AOD-9604

AOD9604, hGH fragment 176-191 (modified), Tyr-hGH(177-191), "anti-obesity drug 9604"

Metabolic & weight

Awaiting medical reviewEN ES DE FR PT ZH+ Follow for updates

Summary

Class: Synthetic 16-amino-acid peptide: the C-terminal fragment of human growth hormone (residues 177–191) with an added tyrosine at the start, and a disulphide bond between its two cysteines
Mechanism: Proposed to copy the fat-mobilising region of growth hormone — increasing fat breakdown and reducing fat storage — without GH's effects on growth, IGF-1 or blood sugar
Routes studied: Oral tablets and subcutaneous injection (human trials); injection and oral (animal); intra-articular (rabbit); subcutaneous and oral (community)
Dose range reported: Human trials: 0.25 mg/kg IV single dose (Phase 1); oral 1–30 mg/day for 12 weeks in Phase 2 obesity trials. Community: 250–300 µg/day subcutaneous, typically fasted; oral 500 µg–1 mg. No approved human dose
Half-life: Short; reported in the range of 10–30 minutes after IV dosing in early human pharmacology †
Storage: Lyophilised: refrigerate, protect from light. Reconstituted: refrigerate, community practice is use within ~4 weeks
Regulatory status: Not approved as a medicine anywhere. FDA compounding Category 2 (2023). WADA-prohibited

Doses are as reported in studies or by the community — never recommendations.

1What it is

AOD-9604 is a man-made copy of the tail end of human growth hormone. In the 1990s, researchers at Monash University in Melbourne noticed that this C-terminal region of GH seemed to carry the hormone's fat-burning activity while the rest of the molecule carried its growth and blood-sugar effects. The Australian company Metabolic Pharmaceuticals developed a stabilised version — the natural fragment 176–191 with an extra tyrosine — and took it through a full clinical programme for obesity between roughly 1999 and 2007.

The programme failed. The largest Phase 2b trials did not show a statistically significant difference in weight loss from placebo, and the company stopped development. The compound then resurfaced as a food-ingredient candidate (the company self-affirmed GRAS status in the US in 2014) and as a community peptide. More recently it has been studied in animals for cartilage repair.

2How it's thought to work

Lipolysis. in rodent fat cells and tissue, AOD-9604 increases fat breakdown and reduces new fat formation. The proposed route is through β3-adrenergic receptor signalling, because the effect disappears in mice lacking that receptor (Heffernan 2001).

No GH-receptor binding. it does not bind the GH receptor, does not raise IGF-1 and does not alter glucose or insulin in the studies that measured them — which was the whole point of the design.

Cartilage. in rabbit osteoarthritis models, intra-articular AOD-9604 with hyaluronic acid improved cartilage scores. The mechanism here is not established; proposed links to collagen synthesis and chondrocyte survival remain speculative.

Proposed: a fragment from the end of the growth hormone molecule that keeps its fat-mobilising effect, so fat cells release stored fat.Schematic — not to scale

3What the research shows

Graded A (negative)

Weight loss in humans

Metabolic Pharmaceuticals ran six clinical trials involving roughly 900 participants. The Phase 2b studies of oral AOD-9604 over 12 weeks in obese adults did not meet their primary weight-loss endpoint; the difference from placebo was small and not statistically significant, and the company discontinued the obesity programme in 2007. The efficacy data were reported in company announcements rather than full peer-reviewed papers, so the detail available is limited — but the overall result is clear: in the best-designed human test it has had, it did not produce meaningful weight loss.

Graded A/B

Human safety

A pooled analysis of the six trials reported that AOD-9604 was well tolerated at oral doses up to 30 mg/day, with an adverse-event profile similar to placebo and no effect on IGF-1, glucose tolerance or insulin (Stier 2013, J Endocrinol Metab). This is the one solid piece of positive human data and it concerns safety, not efficacy. [3]

Fat metabolism in rodents

Obese mice given the GH fragment or AOD-9604 showed increased lipolysis, reduced lipogenesis and weight loss without the hyperglycaemia seen with full GH (Ng 2000, Horm Res; Heffernan 2001, Endocrinology). The β3-adrenergic knockout work points to the receptor involved. [1][2][5]

Cartilage repair and osteoarthritis

In a rabbit model of collagenase-induced knee osteoarthritis, weekly intra-articular AOD-9604 combined with hyaluronic acid improved cartilage histology more than either alone (Kwon & Kim 2015, Ann Rehabil Med). Rabbit-only; no human data. [4]

Early human pharmacology

Phase 1 and early Phase 2 work (around 2001–2004) reported that single IV doses and short oral courses increased fat oxidation and produced small weight changes in obese volunteers, without raising IGF-1 or glucose. These results were released in company summaries and conference material rather than full papers, so they are graded B at best and were not borne out in the larger trials that followed.

