AOD-9604: the monograph

AOD-9604 is a 16-amino-acid piece of human growth hormone: residues 177 to 191 of the hormone's tail, closed by a disulfide bond, with one extra tyrosine added to stabilize it⁷. It is sold online as injectable vials under names like the fat-burning fragment, hGH fragment 176-191, or simply GH frag, on the promise that it delivers growth hormone's effect on body fat and none of its problems.

What separates this compound from most research peptides is that the promise was tested. Not in a forum, not in mice alone: in six randomized, double-blind, placebo-controlled human trials run by an Australian pharmaceutical company across up to 16 hospitals, with about 900 participants³. The program reached a 502-patient, 24-week phase 2b trial in obesity. That trial failed to demonstrate a significant benefit on its primary weight-loss endpoint, and the obesity program was terminated⁴.

Three facts frame the rest of this page. No product containing AOD-9604 has ever been approved by FDA for any use². FDA lists it among bulk substances that may present significant safety risks, stating that it has identified no, or only limited, safety-related information and therefore lacks sufficient information to know whether the drug would cause harm when administered to humans¹. And a 2026 peer-reviewed review concludes there are no robust data supporting clinically meaningful visceral-fat reduction or broader metabolic benefit in humans⁴.

This monograph documents the whole record with primary sources: every human trial with its numbers, the animal literature the marketed benefits actually come from, the pharmacology of a fragment versus the whole hormone, and the parts of the story that exist only in a company press release. Our evidence table holds 25 study rows, each labelled by species; 9 are human, and none of them reports a positive result for the uses this compound is sold for³⁴.

Human growth hormone is a single chain of 191 amino acids³. Research through the 1980s and 1990s mapped different jobs onto different stretches of that chain, and the carboxy-terminal region, residues 177 to 191, was identified as a lipid-mobilizing domain³. AOD-9604 is that domain made synthetically, with a tyrosine bolted onto the front end. Its sequence is YLRIVQCRSVEGSCGF, the two cysteines joined in a loop⁸, giving formula C78H123N23O23S2 and molecular weight 1815.1⁶.

The naming is a persistent source of confusion, and it is worth getting right before reading anything else about this compound. Counting the added tyrosine, the molecule is 16 residues and gets called hGH fragment 176-191. Counting only the native hormone residues, it is hGH 177-191. WADA's Prohibited List names both forms in the same line³¹. The 1980s and 1990s papers you will see cited in marketing generally studied hGH 177-191 or the un-tyrosinated AOD9401, not AOD-9604 itself¹⁴.

Structurally the fragment is not just a floppy string. Two-dimensional NMR showed the cyclic region adopting type I beta-turns and retaining structural similarity to the same region inside the intact hormone's crystal structure⁹. That is the strongest version of the design rationale: the piece keeps the shape it had inside the whole.

For scale, the compound it is a fragment of has 12 approved applications in FDA's drug database³⁶. AOD-9604 has none².

AOD-9604 was a real drug candidate with a real owner. Metabolic Pharmaceuticals Ltd, based in Port Melbourne, Australia, developed it for the treatment of obesity¹⁰. A 2004 industry profile records the state of play in one line: Metabolic is developing AOD-9604 for the potential treatment of obesity; by February 2002, phase IIa trials were underway¹⁰. Through the mid-2000s the compound appeared in obesity-drug pipeline reviews alongside rimonabant, cetilistat and oleoyl-estrone, described as a human growth hormone fragment that increases adipose tissue breakdown³²³³.

The program ran six trials in sequence: a phase 1 dose escalation, three phase 2a safety studies, then two phase 2b efficacy trials, the second of which enrolled 534 and randomized 502³. That is a serious, expensive, conventional development path.

