# AOD-9604: full monograph (AOD-9604 Co)
> Source page: https://aod9604co.com/monograph

Status: Research compound, not FDA-approved
Disclosure: AOD-9604 is not FDA approved. FDA cites limited safety information and immunogenicity concerns; it is sold as a research chemical with no established human efficacy.
Not the same substance as: Somatropin (recombinant human growth hormone; the full 191-amino-acid hormone, of which this is 16 residues); Ipamorelin (a ghrelin-receptor agonist that raises the body's own growth hormone; a different mechanism entirely); CJC-1295 and sermorelin (GHRH analogues acting on the pituitary); Tesamorelin (Egrifta, the approved GHRH analogue for HIV-associated lipodystrophy); Somatostatin (177-191) and Tyr-somatostatin (177-191), which appear in the PubChem synonym list for CID 71300630 but describe a different parent protein; AOD-9604 is a growth hormone fragment, not a somatostatin fragment
Updated: 2026-08-14

## Key facts
- Status: Research compound, not FDA-approved
- Animal half life: About 3 minutes after IV injection in pigs, with almost all drug cleared from plasma by 12 minutes; about 4 minutes in rat plasma in vitro, with intact peptide undetectable at 56 minutes min (source: https://www.jofem.org/index.php/jofem/article/view/213)
- Human cmax: 12.6, 10.2 and 13.8 ng/mL after single IV infusions of 0.8, 1.2 and 1.8 mg/kg respectively (means, healthy volunteers) ng/mL (source: https://clinicaltrials.gov/study/NCT05298306)
- Human tmax: 0.08 hours (about 5 minutes) at every IV dose level h (source: https://clinicaltrials.gov/study/NCT05298306)
- Igf1 response: No significant IGF-1 elevation in any human trial, including at 12 and 24 weeks of daily oral dosing (p = 0.50844 and p = 0.75754 versus placebo). This is the compound's most reproducible human finding, and it is a negative (source: https://www.jofem.org/index.php/jofem/article/view/157)
- Metabolism: Degraded by sequential removal of amino acids from the N-terminus. Six metabolites identified in serum and urine; the fragment CRSVEGSCG is markedly more stable than the parent peptide and is used to extend the doping-control detection window (source: https://europepmc.org/article/MED/25208511)
- Oral bioavailability: Orally bioavailable in pigs and rats: parent peptide and its degradants appear in plasma after oral dosing, with slower absorption than IV and the same degradation products. No human bioavailability figure has been published (source: https://www.jofem.org/index.php/jofem/article/view/213)
- Subcutaneous kinetics: Unstudied. Every human study of this molecule used the intravenous or oral route. No published human subcutaneous pharmacokinetic data exist, which is the route the injectable gray market uses (source: https://pmc.ncbi.nlm.nih.gov/articles/PMC13322892/)
- Class: Synthetic C-terminal fragment of human growth hormone (Tyr-hGH 177-191); a growth hormone fragment, not a growth hormone secretagogue (source: https://europepmc.org/article/MED/25208511)
- Human half-life: Not determinable from posted human data; about 3 minutes IV in pigs min (source: https://clinicaltrials.gov/study/NCT05298306)
- Molecule: Hexadecapeptide, sequence YLRIVQCRSVEGSCGF, disulfide-bridged, C78H123N23O23S2, molecular weight 1815.1 (source: https://pubchem.ncbi.nlm.nih.gov/compound/71300630)
- Developer: Metabolic Pharmaceuticals Ltd (Australia); phase 2a trials were underway by February 2002 (source: https://europepmc.org/article/MED/15134286)
- Human trials: 9 with published or posted results: 6 in the obesity program (about 900 participants) and 3 later pain trials of the same peptide (source: https://www.jofem.org/index.php/jofem/article/view/157)
- Obesity outcome: The 24-week, 502-patient phase 2b trial failed its primary weight-loss endpoint and the program was terminated (source: https://pmc.ncbi.nlm.nih.gov/articles/PMC13322892/)
- Anti-doping: Prohibited at all times under WADA section S2.2.3, growth hormone fragments, named explicitly as AOD-9604 and hGH 176-191 (source: https://www.wada-ama.org/en/prohibited-list)
- IGF-1 effect: None detected in humans at any dose or duration studied, including 24 weeks of daily dosing (source: https://www.jofem.org/index.php/jofem/article/view/157)

## Overview
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 it 7 . 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 participants 3 . 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 terminated 4 . Three facts frame the rest of this page. No product containing AOD-9604 has ever been approved by FDA for any use 2 . 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 humans 1 . And a 2026 peer-reviewed review concludes there are no robust data supporting clinically meaningful visceral-fat reduction or broader metabolic benefit in humans 4 . 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 for 3 4 .
Sources: https://europepmc.org/article/MED/25208511 ; https://www.jofem.org/index.php/jofem/article/view/157 ; https://pmc.ncbi.nlm.nih.gov/articles/PMC13322892/ ; https://www.accessdata.fda.gov/scripts/cder/daf/ ; https://www.fda.gov/drugs/human-drug-compounding/certain-bulk-drug-substances-use-compounding-may-present-significant-safety-risks

## About AOD-9604 (Tyr-hGH 177-191)
Human growth hormone is a single chain of 191 amino acids 3 . 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 domain 3 . 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 loop 8 , giving formula C78H123N23O23S2 and molecular weight 1815.1 6 . 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 line 31 . The 1980s and 1990s papers you will see cited in marketing generally studied hGH 177-191 or the un-tyrosinated AOD9401, not AOD-9604 itself 14 . 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 structure 9 . 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 database 36 . AOD-9604 has none 2 .
Sources: https://pmc.ncbi.nlm.nih.gov/articles/PMC10034483/ ; https://pubchem.ncbi.nlm.nih.gov/compound/71300630 ; https://www.wada-ama.org/en/prohibited-list ; https://europepmc.org/article/MED/11152298 ; https://www.accessdata.fda.gov/scripts/cder/daf/

