AOD-9604: What It Is, Where to Get It Prescribed, and What It Costs

Human growth hormone is a protein of 191 amino acids. AOD-9604 is a synthetic copy of the last fifteen of them — positions 177 to 191, the C-terminal end — with an extra tyrosine added at the front, which makes it a hexadecapeptide of sixteen amino acids joined by a single disulphide bridge. It is often called "hGH fragment 176–191" online; the numbering differs by one depending on whether the added tyrosine is counted, but it is the same molecule.

That region of growth hormone is the part that, in the early animal work, seemed to carry the hormone's effect on fat tissue. The whole point of the fragment was to keep that piece and leave the rest behind.

AOD stands for Anti-Obesity Drug. The compound came out of biochemistry work at Monash University in Melbourne and was developed and patented in the late 1990s by an Australian company, Metabolic Pharmaceuticals, as an oral obesity treatment. The number is a compound code, not a dose or a strength. The company's clinical program is the most important thing to understand about this peptide, and it is covered in full below, because it is one of the few compounded peptides that has actually been through randomised, placebo-controlled human trials — and the result was negative for weight loss.

It is not growth hormone, and it does not behave like it. Cell work reports that it does not bind the growth hormone receptor, animal work reports it does not cause the rise in blood glucose or the fall in insulin sensitivity that full-length growth hormone does, and the human trials reported no change in IGF-1. It is not a growth hormone secretagogue either — it does not prompt the pituitary to release anything, which is what sermorelin, ipamorelin and CJC-1295 / Ipamorelin are for. It is not an appetite drug: nothing in the research describes an effect on hunger or satiety, which is the mechanism behind semaglutide and tirzepatide. And it is not an anabolic agent.

The founding idea, set out in a 2000 paper in Hormone Research from the Monash group, is that growth hormone's effect on fat tissue lives in its C-terminal region and can be separated from its growth-promoting and diabetogenic effects. In that paper, obese Zucker rats given the fragment orally for 19 days gained substantially less weight than controls, their fat tissue showed increased lipolytic activity when tested, and euglycaemic clamp testing found no adverse effect on insulin sensitivity — in contrast to what chronic growth hormone does.

The paper on file for this page, in Endocrinology in 2001, compared the fragment with full-length growth hormone in obese mice and in mice lacking the beta-3 adrenergic receptor, a receptor on fat cells that drives fat breakdown and heat production. In ordinary obese mice, chronic treatment reduced weight gain and was associated with increased expression of beta-3 receptors in white and brown fat. In the knockout mice, those effects were absent. The proposed reading is that the fragment acts through, or at least depends on, that receptor system rather than on the growth hormone receptor.

A companion 2001 paper in the International Journal of Obesity gave obese and lean mice either growth hormone, the fragment, or saline by mini-pump for 14 days. Both growth hormone and the fragment reduced weight gain in the obese animals, and this was associated with increased whole-body fat oxidation and higher plasma glycerol, which is a marker of fat cells releasing their contents. Unlike growth hormone, the fragment did not raise blood glucose or reduce insulin secretion.

The same 2001 paper tested the fragment in cells engineered to carry the human growth hormone receptor. It did not compete with growth hormone for the receptor and did not drive cell proliferation. That is the laboratory basis for the claim, repeated everywhere online, that AOD-9604 "has the fat effect without the growth effect." The human trials are consistent with it on the specific point of IGF-1, which did not change on treatment, and on glucose tolerance, which was not impaired.

The FDA's reviewers, going through this literature in 2024, made a point worth repeating: none of the animal studies established a dose-response relationship, the statistics were not corrected for multiple comparisons, and the actual receptor or binding site has not been found. "Works through beta-3 receptors" is a reasonable inference from the knockout data; it is not an established mechanism.

This is where the case was built. Across the Zucker rat and ob/ob mouse work, chronic treatment reduced weight gain, increased markers of fat breakdown and fat oxidation, and did not produce the glucose and insulin problems seen with growth hormone. The effect sizes were meaningful in those animals. The problem, as the next sections show, is that this did not carry over to people at the doses tested.

A 2015 paper in Annals of Clinical and Laboratory Science injected AOD-9604 into the knees of rabbits with collagenase-induced osteoarthritis, weekly for four to seven weeks, with or without hyaluronic acid. Treated joints scored better on gross and microscopic cartilage assessment than saline-treated joints, and the combination with hyaluronic acid scored better than either alone. This is the origin of the joint and cartilage claims attached to the peptide. It is one study, in one animal model, by intra-articular injection — not subcutaneous — and there is no human study of AOD-9604 for any joint condition.

Between roughly 2001 and 2007 the company ran six randomised, double-blind, placebo-controlled trials in Australia, enrolling close to 900 people in total, mostly with obesity. The early studies were small: a 15-man intravenous dose-escalation study, a 23-man intravenous study, and two short oral studies of 17 and 36 men. The intravenous studies reported a rise in circulating free fatty acids within hours of a dose, but no statistically significant weight loss against placebo over the few weeks involved.

The fifth study gave 300 men and women with obesity oral AOD-9604 at one of five daily doses, or placebo, for 12 weeks. It was reported as a conference abstract rather than a full paper; the abstract described weight loss slightly greater than placebo at every dose, with the largest effect at the lowest dose, and a reduction in waist circumference. The FDA's reviewers later described the differences as small and of unclear meaning.