Then it stopped. The 24-week phase 2b trial failed to demonstrate a significant benefit on its primary weight-loss endpoint⁴. The record of the decision that followed is a 2007 announcement by the sponsor to the Australian Securities Exchange, whose title says it plainly: the phase 2B clinical trial results do not support commercial viability of the obesity project, and the programme is terminated⁴. We cite the 2026 peer-reviewed review that records that announcement rather than the announcement itself, because a direct fetch of the exchange's announcement archive for this delisted company returned nothing on the day this page was built. That is worth stating plainly: the moment the program ended is documented in a press release, not a paper.

Two afterlives followed. The sponsor's authors published the accumulated safety data in 2013 and the non-clinical toxicology and kinetics in 2014, the second under the title of a nutraceutical ingredient for improved metabolic health, recording that an expert panel had determined the compound to be Generally Recognized As Safe for intended uses in foods¹⁹³. The molecule itself then reappeared under a new code, LAT8881, at a different company, Lateral Pharma, which took it into three further human trials for pain indications⁸. Meanwhile, the peptide had become a research chemical sold on the internet and, by 2014, was being identified by government analysts in confiscated vials⁷.

The mechanism claim for AOD-9604 is unusually specific, and unusually testable: that the fragment reproduces growth hormone's effect on fat while bypassing the growth hormone receptor, and therefore bypasses the IGF-1 rise, the blood-sugar effects and the growth signalling that come with the whole hormone.

The receptor part is supported. In transfected cells expressing the human growth hormone receptor, AOD9604 did not compete for the receptor and did not induce cell proliferation, unlike intact hGH¹¹. A later paper on the same molecule states it directly: LAT8881, formerly identified as AOD9604, was found to not act via the GH receptor⁸. So this is not a growth hormone secretagogue, and it is not growth hormone. It is a fragment acting through something else.

The IGF-1 part is supported too, and by human data, which is rare here. No human trial found a significant IGF-1 change at any dose or duration, including 24 weeks of daily dosing, where the mean changes were 1.76 nmol/L at 12 weeks and 1.24 nmol/L at 24 weeks with p values of 0.50844 and 0.75754 against placebo³.

What the fragment does instead is less settled than the marketing suggests. In obese mice, chronic dosing increased fat oxidation and plasma glycerol and reduced weight gain, and treatment raised suppressed beta3-adrenergic receptor RNA toward lean levels; but in beta3-AR knockout mice, chronic treatment failed to change body weight or lipolysis, and the authors concluded the lipolytic actions are not mediated directly through that receptor¹². In 2000, mouse work showed body weight gain diverging from controls from day 16 with no difference in food consumption, which is the basis for calling the effect metabolic rather than appetite-driven¹³.

Two older findings complicate the clean story and are almost never quoted. In 1993, the same C-terminal sequence showed antilipogenic activity identical to intact hGH but no significant lipolytic effect by glycerol release from fat pads, and its authors concluded growth hormone's main physiological effect on lipid metabolism is on lipogenesis, not lipolysis¹⁶. And in 1982, the same region was reported as insulin-antagonistic, causing significant hyperglycaemia and insulin resistance in normal rats at nanomolar quantities, with the active core inside residues 178 to 190¹⁸. The idea that this stretch of the hormone carries only the fat-burning function, and nothing else, is a simplification of its own literature.

Nine human trials of this molecule have published or posted results. Here they all are.

The obesity program, six trials, about 900 participants. METAOD001 was a phase 1 dose escalation, 25 to 400 mcg/kg intravenously in 15 healthy men, with recombinant growth hormone as a positive control. METAOD002 gave single intravenous doses of 25, 50 and 100 mcg/kg to 23 obese men. METAOD003 gave single oral doses of 9, 27 and 54 mg to 17 obese men. METAOD004 gave 9, 27 or 54 mg orally daily for seven days to 36 obese men³. All four were safety studies and all four were uneventful: no serious adverse events in the phase 1 study, no significant glycerol, glucose or IGF-1 trends, and in the oral single-dose study the only event judged definitely treatment-related followed placebo³.