## Regulatory status: what the FDA listing actually says
AOD-9604 is not FDA approved. FDA cites limited safety information and immunogenicity concerns; it is sold as a research chemical with no established human efficacy. Two separate facts sit behind that sentence, and they are worth reading apart. First, approval. A search of Drugs@FDA returns no product containing AOD-9604, and an openFDA query for the ingredient returns NOT_FOUND 2 . There is no approved AOD-9604 product in the United States or, per a 2026 review, with any major regulatory agency 4 . Second, the safety listing. FDA maintains a page of bulk drug substances nominated for use in compounding that may present significant safety risks. AOD-9604 appears there, in the table of substances nominated but withdrawn , meaning the nomination was pulled rather than resolved in the compound's favour 1 . The entry reads, in full: compounded drugs containing AOD-9604 may pose significant risk for immunogenicity for certain routes of administration and may have complexities with regard to peptide-related impurities and API characterization; FDA has identified no, or only limited, safety-related information; therefore, the agency lacks sufficient information to know whether the drug would cause harm when administered to humans; FDA has also identified serious adverse events that may be associated with AOD-9604, though causality is not clear 1 . Read that carefully, because it is easy to misread in either direction. FDA is not saying the compound has been shown to be dangerous. It is saying the safety file is not sufficient to know, and that some serious adverse events exist whose relationship to the drug is unclear. Meanwhile the published trial literature reports tolerability indistinguishable from placebo across roughly 900 participants 3 . Both statements are on this page, next to each other, because both are true and neither cancels the other. One more boundary. Even where a compound can legally be compounded, compounded drugs are not FDA-approved products: FDA does not verify their safety, effectiveness or quality before marketing 37 . Vials sold as research chemicals sit further outside that boundary again.
Sources: https://www.accessdata.fda.gov/scripts/cder/daf/ ; https://www.fda.gov/drugs/human-drug-compounding/certain-bulk-drug-substances-use-compounding-may-present-significant-safety-risks ; https://pmc.ncbi.nlm.nih.gov/articles/PMC13322892/ ; https://www.jofem.org/index.php/jofem/article/view/157 ; https://www.fda.gov/drugs/human-drug-compounding/compounding-and-fda-questions-and-answers

## The abandoned program: from Metabolic Pharmaceuticals to a research chemical
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 obesity 10 . 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 underway 10 . 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 breakdown 32 33 . 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 502 3 . 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 endpoint 4 . 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 terminated 4 . 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 foods 19 3 . 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 indications 8 . Meanwhile, the peptide had become a research chemical sold on the internet and, by 2014, was being identified by government analysts in confiscated vials 7 .
Sources: https://europepmc.org/article/MED/15134286 ; https://www.jofem.org/index.php/jofem/article/view/157 ; https://pmc.ncbi.nlm.nih.gov/articles/PMC13322892/ ; https://www.jofem.org/index.php/jofem/article/view/213 ; https://pmc.ncbi.nlm.nih.gov/articles/PMC10034483/ ; https://europepmc.org/article/MED/25208511

## Mechanism of action
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 hGH 11 . A later paper on the same molecule states it directly: LAT8881, formerly identified as AOD9604, was found to not act via the GH receptor 8 . 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 placebo 3 . 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 receptor 12 . 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-driven 13 . 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 lipolysis 16 . 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 190 18 . The idea that this stretch of the hormone carries only the fat-burning function, and nothing else, is a simplification of its own literature.
Sources: https://europepmc.org/article/MED/11673763 ; https://pmc.ncbi.nlm.nih.gov/articles/PMC10034483/ ; https://www.jofem.org/index.php/jofem/article/view/157 ; https://europepmc.org/article/MED/11713213 ; https://europepmc.org/article/MED/10950816 ; https://europepmc.org/article/MED/8358331 ; https://europepmc.org/article/MED/6751009

## Human evidence: the complete list
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 men 3 . 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 placebo 3 . 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 objective 3 . 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 PMC 3 . 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-1 3 . 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 endpoint 4 . 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 detected 3 . 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 placebo 24 . In acute migraine (21 participants), the change in headache pain score was 0 on drug against 0.2 on placebo 23 . In lumbar radicular pain (26 participants), the Part B pain change was 3.7 on drug against 3.1 on placebo 25 . 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 sold 4 . And a 2026 review classifies the compound as an intermediate-tier agent for which short-term human trials exist but with limited interpretable signals 4 .
Sources: https://www.jofem.org/index.php/jofem/article/view/157 ; https://pmc.ncbi.nlm.nih.gov/articles/PMC13322892/ ; https://clinicaltrials.gov/study/NCT03865953 ; https://clinicaltrials.gov/study/NCT04153409 ; https://clinicaltrials.gov/study/NCT05298306

## Animal evidence: where the marketed benefits come from
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 clamp 5 . In obese mice, 14 days of infusion reduced weight gain with increased fat oxidation and plasma glycerol 11 . In Zucker fatty rats treated for 20 days with the un-tyrosinated parent fragment, mean fat-cell diameter fell from 110 to 80 micrometres 14 . Long-term treatment of obese mice with hGH 177-191 reduced cumulative weight gain and adipose mass 15 . 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 activity 13 , and the peptide stimulates lipolysis and inhibits lipogenesis in vitro in rodent, porcine and human adipose tissue 9 . 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 period 20 . 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 evidence 4 . 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 concentrations 17 . 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 work 18 16 .
Sources: https://europepmc.org/article/MED/11146367 ; https://europepmc.org/article/MED/11673763 ; https://europepmc.org/article/MED/11116208 ; https://europepmc.org/article/MED/10950816 ; https://europepmc.org/article/MED/26275694 ; https://pmc.ncbi.nlm.nih.gov/articles/PMC13322892/ ; https://europepmc.org/article/MED/8118430

