Research profile · Peptide
AOD-9604
Also known as Tyr-hGH177-191, AOD9604
Overview
A synthetic fragment of human growth hormone whose pivotal obesity trial failed, and whose widely claimed regulatory status does not exist.
- Category
- Peptide
- Highest evidence level identified
- Early human evidence
- Last scientifically reviewed
- 20 August 2026
- Last regulatory review
- 20 August 2026
Mechanism under investigation
AOD-9604 is a synthetic 16-amino-acid peptide corresponding to the C-terminal region of human growth hormone with an added stabilising residue. It was designed to reproduce the fat-metabolising activity of growth hormone without its growth-promoting effects, and consistently with that, human trials found no significant effect on IGF-1 and binding assays indicate it cannot induce the receptor dimerisation required for growth hormone signalling. The mechanism by which it would nonetheless act is unresolved, and regulators have noted that its molecular targets remain unknown.
Research areas
- Metabolic research
- Lipolysis models
These are fields in which the compound has been investigated. Listing a field is not a statement that anything was demonstrated within it.
Current evidence
In-vitro evidence
Cells, tissues or biochemical systems outside a living organism.
Thinner than marketing implies. There is receptor-binding work showing no displacement of growth hormone and no proliferative response, and metabolic degradation work. No dedicated study in human adipocytes was verified, so claims of adipocyte studies overstate the record.
Animal evidence
Studies in living non-human animals.
Real but modest, and consistently a reduction in weight gain rather than weight loss. Obese rodent models gained roughly five to fifty per cent less weight depending on model, without reduced food intake. In knockout mice lacking a particular adrenoceptor the effect was lost, suggesting dependence on that signalling — yet the compound shows no direct interaction with that receptor, so the link is unexplained.
Human observational evidence
Studies observing people without assigning an intervention.
None. Regulatory searches of adverse event and food-supplement reporting systems retrieved no reports, with the caveat from the regulator that this absence does not imply safety.
Clinical-trial evidence
Studies assigning an intervention to human participants.
This is where marketing and evidence diverge most sharply. Six company-funded randomised placebo-controlled trials ran between 2001 and 2006 with roughly 900 participants. The pivotal trial randomised 502 adults with obesity over 24 weeks with a primary endpoint of significant weight loss against placebo. It failed. The developer announced in February 2007 that results did not support commercial viability and terminated development for obesity, weight loss against placebo at both 12 and 24 weeks being too small to reach significance. The one apparently positive result exists only as a conference abstract and shows an implausible dose response with the largest effect at the lowest dose.
Study limitations
- The widely repeated claim that this compound has FDA GRAS status does not correspond to any FDA notice. A direct search of the GRAS Notice Inventory returned no records, so no FDA response letter of any kind exists. The claim traces to the sponsor’s own publications describing a self-affirmed conclusion by an independent panel, which requires no FDA involvement and carries no FDA endorsement.
- The pivotal 502-patient trial failed its primary endpoint and obesity development was terminated in 2007. This is routinely omitted from secondary summaries.
- All six human trials were sponsor-funded, and the safety publications were authored by employees and consultants, one holding equity in the parent company. There is no independent human trial.
- Both the best and the worst results sit outside the peer-reviewed record: the positive result exists only as a conference abstract, and the failed pivotal trial is known only from a stock-exchange announcement.
- No human pharmacokinetic studies were identified, and the mechanism remains unidentified, which regulators have judged to undermine biological plausibility.
- The common shorthand "hGH 176-191" is inaccurate. Residue 176 of mature growth hormone is a different amino acid from the one this peptide begins with, and anti-doping listings treat the two as separate substances.
UK regulatory context
Experimental — not authorised for human use in the UK
A compound appearing in research literature that holds no UK authorisation for human use in any indication.
Source: GRAS Notice Inventory — search returning no records for this substance (opens hfpappexternal.fda.gov in a new tab) (US Food and Drug Administration)
Regulatory classification is jurisdiction-specific. A compound authorised elsewhere is not thereby authorised in the UK, and a supplier’s description of a substance does not determine how it is classified in law. See safety and regulation for the framework and the authoritative sources.
Safety and interpretation
Across six trials the sponsor reported a tolerability profile it described as indistinguishable from placebo, with no treatment-related withdrawals, no antibodies detected and no adverse effect on glucose tolerance. A regulator’s reading of the same dataset was more guarded, noting events assessed as possibly related including severe chest tightness, and recording that serious adverse events in one cohort included several malignancies which trial investigators considered unrelated to treatment. Since no product is authorised anywhere, material sold under this name is of unverified identity and purity.
References
- Regulator or official body
US Food and Drug Administration · accessed 20 August 2026
Searched directly and re-verified on alternative terms. No notice exists, therefore no FDA response letter exists. No UK marketing authorisation and no UK novel food authorisation either, so there is no lawful route to sale as a food or supplement in Great Britain.
- Primary research
Safety and Tolerability of the Hexadecapeptide AOD9604 in Humans (opens doi.org in a new tab)
Stier H, Vos E, Kenley D. Journal of Endocrinology and Metabolism, 2013 · doi:10.4021/jem157w
Sponsor-affiliated authorship. Note that this paper is frequently miscited to the Journal of Obesity, which did not publish it.
- Primary research
Moré MI, Kenley D. Journal of Endocrinology and Metabolism, 2014 · doi:10.14740/jem213w
The source of the self-affirmed GRAS claim. Sponsor-affiliated authorship.
- Primary research
Heffernan M, et al.. Endocrinology, 2001 · doi:10.1210/endo.142.12.8522