METAOD005 was the first efficacy trial: 300 obese adults across five Australian hospitals, randomized to 12 weeks of daily oral dosing at 1, 5, 10, 20 or 30 mg or placebo, with reduction in body weight as a stated objective³. Its safety results are published. Its weight-loss result is not, anywhere we could find, and we searched every AOD9604 record indexed in PubMed and Europe PMC³. Five serious adverse events occurred, all neoplasms, all in drug arms: three on 20 mg, one on 5 mg, one on 10 mg. The investigator considered none related to study medication, and since IGF-1 did not move, they could not be attributed to raised IGF-1³.

METAOD006 was the trial that ended the program: 534 enrolled, 502 randomized, 16 Australian sites, 24 weeks of daily oral dosing at 0.25, 0.5 or 1 mg or placebo. It failed to demonstrate a significant benefit on the primary weight-loss endpoint⁴. On safety it was unremarkable: adverse events in 75.6 to 83.2 percent of subjects across arms, with the highest rate in the placebo group, no IGF-1 differences, no glucose differences, no anti-AOD9604 antibodies detected³.

The second program, three trials. The same peptide, recoded LAT8881, went into pain indications at Lateral Pharma. In neuropathic pain (53 participants), the primary endpoint was -0.87 points on an 11-point pain scale against -0.74 for placebo²⁴. In acute migraine (21 participants), the change in headache pain score was 0 on drug against 0.2 on placebo²³. In lumbar radicular pain (26 participants), the Part B pain change was 3.7 on drug against 3.1 on placebo²⁵. All three are completed with results posted on the registry, and none is published as a peer-reviewed efficacy paper.

Note what is absent from that list. There is no human trial of AOD-9604 for muscle gain, athletic recovery, injury healing, joint repair, sleep or anti-aging. There is no human trial at all of the subcutaneous injections that are actually sold⁴. And a 2026 review classifies the compound as an intermediate-tier agent for which short-term human trials exist but with limited interpretable signals⁴.

Every benefit claim you will read on a sales page traces to this section, not the last one. The animal literature is genuinely positive, and it is genuinely animal.

Weight and fat. In obese Zucker rats, 500 mcg/kg orally for 19 days cut body weight gain by more than half, 15.8 g against 35.6 g in controls, with increased lipolytic activity in fat tissue and, unlike intact growth hormone, no adverse effect on insulin sensitivity by euglycemic clamp⁵. In obese mice, 14 days of infusion reduced weight gain with increased fat oxidation and plasma glycerol¹¹. In Zucker fatty rats treated for 20 days with the un-tyrosinated parent fragment, mean fat-cell diameter fell from 110 to 80 micrometres¹⁴. Long-term treatment of obese mice with hGH 177-191 reduced cumulative weight gain and adipose mass¹⁵.

Human tissue, but not humans. The compound has been applied to human fat tissue, in a dish: isolated adipose tissue from obese humans showed increased lipolytic and decreased lipogenic activity¹³, and the peptide stimulates lipolysis and inhibits lipogenesis in vitro in rodent, porcine and human adipose tissue⁹. That is a real result and it is not the same thing as an effect in a person, which is what the phase 2b trials were built to measure.

Joints. The entire joint-repair story rests on one study in 32 rabbits with chemically induced knee osteoarthritis. Weekly ultrasound-guided injections directly into the joint, of 0.25 mg AOD9604 with or without 6 mg hyaluronic acid, produced better cartilage scores than saline, and the combination beat either agent alone with the shortest lameness period²⁰. Note the route: into the joint capsule, under ultrasound guidance, weekly. A 2026 review states that claims around osteoarthritis, joint repair or tissue regeneration are grounded mainly in animal work with a lack of convincing human clinical trial evidence⁴.

