic findings; a larger human obesity trial did not show significant weight-loss efficacy.

What the visual panels show

Original diagrams summarize the cited research or documented evidence search. They are not copied publication figures or claims of treatment benefit.

  • EXPERIMENTAL LIPID READOUTS[1][2][3]

    Publication-grounded mechanism schematic · Original publication-grounded diagram

    Exposure in obese rodent models · Measure lipid oxidation and adipose lipolysis · Compare weight outcomes with controls

    Interpretation: No clinically validated receptor pathway established here.

  • Obese Zucker rats[1]

    RAT STUDY · Original publication-grounded diagram

    Less weight gain; higher adipose lipolysis

    19 days; weight gain, not human weight loss.

    Interpretation: A generic rodent icon represents rats. No human fat-loss claim or fabricated weight curve.

  • Distinct from intact GH[2][3]

    CELL / MOUSE STUDY · Original publication-grounded diagram

    No conventional hGH-receptor activity detected

    Experimental comparison; not direct β3-receptor agonism.

    Interpretation: Do not show AOD docking to GHR or β3-AR. Pathway involvement is not direct binding.

  • OPTIONS · adults with obesity[5]

    HUMAN RCT · FDA REVIEW · Original publication-grounded diagram

    No significant weight-loss advantage at 12 weeks

    536 enrolled; 502 randomized; FDA summarizes company disclosures.

    Interpretation: Negative primary endpoint stays prominent. FDA could not locate a full primary trial publication; no invented quantitative plot.

Follow the evidence

Sources & what they support

  1. Metabolic studies of a synthetic lipolytic domain (AOD9604) of human growth hormone.

    Horm Res · 2000 · PMID: 11146367 · DOI: 10.1159/000053183

    Supports: 19-day obese-rat study

  2. Increase of fat oxidation and weight loss in obese mice caused by chronic treatment with human growth hormone or a modified C-terminal fragment.

    Int J Obes Relat Metab Disord · 2001 · PMID: 11673763 · DOI: 10.1038/sj.ijo.0801740

    Supports: Mouse outcomes and absence of conventional hGH-receptor activity

  3. The effects of human GH and its lipolytic fragment (AOD9604) on lipid metabolism following chronic treatment in obese mice and beta(3)-AR knock-out mice.

    Endocrinology · 2001 · PMID: 11713213 · DOI: 10.1210/endo.142.12.8522

    Supports: β3-pathway experiments; not direct β3 receptor agonism

  4. PubChem CID 71300630

    Supports: Reference chemical graph, formula and molecular mass; not product identity

    Original structure record · Download source SDF

    Original PubChem 2D source structure record.

  5. FDA AOD-9604-related bulk substances briefing document, November 2024, pages 21–22

    2024

    Supports: FDA review of OPTIONS study design and negative weight-loss result; original trial report not found in peer-reviewed literature

Source-linked educational drafts. Scientific and clinical review is pending. These cards describe molecules and study context, not product quality, approval or treatment recommendations.

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