The sixth and decisive study, called OPTIONS, enrolled 536 adults with obesity (502 randomised) and gave them 0.25, 0.5 or 1 mg of oral AOD-9604 or placebo once daily for 24 weeks, on top of a dietitian-supervised diet and exercise program. The primary endpoint was statistically significant weight loss versus placebo at 12 weeks; the trial was powered to detect a difference of 1.8 kg. It did not find one. On 21 February 2007 the company announced that the results did not support the commercial viability of AOD-9604 as an obesity treatment and terminated development for that condition. The company's own statement said weight loss versus placebo at 12 and 24 weeks was too low to reach statistical significance and that the overall population did not respond consistently.

That is the honest summary: the biggest and best-designed human trial of this peptide, run by the company that invented it, found no significant weight loss over placebo.

Unusually for a compounded peptide, there are real randomised human trials — six of them. What they establish is mostly about safety and pharmacology: no change in IGF-1, no impairment of glucose tolerance, no anti-AOD-9604 antibodies detected in the subjects tested, and no serious adverse event judged related to treatment. A 2013 paper in the Journal of Endocrinology and Metabolism, written by people connected to the company, summarises that safety data across all six studies.

Two limits matter. First, every one of those trials used intravenous or oral AOD-9604. There is no published human trial of the subcutaneous injection that is actually prescribed, which the FDA specifically noted in 2024. Second, the efficacy result for obesity was negative. Anyone presenting AOD-9604 as a "clinically proven" fat-loss peptide is describing trials that reached the opposite conclusion.

• It does not establish weight loss in humans. The largest trial found none over placebo, and the smaller ones found nothing significant.
• It does not establish an effect size or a timeline for body composition change by subcutaneous injection, because that has never been studied in people.
• It does not establish any effect on joints or cartilage in humans. That claim rests on one rabbit study using intra-articular injection.
• It does not establish long-term safety beyond the 24 weeks of the longest trial.
• It does not establish efficacy for any condition as an FDA-approved treatment. It is not approved for anything.

Nothing measurable should be expected. The intravenous studies reported changes in circulating fatty acids within hours of a dose, but that is a blood marker, not a change in body composition. Most people report nothing in this window, which is normal.

If prescribers describe change at all, it is in this window and it is modest — usually framed as support for a diet and training program that is already producing results, not as a driver of results on its own. A vial is sized at four weeks of Monday-to-Friday dosing, and a physician will usually want to see at least two fills before forming a view.

There is no withdrawal or rebound described in the literature. Whether there is anything to maintain depends on whether anything changed, and the honest position is that the human evidence does not predict that it will for most people.

The OPTIONS trial gave 502 people with obesity a supervised diet and exercise program with or without oral AOD-9604 for six months, and the peptide did not add significant weight loss on top of the program. Anyone whose primary goal is meaningful weight loss should start from that fact. Injection is a different route from the oral tablets used in the trials, and physicians who prescribe it are relying on the animal mechanism and their own clinical judgement, not on a human result that the trials failed to produce.

The directions are written in millilitres and in insulin-syringe units because that is what you can read off the barrel. 0.25 mL is 25 units on a U-100 syringe. You are not calculating anything — the number is printed on your medication.

Subcutaneous means into the fat layer, not the muscle. Abdomen and thigh are the usual sites, rotated so the same spot is not used repeatedly. The five-days-on, two-days-off pattern is a prescribing convention rather than anything derived from the trials, which used daily oral tablets; it is common across peptide protocols and gives injection sites a rest. Some prescribers direct the injection in the morning before eating, on the theory that it fits the fasted-state fatty-acid changes seen in the intravenous studies. Your directions will say.

20 doses at Monday through Friday is four weeks, which is why refills run on a 28-day cycle. One vial per fill, always — not a stockpile. Both strengths are the same 5 mL volume with more peptide in it, so the dose volume and the number of doses per vial do not change.

Refrigerated, and it ships that way in insulated packaging with ice packs. The peptide's disulphide bridge and its tendency, like most peptides, to aggregate if mishandled are the reasons the pharmacy's storage directions matter. Beyond-use dating runs from first puncture and is on the label.

Different mechanism, different evidence, different price. Semaglutide and tirzepatide act on appetite and gut hormone receptors, have FDA-approved branded versions with large randomised trials showing substantial weight loss, and are the reference standard for medical weight management. AOD-9604 is described around fat-cell signalling in animals and its human obesity trials were negative. It is not a substitute for a GLP-1 medication, and a physician will not present it as one.

Both are connected to growth hormone, from opposite directions. Tesamerelin is a growth-hormone-releasing hormone analogue that raises the body's own growth hormone and IGF-1, and its approved product has human trial data on visceral fat in a specific population. AOD-9604 is a fragment of growth hormone that, by design and by the trial data, does not raise IGF-1 at all. Someone wanting to avoid any effect on the growth hormone axis would look at AOD-9604; someone wanting the visceral fat evidence would look at tesamorelin. They are not interchangeable.

The SHRED blend combines AOD-9604 with CJC-1295, ipamorelin and MOTS-c; the PHYSIQ blend combines it with tesamorelin, ipamorelin and MOTS-c. Both put the fragment alongside peptides that do act on the growth hormone axis, which is a deliberate choice rather than an accident: the fragment on its own leaves that axis alone. A single-agent vial is the simpler and cheaper option and the one to start with if the physician wants to see what one compound does before adding others.

AOD-9604 is not available as a pepti Pen cartridge, a capsule or a nasal spray. The oral tablets used in the company's trials are not a compounded format Pepti supplies, and the trial result gives no reason to prefer them.