The counterweights. The animal record is not uniformly favourable to the marketing story. Isolated rat adipocytes showed reduced basal and insulin-stimulated glucose uptake, with the fragment more potent than intact hGH at equimolar concentrations¹⁷. And the 1982 and 1993 findings covered in the mechanism section, insulin antagonism in normal rats and no significant lipolytic effect by glycerol release, come from this same body of work¹⁸¹⁶.

This is the central claim, so it deserves its own answer rather than a line in a table.

The honest version is: it is a real functional domain of growth hormone, the design was rational, the separation from growth hormone signalling is real, and the fat-loss part did not reproduce in humans.

Taking those in order. The C-terminal region of growth hormone was identified decades ago as a lipid-mobilizing domain, inhibiting acetyl-CoA carboxylase in fat and liver cells³, and the synthetic version keeps the shape it had inside the whole protein⁹. So the premise is not invented.

The separation is real and measurable. No growth hormone receptor binding, no receptor-mediated cell proliferation¹¹, and in humans no IGF-1 movement across nine trials up to 24 weeks³. Growth hormone raises IGF-1; this does not. Growth hormone's long-term use carries glucose intolerance, insulin resistance and diabetes risk³; in the human trials, this compound showed no significant glucose or oral glucose tolerance changes³.

And then the part the marketing omits. Growth hormone reduces body fat mass in people. AOD-9604, in a 502-patient randomized trial over 24 weeks, did not beat placebo on weight⁴. The side effects were successfully left behind. On the human evidence, so was the effect. A fragment that avoids the receptor also avoids what the receptor does.

There is also a wrinkle inside the fragment's own literature worth knowing if you are going to make the pro-hormone argument. The same C-terminal sequence was reported in 1982 to cause hyperglycaemia and insulin resistance in rats¹⁸, and in 1993 to be antilipogenic but not significantly lipolytic in a fat-pad assay¹⁶. The clean division of growth hormone into a fat-burning half and a growth half is a story that this stretch of amino acids does not fully support.

There is no established dose of AOD-9604, because no dose of it has been shown to do anything in a person. What exists is a record of what trials administered, and a separate record of what the market recommends. They do not match on amount, route or frequency.

What the trials gave. Intravenously: 25 to 400 mcg/kg as single infusions in phase 1, then 25, 50 and 100 mcg/kg singles in obese men³. Orally: single doses of 9, 27 and 54 mg, then 9 to 54 mg daily for a week, then 1 to 30 mg daily for 12 weeks, and finally 0.25, 0.5 and 1 mg daily for 24 weeks³. The later pain trials used two 30 mg oral capsules per migraine attack²³, oral capsules over three weeks in neuropathic pain²⁴, and single intravenous infusions of 0.8, 1.2 and 1.8 mg/kg²⁵.

Notice the direction the program moved: from 54 mg down to 1 mg, and the largest, longest, lowest-dose trial is the one that failed. Notice also that the highest dose tested, 54 mg, was the one associated with an increased incidence of gastrointestinal adverse events³.

What the market recommends. A 2026 peer-reviewed review documents the practice directly: bodybuilding-related forums describe 250 to 500 mcg per day subcutaneously, split across 2 to 3 injections, ideally before exercise or fasted in the morning, in cycles of 8 to 12 weeks⁴.

The gap that matters most is not the number, it is the route. Not one human study of this molecule used subcutaneous injection. Every human dose on record was intravenous or oral³⁴. The compound is orally bioavailable in animals, and the development program deliberately moved to capsules and tablets¹⁹. A subcutaneous injectable is a formulation this molecule's own developers did not take into humans.

The honest answer has two halves that point in different directions, and anyone telling you only one half is selling something.