## Is it really the fat-loss part of growth hormone?
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 cells 3 , and the synthetic version keeps the shape it had inside the whole protein 9 . So the premise is not invented. The separation is real and measurable. No growth hormone receptor binding, no receptor-mediated cell proliferation 11 , and in humans no IGF-1 movement across nine trials up to 24 weeks 3 . Growth hormone raises IGF-1; this does not. Growth hormone's long-term use carries glucose intolerance, insulin resistance and diabetes risk 3 ; in the human trials, this compound showed no significant glucose or oral glucose tolerance changes 3 . 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 weight 4 . 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 rats 18 , and in 1993 to be antilipogenic but not significantly lipolytic in a fat-pad assay 16 . 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.
Sources: https://www.jofem.org/index.php/jofem/article/view/157 ; https://europepmc.org/article/MED/11152298 ; https://europepmc.org/article/MED/11673763 ; https://pmc.ncbi.nlm.nih.gov/articles/PMC13322892/ ; https://europepmc.org/article/MED/6751009 ; https://europepmc.org/article/MED/8358331

## Dosage: what was studied versus what is sold
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 men 3 . 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 weeks 3 . The later pain trials used two 30 mg oral capsules per migraine attack 23 , oral capsules over three weeks in neuropathic pain 24 , and single intravenous infusions of 0.8, 1.2 and 1.8 mg/kg 25 . 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 events 3 . 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 weeks 4 . 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 oral 3 4 . The compound is orally bioavailable in animals, and the development program deliberately moved to capsules and tablets 19 . A subcutaneous injectable is a formulation this molecule's own developers did not take into humans.
Sources: https://www.jofem.org/index.php/jofem/article/view/157 ; https://clinicaltrials.gov/study/NCT04153409 ; https://clinicaltrials.gov/study/NCT03865953 ; https://clinicaltrials.gov/study/NCT05298306 ; https://pmc.ncbi.nlm.nih.gov/articles/PMC13322892/ ; https://www.jofem.org/index.php/jofem/article/view/213

## Is AOD-9604 safe?
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 group 3 . No adverse event was deemed definitely related to study treatment. No anti-AOD9604 antibodies were detected in any assayed subject, in either long-term trial 3 . IGF-1 did not move; glucose tolerance did not deteriorate 3 . 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 monkeys 19 . The one dose-related signal was gastrointestinal events at the highest oral dose, 54 mg 3 . 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 clear 1 . 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 concerns 3 . 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 conditions 3 . None of it describes subcutaneous injection of a research chemical of unverified content, which is what is being sold 4 .
Sources: https://www.jofem.org/index.php/jofem/article/view/157 ; https://www.jofem.org/index.php/jofem/article/view/213 ; https://www.fda.gov/drugs/human-drug-compounding/certain-bulk-drug-substances-use-compounding-may-present-significant-safety-risks ; https://pmc.ncbi.nlm.nih.gov/articles/PMC13322892/

## Who should not consider AOD-9604?
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 trial 3 . 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 below 31 . 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 humans 1 . A contraindication list requires knowing the harms. Nobody publishing on this compound claims to.
Sources: https://www.jofem.org/index.php/jofem/article/view/157 ; https://www.wada-ama.org/en/prohibited-list ; https://www.fda.gov/drugs/human-drug-compounding/certain-bulk-drug-substances-use-compounding-may-present-significant-safety-risks

## Which medicines and conditions interact with AOD-9604?
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 them 3 . 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 humans 11 3 , which removes the most obvious interaction pathway that growth hormone itself has. Its measured effects on glucose handling in humans were null 3 , though the same C-terminal sequence has shown insulin-antagonistic activity in rats and reduced insulin-stimulated glucose uptake in isolated rat fat cells 18 17 . 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 systems 7 , which is a reason to expect fewer classical drug interactions, and not a substitute for having looked.
Sources: https://www.jofem.org/index.php/jofem/article/view/157 ; https://europepmc.org/article/MED/11673763 ; https://europepmc.org/article/MED/6751009 ; https://europepmc.org/article/MED/8118430 ; https://europepmc.org/article/MED/25208511

## What about pregnancy and breastfeeding?
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 potential 3 . The first four trials enrolled only men 3 . 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 pharmacokinetics 19 . 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 limited 1 .
Sources: https://www.jofem.org/index.php/jofem/article/view/157 ; https://www.jofem.org/index.php/jofem/article/view/213 ; https://www.fda.gov/drugs/human-drug-compounding/certain-bulk-drug-substances-use-compounding-may-present-significant-safety-risks

## How is AOD-9604 stored and handled?
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 manufacturer 3 . 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 loss 19 . 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 study 30 . 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.
Sources: https://www.jofem.org/index.php/jofem/article/view/157 ; https://www.jofem.org/index.php/jofem/article/view/213 ; https://europepmc.org/article/MED/42328738

## What is actually in the vials?
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 label 27 . 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 USA 7 . 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 administration 1 . 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 patients 34 . Orthopaedic review literature places AOD-9604 in the same category of peptides where preclinical work is promising and clinical trials are lacking 35 .
Sources: https://europepmc.org/article/MED/24976118 ; https://europepmc.org/article/MED/25208511 ; https://www.fda.gov/drugs/human-drug-compounding/certain-bulk-drug-substances-use-compounding-may-present-significant-safety-risks ; https://europepmc.org/article/MED/41966639

