Could the part of growth hormone that acts on fat be separated from the parts that drive growth? AOD-9604 was Australia's attempt to find out, and its clinical programme is a lesson in how ideas get tested.
AOD-9604 · Growth hormone C-terminal fragment
Growth hormone does many things: it drives growth, raises blood glucose and prompts fat cells to release stored fat. Researchers asked whether a small piece of the hormone could keep only the fat-related action. AOD-9604 is that piece. The evidence is from rodent studies and from human obesity trials that ended without showing a weight-loss effect.
AOD-9604 is a synthetic 16-amino-acid peptide, sometimes called a hexadecapeptide, corresponding to residues 177 to 191 at the C-terminal end of human growth hormone with an added tyrosine at the start. It was designed at Monash University and developed by Metabolic Pharmaceuticals in Melbourne through the late 1990s and 2000s.
The idea came from earlier work on a related synthetic fragment, AOD9401, which covers the same region without the added tyrosine. In isolated rat fat tissue AOD9401 stimulated the enzyme that releases stored fat, hormone-sensitive lipase, and in obese Zucker rats it reduced weight gain without the glucose intolerance that whole growth hormone causes (Ng et al., 2000); that paper is historical context for the fragment concept rather than data on AOD-9604 itself. In the human trials described below, AOD-9604 did not raise IGF-1, the liver hormone that carries growth hormone's growth effects, and did not alter glucose handling.
Animal work: in obese mice given AOD-9604 by intraperitoneal injection for 14 days, body weight and fat fell, and the expression of the beta-3 adrenergic receptor in fat tissue rose; in mice lacking that receptor the chronic effect disappeared, pointing to an indirect mechanism (Heffernan et al., 2001).
Human work: Metabolic Pharmaceuticals ran six randomised, placebo-controlled trials, METAOD001 to METAOD006, in roughly 900 people, moving from single intravenous doses to oral tablets taken for up to 24 weeks. The final study, METAOD006 (announced as the OPTIONS study), was a 24-week oral phase 2b trial in about 500 adults with obesity that included a structured diet and exercise programme. Weight-loss effects seen in the earlier, shorter studies were not seen in that trial, and development as an obesity drug stopped in 2007. The company's later summary reported adverse events similar to placebo and no change in IGF-1 or glucose handling across the programme (Stier et al., 2013; More and Kenley, 2014).
Since then the only new line is preclinical: in a rabbit model of collagenase-induced knee osteoarthritis, intra-articular AOD-9604 with or without hyaluronic acid was associated with better cartilage scores (Kwon and Park, 2015).
The central question, whether the fragment reduces body fat in people, was tested and not confirmed: the largest and longest trial found no effect beyond diet and exercise. Tolerability data from that programme describe oral tablets and intravenous doses in a supervised trial setting; they were published in a small journal by authors connected to the developer and do not speak to other routes or to research material.
The osteoarthritis finding is a single rabbit study with no human follow-up. Why the animal mechanism did not translate is unresolved.
AOD-9604 is not an approved medicine in Australia and has not been approved by any regulator; its clinical development for obesity ended in 2007. It is named on the WADA 2026 Prohibited List under S2.2.3, growth hormone fragments, and is prohibited at all times in sport.
Sources and status checked 2026-09-22
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