What the trials found. Across roughly 900 participants in six randomized placebo-controlled trials, tolerability was indistinguishable from placebo. In the 24-week trial, adverse events occurred in 75.6 to 83.2 percent of subjects across arms, and the highest rate was in the placebo group³. No adverse event was deemed definitely related to study treatment. No anti-AOD9604 antibodies were detected in any assayed subject, in either long-term trial³. IGF-1 did not move; glucose tolerance did not deteriorate³. Non-clinical work found no genotoxicity across Ames, chromosomal aberration and micronucleus assays, and no toxicological concerns after 6 months of oral dosing in rats and 9 months in monkeys¹⁹. The one dose-related signal was gastrointestinal events at the highest oral dose, 54 mg³.

What FDA says. That it has identified no, or only limited, safety-related information; that it therefore lacks sufficient information to know whether the drug would cause harm when administered to humans; that compounded drugs containing AOD-9604 may pose significant risk for immunogenicity for certain routes of administration and may have complexities regarding peptide-related impurities and API characterization; and that FDA has identified serious adverse events that may be associated with AOD-9604, though causality is not clear¹.

The item both halves touch. Five serious adverse events were reported in the 12-week trial, all neoplasms, all in drug arms: basal cell carcinoma, a moderate lipoma and squamous cell carcinoma on 20 mg, breast cancer on 5 mg, malignant melanoma on 10 mg. The investigator considered none of them related to study medication, and because IGF-1 did not change, they could not be attributed to the IGF-1 mechanism that drives growth hormone cancer concerns³. We report the finding and the investigator's assessment together, and we do not assert that these are the events FDA refers to, because no public document establishes that link.

Two limits on all of the above. Every safety observation here comes from intravenous or oral dosing in medically supervised trials of a pharmaceutical-grade product manufactured under cGMP conditions³. None of it describes subcutaneous injection of a research chemical of unverified content, which is what is being sold⁴.

There is no approved label for this compound, so there is no official contraindication list. What follows is not a list of exclusions from a label that does not exist; it is a description of who the evidence base cannot speak for at all.

The trials enrolled obese but otherwise healthy adults, aged 30 to 65 in the 12-week study, with the first four studies male-only and the two long-term studies excluding women of child-bearing potential in the 12-week trial³. Anyone outside those groups, meaning anyone with significant comorbidity, anyone outside that age band, and anyone who could become pregnant, is outside the population in which this compound was ever studied.

Athletes subject to anti-doping rules are in a different category: for them this is not a question of caution but of a prohibited substance, covered in its own section below³¹.

Beyond that, the honest statement is that FDA has said it lacks sufficient information to know whether this drug would cause harm when administered to humans¹. A contraindication list requires knowing the harms. Nobody publishing on this compound claims to.

No drug-interaction study of AOD-9604 has been published. The trials were not designed to detect interactions, and no interaction data appear in the safety review that summarizes all six of them³.

What the pharmacology suggests is worth stating carefully, as mechanism rather than evidence. The compound does not bind the growth hormone receptor and does not raise IGF-1 in humans¹¹³, which removes the most obvious interaction pathway that growth hormone itself has. Its measured effects on glucose handling in humans were null³, though the same C-terminal sequence has shown insulin-antagonistic activity in rats and reduced insulin-stimulated glucose uptake in isolated rat fat cells¹⁸¹⁷. Anyone taking insulin or other glucose-lowering medication is therefore in territory where animal data and human data disagree and no interaction study exists.

The compound is metabolized by rapid sequential cleavage of amino acids from its N-terminus rather than by hepatic enzyme systems⁷, which is a reason to expect fewer classical drug interactions, and not a substitute for having looked.

No data exist. No trial of this compound enrolled pregnant or breastfeeding participants, and the 12-week phase 2b trial specifically restricted female participants to those of non-child-bearing potential³. The first four trials enrolled only men³.

Reproductive toxicology is not among the non-clinical studies reported for this compound; the published non-clinical program covers genotoxicity, chronic oral toxicity in rats and monkeys, and pharmacokinetics¹⁹.

So the position is a complete absence of evidence, in a compound with no approved product, no label and an FDA statement that safety information is limited¹.