## What should athletes know?
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 176-191 31 . 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 immunoassay 28 . 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 recovery 7 , direct-urine-injection screening covers it alongside other sub-2 kDa peptides at 50 to 500 pg/mL 29 , and current workflows detect it in dried blood spots, serum and plasma 30 . 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 window 7 . 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 months 30 .
Sources: https://www.wada-ama.org/en/prohibited-list ; https://europepmc.org/article/MED/24124033 ; https://europepmc.org/article/MED/25208511 ; https://europepmc.org/article/MED/26578461 ; https://europepmc.org/article/MED/42328738

## Pharmacokinetics
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 met 25 . A 2026 review records the same absence in one phrase: half-life not reported in human trials 4 . 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 expected 19 . 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 injection 19 . 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 parent 7 . What is missing. There is no published human subcutaneous pharmacokinetic data of any kind, because no human study used that route 4 . For a compound sold as a subcutaneous injection, the kinetics of the route being sold are entirely unstudied.
Sources: https://clinicaltrials.gov/study/NCT05298306 ; https://pmc.ncbi.nlm.nih.gov/articles/PMC13322892/ ; https://www.jofem.org/index.php/jofem/article/view/213 ; https://europepmc.org/article/MED/25208511

## What we do not know yet
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.
Sources: https://pmc.ncbi.nlm.nih.gov/articles/PMC13322892/ ; https://www.fda.gov/drugs/human-drug-compounding/certain-bulk-drug-substances-use-compounding-may-present-significant-safety-risks ; https://www.jofem.org/index.php/jofem/article/view/157

## Comparisons
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 market 4 3 . 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 searched 1 .
Sources: https://pmc.ncbi.nlm.nih.gov/articles/PMC13322892/ ; https://www.jofem.org/index.php/jofem/article/view/157 ; https://www.fda.gov/drugs/human-drug-compounding/certain-bulk-drug-substances-use-compounding-may-present-significant-safety-risks

## References
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.

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

## Related compounds and comparisons
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-1 4 . AOD-9604 does the opposite of that by design: it does not touch the growth hormone receptor and does not raise IGF-1 11 3 . 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 data 4 .
Sources: https://pmc.ncbi.nlm.nih.gov/articles/PMC13322892/ ; https://europepmc.org/article/MED/11673763 ; https://www.jofem.org/index.php/jofem/article/view/157

