AOD-9604
| Category | Metabolic & GLP-1 |
| Goals | Fat Loss |
| Evidence level | Anecdotal (positive rodent data; human trials failed efficacy endpoints) |
| Legal status | Research-only — not approved for human use |
| FDA status | Not approved; flagged as a bulk substance of possible concern (2026) |
| Half-life | Short (~minutes in available data); human PK not well established |
| Routes | Subcutaneous · Oral · Transdermal (reported) |
| CAS / MW / Sequence | 221231-10-3 · 1815.1 g/mol · YLRIVQCRSVEGSCGF (16 aa) |
| Last reviewed | 2026-06-05 |
In one line
A modified fragment of the C-terminal “lipolytic” region of human growth hormone, developed as an anti-obesity drug but discontinued after human trials showed only modest, non-viable weight loss.
Evidence at a glance
AOD-9604 reached human clinical trials but was abandoned in Phase II because weight loss was small and not commercially meaningful. The promising effects are mostly from rodent studies. Popular fat-loss marketing overstates the human evidence. See Evidence Grading Explained and the Disclaimer.
Key Takeaways
- A 16-amino-acid peptide based on hGH residues 176–191, with an added N-terminal tyrosine for stability and a disulfide bridge between its two cysteines.
- Designed to isolate the fat-burning (lipolytic) action of growth hormone without raising IGF-1 or affecting blood glucose/insulin.
- Strong rodent data, but human trials (~900 subjects, Phase I/II) did not show clinically meaningful weight loss; development was halted.
- Not FDA-approved; sold as a research chemical and flagged by the FDA as a bulk substance of possible concern.
- Frequently marketed for “spot fat loss” and joint/cartilage support — claims that outrun the controlled evidence.
What Is It
AOD-9604 (“Anti-Obesity Drug 9604”) is a synthetic peptide corresponding to amino acids 176–191 of human growth hormone (hGH) — the C-terminal region thought to carry GH’s fat-metabolizing activity — with a tyrosine added at the N-terminus to improve stability. The two cysteine residues form an intramolecular disulfide bridge that holds the C-terminal loop in the conformation believed to be required for lipolytic activity. It was developed in Australia (Metabolic Pharmaceuticals) explicitly as a weight-loss drug candidate, the idea being to capture GH’s fat-burning effect while avoiding GH’s growth-promoting (IGF-1) and glucose-disrupting effects.
Mechanism of Action
Proposed mechanisms are drawn mostly from preclinical models:
- Stimulation of lipolysis (preclinical) — increases the breakdown of stored fat in adipocytes, reportedly via β3-adrenergic-receptor pathways.
- Inhibition of lipogenesis (preclinical) — reduces new fat formation/storage.
- IGF-1-sparing (by design) — unlike full GH, it is reported not to raise IGF-1 or impair glucose tolerance, suggesting a mechanism distinct from the GH receptor.
- Cartilage / repair claims (preclinical / anecdotal) — some studies explored effects on cartilage, but this is not an established human use.
Limitations
The fat-loss mechanism is well characterized in rodents but did not translate into meaningful weight loss in humans. The molecular target underlying its lipolytic effect is not fully established.
Evidence by Outcome
| Outcome | Evidence | Notes |
|---|---|---|
| Weight loss (humans) | Anecdotal | 12-wk trial: ~2.6 kg vs ~0.8 kg placebo; Phase IIb halted for lack of viable efficacy |
| Fat oxidation / lipolysis | Preclinical | Robust in rodent and in-vitro models |
| IGF-1 / glucose neutrality | Clinical (safety) | Human trials reported no IGF-1 rise or glucose impairment |
| Cartilage / joint repair | Preclinical | Some animal/in-vitro work; no confirmatory human data |
| ”Targeted/spot” fat loss | Anecdotal | No controlled human evidence supports localized fat loss |
Reported Dosing
Not medical advice
Protocols as reported in community sources and discontinued-trial literature. There is no approved human dose. See Reconstitution & Dosing Math.