No validated storage standard exists for the vials sold online, because no approved product exists to carry one. What can be said comes from how the compound behaved in laboratories.

In the trials, the intravenous product was supplied in lyophilized form and reconstituted before use with a designated volume of sterile water for injection, and the oral forms were capsules and tablets made with conventional excipients, all manufactured under cGMP conditions by a named contract manufacturer³.

The peptide is fragile in solution. In rat plasma at room temperature, 75 to 80 percent was lost within an hour, with a serum half-life of about 4 minutes and intact peptide undetectable at 56 minutes; chilling and processing immediately prevented significant loss¹⁹. In doping-control work, at 4 and 22 degrees Celsius the compound was extensively degraded after one week in serum and plasma, while remaining detectable in dried matrices for the full two-month study³⁰.

Those figures describe biological matrices, not a vial of powder in a refrigerator, and should not be read as a shelf-life. They do establish that this is a peptide that comes apart readily once it is wet and warm.

Nobody selling this compound can tell you, and the question has a documented history rather than a hypothetical one.

In 2014, Belgian government analysts published a case report on identifying AOD9604 in unknown pharmaceutical preparations seized by the authorities, work carried out because the products' contents had to be established forensically rather than read from a label²⁷. In 2015, an American anti-doping laboratory reported that the peptide is available on several internet websites and was recently identified in confiscated vials in the USA⁷.

FDA's own concern is partly about exactly this: complexities with regard to peptide-related impurities and API characterization, alongside immunogenicity risk for certain routes of administration¹. Peptide-related impurities are not a theoretical category; they are what you get when synthesis, purification and storage are unverified.

A certificate of analysis supplied by a seller does not resolve this. It is a document about a sample, produced by or for the party selling the product, and it establishes neither that the tested sample matches your vial nor that the analysis was performed to any particular standard. Peer-reviewed reviews describe this market plainly: unapproved compounds operating largely outside regulatory oversight, where rigorous human safety data are scarce and there is potential for serious harm to patients³⁴. Orthopaedic review literature places AOD-9604 in the same category of peptides where preclinical work is promising and clinical trials are lacking³⁵.

AOD-9604 is prohibited at all times. The 2026 WADA Prohibited List names it explicitly in section S2.2.3, growth hormone fragments, in the same line as hGH 176-191³¹. Being a fragment rather than the hormone offers no exemption; the category exists precisely to cover fragments.

The belief that it is undetectable comes from a real finding, misapplied. AOD-9604 does not influence the WADA growth hormone isoform immunoassay²⁸. That is true, and it is why anti-doping laboratories built dedicated assays instead. A validated urine method detects it down to 50 pg/mL with 62 percent recovery⁷, direct-urine-injection screening covers it alongside other sub-2 kDa peptides at 50 to 500 pg/mL²⁹, and current workflows detect it in dried blood spots, serum and plasma³⁰.

Detection windows have their own quirk. The parent peptide degrades fast, but a metabolite, the fragment CRSVEGSCG, is significantly more stable than the parent compound and screening for it may extend the detection window⁷. Sample handling matters too: the compound degrades extensively within a week in liquid serum and plasma at 4 and 22 degrees Celsius, while staying detectable in dried matrices for months³⁰.

The pharmacokinetic picture is thin in humans and clear in animals, and the shape of the gap is itself informative.

In humans. The only posted human pharmacokinetic dataset comes from the 2023 intravenous study of this peptide: mean Cmax 12.6, 10.2 and 13.8 ng/mL at 0.8, 1.2 and 1.8 mg/kg, and Tmax 0.08 hours at every dose. Terminal half-life could not be determined at any dose level, because the criterion of at least three quantifiable elimination-phase data points was not met²⁵. A 2026 review records the same absence in one phrase: half-life not reported in human trials⁴. The drug leaves too fast to measure its leaving.