## Study results
| Study | Species/model | n | Duration | Outcome | Effect size | Publication status |
| --- | --- | --- | --- | --- | --- | --- |
| S1 (https://www.jofem.org/index.php/jofem/article/view/157) | human (METAOD001. Double-blind, placebo-controlled, dose-escalation safety study in healthy adult males, BMI 24 to 30, with single-dose recombinant hGH 0.12 IU/kg IV as a positive control) | 15 | Single doses | Well tolerated. 29 adverse events in 12 subjects, no serious adverse events; most common was headache (6). No clinically significant changes in vital signs, laboratory values or ECG, and no significant glycerol, glucose or IGF-1 trends for AOD9604, rhGH or placebo | No efficacy endpoint; this was a safety and tolerability study | Summarized in a peer-reviewed safety review by the sponsor's authors; no standalone trial report is indexed in PubMed |
| S2 (https://www.jofem.org/index.php/jofem/article/view/157) | human (METAOD002. Double-blind, placebo-controlled 4 x 4 Latin square safety study in clinically obese males, BMI at or above 35) | 23 | Single doses | No clinically relevant changes in safety laboratory parameters, vital signs or ECG through 24 hours. No significant changes in glucose or IGF-1 versus placebo | No efficacy endpoint | Summarized in the same peer-reviewed safety review; no standalone trial report indexed |
| S3 (https://www.jofem.org/index.php/jofem/article/view/157) | human (METAOD003. Double-blind, placebo-controlled 4 x 4 Latin square study in clinically obese males, BMI at or above 35) | 17 | Single doses | No significant IGF-1 changes over 24 hours at any dose. One isolated glucose signal: an 8 percent increase 12 hours post-dose in one subject on 54 mg. The only event judged definitely treatment-related in the study was taste perversion, and it followed placebo | No efficacy endpoint | Summarized in the peer-reviewed safety review; no standalone trial report indexed |
| S4 (https://www.jofem.org/index.php/jofem/article/view/157) | human (METAOD004. Double-blind, placebo-controlled dose-escalation study in clinically obese males, BMI at or above 30) | 36 | 7 days | Fasting plasma glucose and serum insulin unchanged across the treatment period; no changes in any oral glucose tolerance test parameter from day 1 to day 7; no clinically significant laboratory, vital sign or ECG findings | No efficacy endpoint | Summarized in the peer-reviewed safety review; no standalone trial report indexed |
| S5 (https://www.jofem.org/index.php/jofem/article/view/157) | human (METAOD005. Randomized, double-blind, placebo-controlled, parallel-group study at 5 Australian hospitals in healthy obese adults, BMI at or above 35 (median 40), with a 2-week single-blind placebo run-in) | 300 (about 50 per group) | 12 weeks after a 2-week run-in | Stated objective was to assess efficacy measured as reduction in body weight, plus safety and tolerability. The peer-reviewed publication reports the safety results only: no significant change in IGF-1 in any group, no significant oral glucose tolerance test changes, no anti-AOD9604 antibodies at any timepoint. Five serious adverse events occurred, all neoplasms, all in AOD9604 arms: three on 20 mg (basal cell carcinoma, moderate lipoma, squamous cell carcinoma), one on 5 mg (breast cancer), one on 10 mg (malignant melanoma). The investigator considered none of them related to study medication | No weight-loss result has ever been published for this trial | Safety results peer-reviewed; the efficacy result was never published in any form we could locate |
| S6 (https://pmc.ncbi.nlm.nih.gov/articles/PMC13322892/) | human (METAOD006. Randomized, double-blind, placebo-controlled, multi-center, parallel-group study at 16 Australian hospitals and medical centres in clinically obese adults, BMI 30 to 45 (median 36.3), with a 4-week single-blind placebo run-in and 4-week follow-up) | 534 enrolled, 502 randomized | 24 weeks | Failed to demonstrate a significant benefit on the primary weight-loss endpoint. Safety was indistinguishable from placebo: adverse event incidence 75.6 to 83.2 percent across arms with the highest rate in the placebo group, no significant IGF-1 differences (p = 0.50844 at 12 weeks, p = 0.75754 at 24 weeks), no significant glucose differences, no anti-AOD9604 antibodies detected | No significant benefit versus placebo on the primary weight-loss endpoint | DOCUMENTED ABSENCE. The safety data are peer-reviewed; the efficacy failure is sourced to a 2007 sponsor stock-exchange announcement, and a 2026 peer-reviewed review states that conclusions about the lack of efficacy rest on sponsor-reported program outcomes rather than peer-reviewed randomized efficacy trials |
| S7 (https://clinicaltrials.gov/study/NCT03865953) | human (NCT03865953. Randomized, double-blind, placebo-controlled, crossover phase 2a study of oral LAT8881 in neuropathic pain (Lateral Pharma)) | 53 | 3 weeks per period | Primary endpoint, absolute change in mean pain score on an 11-point numeric pain rating scale: LAT8881 -0.87 (SD 1.53) versus placebo -0.74 (SD 2.09) | Difference of 0.13 points on an 11-point scale, favouring drug | Results posted on ClinicalTrials.gov; no peer-reviewed efficacy publication indexed for this trial |
| S8 (https://clinicaltrials.gov/study/NCT04153409) | human (NCT04153409. Randomized, double-blind, placebo-controlled, crossover proof-of-concept study of oral LAT8881 in acute migraine) | 21 | Single treated attacks in crossover | Primary endpoint, change in migraine headache pain score on an 11-point numeric rating scale: active 0 (SD 1.10) versus placebo 0.2 (SD 1.33) | No reduction from baseline in the active arm | Results posted on ClinicalTrials.gov; no peer-reviewed efficacy publication indexed for this trial |
| S9 (https://clinicaltrials.gov/study/NCT05298306) | human (NCT05298306. Two-part study: Part A ascending-dose IV safety and pharmacokinetics in healthy volunteers, Part B single IV dose versus placebo in lumbar radicular pain) | 26 | Single dose, sampling to 6 hours | Part B primary endpoint, change in baseline pain: LAT8881 3.7 (SD 2.7) versus placebo 3.1 (SD 2.3). Part A pharmacokinetics: Cmax 12.6, 10.2 and 13.8 ng/mL across the three ascending doses, Tmax 0.08 hours. Terminal half-life could not be determined at any dose because the criterion of at least three quantifiable elimination-phase data points was not met | No separation from placebo on the primary pain endpoint | Results posted on ClinicalTrials.gov; no peer-reviewed efficacy publication indexed for this trial |
| S10 (https://europepmc.org/article/MED/11146367) | rat (Obese Zucker rats, daily oral dosing) | Not stated in abstract | 19 days | Body weight gain reduced by over 50 percent versus control (15.8 +/- 0.6 g versus 35.6 +/- 0.8 g). Adipose tissue showed increased lipolytic activity. Unlike chronic intact hGH, no adverse effect on insulin sensitivity by euglycemic clamp | Weight gain 15.8 g versus 35.6 g in controls | Peer-reviewed |
| S11 (https://europepmc.org/article/MED/11673763) | mouse; in vitro (Obese (ob/ob) and lean C57BL/6J mice by mini-osmotic pump, plus BaF-BO3 cells transfected with the hGH receptor) | Not stated in abstract | 14 days | Both hGH and AOD9604 significantly reduced body weight gain in obese mice, with increased in vivo fat oxidation and increased plasma glycerol. Unlike hGH, AOD9604 did not induce hyperglycaemia or reduce insulin secretion. In vitro, AOD9604 did not compete for the hGH receptor and did not induce cell proliferation, unlike hGH | Not stated numerically in abstract | Peer-reviewed. This is the single study that anchors the whole fragment-versus-hormone marketing story |
| S12 (https://europepmc.org/article/MED/11713213) | mouse (Obese mice and beta3-adrenergic receptor knock-out mice, chronic intraperitoneal dosing) | Not stated in abstract | 14 days | Both hGH and AOD9604 reduced body weight and body fat in obese mice and raised repressed beta3-AR RNA levels to those of lean mice. In beta3-AR knock-out mice, chronic treatment failed to change body weight or lipolysis, yet acutely AOD9604 still increased energy expenditure and fat oxidation. The authors concluded the lipolytic actions are not mediated directly through beta3-AR | Not stated numerically in abstract | Peer-reviewed |