Body composition, recovery, "fat loss without diet"

Community use for fat loss rests on the rodent data and anecdote, and runs directly against the human trial results. There are no human studies of injectable AOD-9604 for body composition.

4Reported side effects and interactions

Literature-reported

Oral doses up to 30 mg/day for 12 weeks produced no safety signals different from placebo across ~900 trial participants (Stier 2013). No change in IGF-1, glucose or insulin.

Community-reported

injection-site irritation, headache, occasional nausea; some report mild water retention. Many report no noticeable effect at all.

Theoretical. because it does not engage the GH receptor, GH-class concerns (IGF-1 rise, insulin resistance) should not apply — and the trial data support this. Long-term injectable use has never been studied.

Interactions. none established. Fat-mobilising effect, if present, would in theory be influenced by β-blockers (which blunt β3 signalling), but this has not been tested.

Markers researchers commonly monitor

Marker	Why it's watched
IGF-1	expected not to change; a rise would suggest contamination with GH or a GH secretagogue rather than AOD-9604.
Fasting glucose and insulin	trials showed no effect; worth confirming given the GH-derived origin.
Lipid panel and free fatty acids	the proposed lipolytic effect would show here if it exists.
Body weight and waist circumference	the only meaningful efficacy readouts, and the ones that disappointed in trials.
No compound-specific safety markers are established; general baseline panels (CBC, CMP) are reasonable

Free for everyone. Safety information is never behind a paywall.

5Reconstitution and handling

Typically supplied as powder in 2 mg or 5 mg vials. with , swirl gently, protect from light. Community practice favours morning fasted dosing on the theory that it works best when insulin is low; this is not supported by human data.

Open in calculator, pre-loaded →

6Commonly studied alongside

In the literature: hyaluronic acid (cartilage models). In the community: discussed with GH secretagogues (ipamorelin, CJC-1295) and with other "fat-loss" peptides such as tesamorelin or 5-amino-1MQ; no combined studies exist.

Informational cross-links. Not stack recommendations.

7Regulatory status by region

Region	Status (checked —)
United States	Not FDA-approved as a drug. Placed in Category 2 of FDA's compounding bulk substances list (2023), restricting compounding. The company's 2014 GRAS self-affirmation as a food ingredient was not an FDA approval †
European Union	Not authorised; not a permitted novel food ingredient
United Kingdom	Not licensed
Australia	Not an approved product despite its Australian origin; prescription-only classification for peptides applies †
South Africa	Not registered
Sport	Prohibited by WADA under S2 (growth hormone fragments are named explicitly, including AOD-9604)

8Open questions

Why did strong rodent lipolysis fail to translate into human weight loss? Species differences in β3-adrenergic receptor biology are the leading explanation.
Does injectable (rather than oral) dosing change the human result? Never tested at scale.
Is the cartilage signal real in humans? No trial exists.
Does research-market material match the clinical-trial molecule (with its disulphide bond intact)? Degradation of the bond would be expected to abolish activity.

9References

1Ng FM et al. (2000). Metabolic studies of a synthetic lipolytic domain (AOD9604) of human growth hormone. Horm Res. PubMed · DOI
2Heffernan M et al. (2001). The effects of human GH and its lipolytic fragment (AOD9604) on lipid metabolism following chronic treatment in obese mice and β3-AR knock-out mice. Endocrinology. PubMed · DOI
3Stier H, Vos E, Kenley D (2013). Safety and tolerability of the hexadecapeptide AOD9604 in humans. J Endocrinol Metab. DOI
4Kwon DR, Kim YG (2015). Effects of intra-articular injection of AOD9604 with or without hyaluronic acid in a rabbit model of knee osteoarthritis. Ann Rehabil Med. PubMed
5Heffernan MA et al. (2001). 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. PubMed · DOI
6FDA (2023). Bulk drug substances for compounding — AOD-9604 category 2 listing. PubMed

References are being resolved to PubMed/DOI identifiers; links search PubMed for the citation until then.

† Being confirmed by our reviewers against current sources.

10Community

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Self-reported side effects Phase 2

Not enough data yet. 0 of the 50 members needed have logged this compound for 4+ weeks. We don't show anything below 50, so no one can be identified.

11Page history

25 Oct 2026Profile published — awaiting medical review

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