In animals. In pigs, the half-life after intravenous injection was approximately 3 minutes, with almost all drug cleared from plasma by 12 minutes. In rat plasma in vitro, the half-life was approximately 4 minutes with intact peptide undetectable at 56 minutes. The same paper cites about 21 minutes for growth hormone itself, and notes that a fragment being briefer is expected¹⁹.

Route and metabolism. The compound is orally bioavailable in animals: after oral dosing, parent peptide and its degradants appear in plasma, more slowly than after injection¹⁹. Elimination is by sequential removal of amino acids from the N-terminus; six metabolites have been identified in serum and urine, one of which, CRSVEGSCG, is markedly more stable than the parent⁷.

What is missing. There is no published human subcutaneous pharmacokinetic data of any kind, because no human study used that route⁴. For a compound sold as a subcutaneous injection, the kinetics of the route being sold are entirely unstudied.

What we do not know yet, as of 2026-08-14. No human efficacy has been demonstrated for any use of AOD-9604. The 24-week, 502-patient randomized trial in obesity failed its primary weight-loss endpoint, and that failure is documented in a peer-reviewed review citing a company stock-exchange announcement rather than in a published trial report. The 12-week, 300-patient trial's weight-loss result has never been published in any form we could locate, and we searched every record indexed for this compound in PubMed and Europe PMC. No human study has tested muscle gain, athletic recovery, injury healing, joint repair, skin, sleep or longevity. No human study has used the subcutaneous route the injectable market assumes, so subcutaneous pharmacokinetics, dose-response and safety are entirely unstudied in people. Human terminal half-life is unknown: in the only human intravenous study with posted kinetics, it could not be calculated because the peptide cleared too quickly to yield three quantifiable elimination-phase points. There are no drug-interaction studies, no reproductive toxicology, no data in pregnancy or breastfeeding, and no data in anyone outside the obese, otherwise healthy adult populations the trials enrolled. The joint and cartilage claims rest on a single rabbit study using weekly ultrasound-guided injections into the joint capsule, and a 2026 review states human clinical trial evidence in those indications is lacking. Five serious adverse events, all neoplasms, occurred in drug arms of the 12-week trial and were judged unrelated to treatment by the investigator; whether they bear any relationship to the serious adverse events FDA refers to is not established by any public document. FDA states it has identified no, or only limited, safety-related information and therefore lacks sufficient information to know whether the drug would cause harm when administered to humans. Where marketing quotes benefit numbers for this compound, they trace to rodent and rabbit studies, to isolated fat tissue in a dish, or to the early-phase safety trials of a program that its own sponsor terminated.

Two tables carry most of the argument on this site. The first sets AOD-9604 against the hormone it is a fragment of, row by row, because that comparison is what the product's entire pitch rests on. The second sets the trial and regulatory record against the claims made for the compound in the market⁴³.

Every row in both tables carries its own source. Where a row states an absence, the absence is the finding, and the citation shows what was searched¹.

Every source below was fetched and read on 2026-08-14. Where free full text exists, the primary link goes to it; otherwise the primary link goes to the Europe PMC record, which mirrors the MEDLINE entry and carries the PMID. The same list ships as this page's machine-readable citation manifest.

The questions below are answered from the same claims ledger as the rest of this page; each answer carries its sources inline.

AOD-9604 is often stacked with or compared to other growth hormone axis peptides, which work by entirely different mechanisms. Growth hormone secretagogues such as ipamorelin, and GHRH analogues such as sermorelin, CJC-1295 and tesamorelin, act on the pituitary to raise the body's own growth hormone and IGF-1⁴. AOD-9604 does the opposite of that by design: it does not touch the growth hormone receptor and does not raise IGF-1¹¹³.

That distinction matters when reading any claim that stacks them. A 2026 review notes that AOD9604 is omitted from its cross-class endocrine comparison as a separate column precisely because it acts independently of the GH receptor and shows no systematic somatotropic activation in available data⁴.