| Route | Dose (reported) | Frequency | Cycle |
|---|---|---|---|
| Subcutaneous | ~300 µg/day (≈1 mg used in trials) | 1× daily, often AM/fasted | Variable (weeks) |
| Oral | Marketed, but bioavailability questionable for a peptide | 1× daily | Variable |
| Transdermal | Sometimes marketed; absorption uncertain | — | — |
Pharmacokinetics
AOD-9604 is a small peptide with a short half-life (on the order of minutes in available data); human PK is not well established. Oral and transdermal products are marketed, but peptide oral bioavailability is generally poor and these routes are not well validated. See Half-Life & Pharmacokinetics.
Side Effects & Risks
- Reassuring trial safety: across ~900 participants in Phase I/II, AOD-9604 was generally well tolerated, with no IGF-1 elevation or glucose impairment reported — a notable point in its favor.
- However, “well tolerated short-term in trials” is not proof of long-term safety, and chronic real-world use is unstudied.
- Anecdotal reports: injection-site reactions, headache, mild GI upset — not systematically documented.
- Sourcing risk: as a research chemical, identity/purity vary widely — see Sourcing and Red Flags & Scams.
- See Side Effects & Risk Management and Bloodwork & Monitoring.
Cycling
No evidence-based cycling standard exists; anecdotal protocols run it for several weeks during a fat-loss phase, alongside diet and training. See Cycling.
Stacks It Appears In
- Often combined anecdotally with CJC-1295 and Ipamorelin (GH secretagogues) for body-composition goals.
- Sometimes paired with GLP-1 agents like Semaglutide or Tirzepatide in community fat-loss stacks — no controlled data supports these combinations.
Comparisons
- vs GLP-1 agonists (Semaglutide, Tirzepatide): those have robust, FDA-approved human weight-loss data; AOD-9604’s human weight-loss data is weak and led to discontinuation.
- vs GH secretagogues (CJC-1295, Ipamorelin, Tesamorelin): those raise endogenous GH/IGF-1; AOD-9604 is specifically designed not to.
Sourcing & Quality
Sold almost exclusively as a lyophilized “research chemical,” so identity and purity are not guaranteed. Evaluate quality before trusting a product: How to Read a CoA, Sourcing, Red Flags & Scams. Reconstitution and storage: Reconstitution & Dosing Math. No vendors are endorsed here.
Legal & Regulatory Status
(As of 2026-06-05.) Not FDA-approved for any use. Clinical development was halted after Phase IIb trials failed to meet efficacy endpoints. The FDA has identified AOD-9604 among bulk drug substances that may present safety risks for compounding. It is sold as a research chemical; status varies by country and it may be prohibited in tested sport. See Regulatory & Legal Status.
FAQ
Is AOD-9604 FDA-approved? No. It was studied as a drug candidate but never approved, and development stopped after Phase II.
Does it cause weight loss in humans? Human trials showed only small weight loss — statistically detectable but not commercially meaningful — which is why the program was discontinued.
Does it raise IGF-1 like growth hormone? By design, no. Trials reported no IGF-1 elevation and no glucose impairment, distinguishing it from full GH and GH secretagogues.
Can it target fat in specific areas? There is no controlled human evidence for localized (“spot”) fat loss.
References
- Ng F.M. et al. (2000). “Metabolic studies of a synthetic lipolytic domain (AOD9604) of human growth hormone.” Hormone Research.
- Heffernan M.A. et al. (2001). “The effects of human GH and its lipolytic fragment (AOD9604) on lipid metabolism…” Endocrinology.
- Metabolic Pharmaceuticals — Phase I/II clinical trial program (AOD-9604, obesity); subsequently discontinued.
- PubChem CID 71300630 — AOD-9604 (C78H123N23O23S2).
- U.S. FDA — bulk drug substances nominated/evaluated for compounding; AOD-9604 flagged for possible safety concern.
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