| S13 (https://europepmc.org/article/MED/10950816) | mouse; human adipose tissue in vitro (C57BL/6J (ob/ob) mice treated orally, plus isolated adipose tissue from obese rodents and from humans) | 18 mice (8 saline, 10 AOD-9401) | 30 days | From day 16 onward body weight gain was significantly lower than saline controls with no difference in food consumption. Ex vivo adipose tissue showed reduced lipogenic and increased lipolytic activity, and acute energy expenditure and glucose and fat oxidation rose. In vitro, lipolytic activity increased and lipogenic activity decreased in isolated adipose tissue from obese rodents and humans | Not stated numerically in abstract | Peer-reviewed. The human component is isolated tissue in a dish, not a person |
| S14 (https://europepmc.org/article/MED/11116208) | rat (Obese Zucker fatty rats plus isolated rat adipose tissue) | Not stated in abstract | 20 days | Reduced body weight gain; mean adipocyte diameter fell from 110 to 80 micrometres. The peptide stimulated hormone-sensitive lipase and inhibited acetyl-CoA carboxylase in isolated rat adipose tissue, mimicking intact hGH, without inducing insulin resistance or glucose intolerance | Adipocyte diameter 110 to 80 micrometres | Peer-reviewed |
| S15 (https://europepmc.org/article/MED/7987248) | mouse (C57BL/6J (ob/ob) obese mice, long-term treatment) | Not stated in abstract | Long-term (not further specified in abstract) | Reduced cumulative body weight gain and decreased adipose tissue mass; lipogenesis in adipose tissue was significantly inhibited | Not stated numerically in abstract | Peer-reviewed |
| S16 (https://europepmc.org/article/MED/8358331) | rat (Peptide-treated rats, glycerol release from epididymal fat pads) | Not stated in abstract | Not stated in abstract | Antilipogenic activity identical to intact hGH, but NO significant lipolytic effect was found as measured by glycerol release from epididymal fat pads. The authors concluded the main physiological effect of hGH on lipid metabolism is at the level of lipogenesis | No significant lipolytic effect in this assay | Peer-reviewed. Rarely cited in marketing, which describes the compound as lipolytic |
| S17 (https://europepmc.org/article/MED/8118430) | rat (in vitro adipocytes) (Adipocytes isolated from genetically obese Zucker rats) | Not applicable | Acute | Reduced basal and insulin-stimulated 2-deoxyglucose uptake. At equimolar concentrations the fragment was more potent than intact hGH | More potent than intact hGH at equimolar concentrations | Peer-reviewed |
| S18 (https://europepmc.org/article/MED/6751009) | rat (Normal rats, in vivo insulin-antagonism assay) | Not stated in abstract | Acute | Cam-hGH 177-191 caused significant hyperglycaemia and insulin resistance in normal rats at nanomolar quantities; shorter fragments (177-180, 177-185, 177-187, 177-189) were inactive even at up to one hundred times the dose. The insulin-antagonistic core sits within residues 178 to 190 | Active at nanomolar quantities; shortened fragments inactive at 100x dose | Peer-reviewed. Complicates the claim that this region carries only the fat-burning half of growth hormone |
| S19 (https://europepmc.org/article/MED/11152298) | in vitro (rodent, porcine and human adipose tissue) (Two-dimensional proton NMR structure determination plus tissue assays) | Not applicable | Not applicable | The cyclic region adopts type I beta-turns and retains structural similarity to the corresponding region of the intact hGH crystal structure. The peptide stimulates lipolysis and inhibits lipogenesis in vitro in rodent, porcine and human adipose tissues | Not stated numerically in abstract | Peer-reviewed |
| S20 (https://europepmc.org/article/MED/26275694) | rabbit (Collagenase-induced knee osteoarthritis in mature New Zealand white rabbits, ultrasound-guided intra-articular injection) | 32 | 4 to 7 weeks of injections, assessment at 8 weeks | Gross morphological and histopathological scores were significantly worse in saline controls than in the hyaluronic acid, AOD9604 and combination groups, and significantly better in the combination group than in either alone. The combination group had the shortest lameness period | Combination superior to either agent alone on cartilage scores | Peer-reviewed. This single rabbit study is the origin of essentially all joint-repair marketing for this compound |
| S21 (https://www.jofem.org/index.php/jofem/article/view/213) | pig; rat; cynomolgus monkey; in vitro (Pig pharmacokinetics after IV and oral dosing, rat whole-body radiography with carbon-14 label, 6-month rat and 9-month cynomolgus monkey oral gavage toxicology, Ames test, CHO chromosomal aberration assay, rat bone micronucleus assay) | 1 pig IV and 1 pig oral for the kinetic study | Single doses for kinetics; 6 and 9 months for chronic toxicology | Very short half-life of approximately 3 minutes after IV injection in pigs, with almost complete clearance from plasma by 12 minutes; in rat plasma in vitro the half-life was approximately 4 minutes with intact peptide undetectable at 56 minutes. Orally the peptide and its degradants appeared in plasma, so it is orally bioavailable, with slower kinetics. No evidence of genotoxicity in any assay and no toxicological concerns after chronic oral dosing in rats and monkeys | IV half-life about 3 minutes in pigs; in vitro rat plasma half-life about 4 minutes | Peer-reviewed, sponsor-authored, published as nutraceutical-ingredient safety documentation |
| S22 (https://europepmc.org/article/MED/25208511) | in vitro (human serum and urine) (Incubation of AOD9604 in serum and urine with mass-spectrometric metabolite identification, plus validation of a urinary solid-phase extraction assay) | Not applicable | Not applicable | Six potential metabolites identified. A single serum metabolite, the peptide CRSVEGSCG, is significantly more stable than the other metabolites or the parent compound. Urinary limit of detection 50 pg/mL, recovery 62 percent. The paper records that the peptide is available on several internet websites and was recently identified in confiscated vials in the USA | Limit of detection 50 pg/mL in urine | Peer-reviewed |
| S23 (https://europepmc.org/article/MED/24976118) | not applicable (seized pharmaceutical preparations) (Analytical identification and characterization of peptide drugs in unknown preparations seized by the Belgian authorities, reported as a case report on AOD9604) | Not applicable | Not applicable | AOD9604 was identified in unlabelled seized pharmaceutical preparations, documenting that this compound circulates through channels where product identity has to be established forensically rather than read off a label | Not applicable | Peer-reviewed (abstract not distributed by PubMed; title, journal and year verified through PubMed and Europe PMC records) |
| S24 (https://europepmc.org/article/MED/24124033) | not applicable (immunoassay study) (Laboratory evaluation of whether AOD-9604 interferes with the WADA growth hormone isoform immunoassay) | Not applicable | Not applicable | AOD-9604 does not influence the WADA hGH isoform immunoassay, which is why anti-doping laboratories developed dedicated peptide assays for it rather than relying on growth hormone tests | No influence on the isoform assay | Peer-reviewed (abstract not distributed by PubMed; finding is stated in the article title and corroborated by subsequent detection literature) |
| S25 (https://europepmc.org/article/MED/42328738) | not applicable (analytical matrices) (Harmonized analytical workflow across dried blood spots, serum and plasma) | Not applicable | Up to two months of storage testing | At 4 and 22 degrees Celsius, AOD9604 (along with alexamorelin, buserelin, hGH 176-191, kisspeptin-10 and LHRH) was extensively degraded after one week in serum and plasma, while remaining detectable in dried matrices throughout the study | Extensive degradation within one week at 4 and 22 degrees Celsius in liquid matrices | Peer-reviewed |

## What we do not know yet
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.

## Questions and answers
### Did the AOD-9604 trials actually work?
No. The pivotal 24-week trial in 502 randomized obese adults failed its primary weight-loss endpoint, the 12-week trial's efficacy result was never published, and three later pain trials posted results that did not separate from placebo.

No. This is the question the whole compound turns on, and it has a documented answer.Six randomized, double-blind, placebo-controlled trials were run in the obesity program, with about 900 participants. The four early ones were safety studies and passed as safety studies. The two that measured weight are what matter. The larger of them, 24 weeks in 502 randomized obese adults across 16 Australian sites, failed to demonstrate a significant benefit on the primary weight-loss endpoint. The smaller one, 12 weeks in 300 adults, had weight reduction as a stated objective and its efficacy result has never been published anywhere we could find.Three later trials of the same peptide in pain indications, run under the code LAT8881, posted primary results that did not separate from placebo: -0.87 versus -0.74 points in neuropathic pain, 0 versus 0.2 in acute migraine, and 3.7 versus 3.1 in lumbar radicular pain.So across nine human trials with published or posted outcomes, this compound has never reported a positive efficacy result for anything.

### Why was AOD-9604 abandoned as a drug?
Its pivotal 24-week obesity trial failed the primary weight-loss endpoint, and the sponsor announced in 2007 that the results did not support commercial viability and the programme was terminated. That announcement, not a published paper, is the primary record.

Because the efficacy did not hold up in the trial that mattered. Metabolic Pharmaceuticals Ltd of Australia developed AOD-9604 for obesity, with phase 2a trials underway by February 2002, and took it through to a 502-patient, 24-week phase 2b trial. That trial failed on its primary weight-loss endpoint.The record of what happened next is a 2007 announcement by the sponsor to the Australian Securities Exchange, titled to the effect that the phase 2B results do not support commercial viability of the obesity project and that the programme is terminated. We cite the 2026 peer-reviewed review that records that announcement, because a direct fetch of the exchange archive for this delisted company returned nothing on the day this page was built.That is a notable fact in its own right. The efficacy failure that ended a decade of development exists in the public record as a press release, and a 2026 review says so explicitly: conclusions regarding the lack of clinical efficacy in obesity are based primarily on sponsor-reported phase 2 programme outcomes rather than peer-reviewed randomized efficacy trials.

### Is AOD-9604 really the fat-loss part of HGH?
It is a genuine growth hormone fragment, residues 177-191 plus a tyrosine, and it genuinely avoids the GH receptor and any IGF-1 rise. But it also produced no weight loss in a 502-patient randomized trial. The side effects were avoided; so was the effect.

It is a real fragment of growth hormone, and the design premise is legitimate. AOD-9604 is residues 177 to 191 of the hormone's 191-amino-acid chain, plus a stabilizing tyrosine, and that C-terminal region was identified decades ago as a lipid-mobilizing domain. NMR work shows the synthetic piece keeps the shape it had inside the intact protein.The separation from growth hormone signalling is also real. The fragment does not compete for the growth hormone receptor and does not drive receptor-mediated cell proliferation, and across nine human trials it never moved IGF-1, including 24 weeks of daily dosing where p values against placebo were 0.50844 and 0.75754.What did not carry over is the effect. Growth hormone reduces fat mass in people; AOD-9604, in a 502-patient randomized trial, did not beat placebo on weight. The side effects were left behind, and on the human evidence so was the benefit.The fragment's own older literature complicates the story further: the same sequence caused hyperglycaemia and insulin resistance in rats in 1982, and in 1993 showed antilipogenic but no significant lipolytic activity by glycerol release.

### What is the FDA status of AOD-9604?
Not approved for anything. Drugs@FDA returns no product, and FDA lists it among compounding substances that may present significant safety risks, citing immunogenicity concerns, impurity complexities, and no or only limited safety information.

AOD-9604 is not FDA approved. FDA cites limited safety information and immunogenicity concerns; it is sold as a research chemical with no established human efficacy.In detail: no product containing AOD-9604 appears in Drugs@FDA, and an openFDA query for the ingredient returns NOT_FOUND. The compound appears on FDA's compounding safety-risks page, in the table of substances nominated but withdrawn.FDA's entry says that compounded drugs containing AOD-9604 may pose significant risk for immunogenicity for certain routes of administration and may have complexities with regard to peptide-related impurities and API characterization; that FDA has identified no, or only limited, safety-related information; that the agency therefore lacks sufficient information to know whether the drug would cause harm when administered to humans; and that FDA has also identified serious adverse events that may be associated with AOD-9604, though causality is not clear.Separately, compounded drugs are not FDA-approved products at all: FDA does not verify their safety, effectiveness or quality before marketing.

### Is AOD-9604 banned by WADA, and is it detectable?
Yes. It is prohibited at all times under WADA section S2.2.3 as a growth hormone fragment. It does not register on the hGH isoform immunoassay, which is why labs use dedicated urine assays detecting it down to 50 pg/mL.

Yes to both. The 2026 WADA Prohibited List names AOD-9604 explicitly in section S2.2.3, growth hormone fragments, alongside hGH 176-191, making it prohibited at all times.The undetectable claim comes from one true finding used misleadingly. AOD-9604 does not influence the WADA growth hormone isoform immunoassay, which is exactly why anti-doping laboratories built dedicated peptide assays instead of relying on growth hormone tests. A validated urine method detects it to 50 pg/mL with 62 percent recovery, direct-urine-injection screening covers it at 50 to 500 pg/mL, and current workflows detect it in dried blood spots, serum and plasma.There is also a stable metabolite, the peptide CRSVEGSCG, which outlasts the parent compound and may extend the detection window.

### How do I know what is actually in a vial or troche?
You cannot verify it. Government analysts have identified this peptide in seized unlabelled preparations and in confiscated US vials, and FDA cites peptide-related impurity and API characterization complexities.

You do not, and this is documented rather than hypothetical. In 2014 Belgian government analysts published a case report on identifying AOD9604 in unknown pharmaceutical preparations seized by the authorities. 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 USA.FDA's stated concerns include exactly this problem: complexities with regard to peptide-related impurities and API characterization, alongside immunogenicity risk for certain routes of administration.A seller-supplied certificate of analysis does not close this gap. It describes a sample, it is produced by or for the seller, and it establishes neither that the tested sample matches your vial nor the standard the analysis met. Note also that the clinical trial material was made under cGMP conditions by a named contract manufacturer, which is a different category of product from anything sold as a research chemical. Oral troches and capsules circulate too, and carry the same verification problem plus an additional formulation variable.

### Was AOD-9604 ever studied as a subcutaneous injection?
No. Every human study used intravenous infusion or oral capsules and tablets; the program moved toward oral dosing. The subcutaneous route the market sells has no human pharmacokinetic, dose-response or safety data behind it.

No. Not once, in any published or posted human study of this molecule.The obesity program used intravenous infusion in two trials and oral capsules or tablets in four. The three later pain trials used oral capsules or intravenous infusion. The development program actually moved toward oral dosing, because the compound is orally bioavailable in animals.Meanwhile the market sells it as a subcutaneous injectable, with forum protocols documented in the peer-reviewed literature at 250 to 500 mcg per day split across 2 to 3 injections. That means the route being sold has no human pharmacokinetic data, no human dose-response data, and no human safety data specific to it. FDA's immunogenicity language is itself route-specific: risk for immunogenicity for certain routes of administration.

### What is the half-life of AOD-9604?
Unknown in humans: the only human IV study could not calculate terminal half-life because too few quantifiable elimination-phase points were obtained. In pigs it is about 3 minutes after IV injection, against about 21 minutes for growth hormone.

In humans it is unknown, and the reason is informative. In the only human study with posted pharmacokinetics, a 2023 intravenous ascending-dose study, terminal half-life could not be determined at 0.8, 1.2 or 1.8 mg/kg because the criterion of at least three quantifiable elimination-phase data points was not met. The peptide left the blood too quickly to characterize its elimination. Mean Cmax was 12.6, 10.2 and 13.8 ng/mL, with Tmax 0.08 hours at every dose. A 2026 review records the same absence: half-life not reported in human trials.In animals the numbers exist and are very short. In pigs, about 3 minutes after intravenous injection, with almost complete clearance from plasma by 12 minutes. In rat plasma in vitro, about 4 minutes, with intact peptide undetectable at 56 minutes. The same paper cites about 21 minutes for growth hormone itself.

### Does AOD-9604 repair joints or cartilage?
No human trial has tested this. The claim rests on one study in 32 rabbits with chemically induced knee osteoarthritis, using weekly ultrasound-guided injections into the joint; a 2026 review states human evidence in these indications is lacking.

The entire joint claim traces to one study, in rabbits. Thirty-two New Zealand white rabbits with collagenase-induced knee osteoarthritis received weekly ultrasound-guided injections directly into the joint of saline, 6 mg hyaluronic acid, 0.25 mg AOD9604, or AOD9604 plus hyaluronic acid. Cartilage scores were better in all treatment groups than saline, and the combination beat either agent alone, with the shortest lameness period.That is a real result with two important qualifiers. The species is rabbit, and the route is intra-articular under ultrasound guidance, weekly. A subcutaneous injection into abdominal fat does not reproduce either.A 2026 peer-reviewed review puts it directly: claims around osteoarthritis, joint repair or tissue regeneration are currently grounded mainly in animal work, with a lack of convincing human clinical trial evidence in these indications.

### Is AOD-9604 safe?
The trials found tolerability indistinguishable from placebo with no antibodies detected. FDA separately states it has no, or only limited, safety information, lacks sufficient information to know whether it would cause harm, and has identified serious adverse events of unclear causality.

Two things are true at once, and honest answers include both.The trials found tolerability indistinguishable from placebo. Across about 900 participants, adverse event rates in the 24-week trial ranged from 75.6 to 83.2 percent across arms, with the highest rate in the placebo group; no event was deemed definitely treatment-related; no anti-AOD9604 antibodies were detected; IGF-1 and glucose tolerance did not move. Non-clinical work found no genotoxicity and no toxicological concerns over 6 months in rats and 9 months in monkeys.FDA says 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; and that it has identified serious adverse events that may be associated with AOD-9604, though causality is not clear.One finding sits near both statements. Five serious adverse events occurred in the 12-week trial, all neoplasms, all in drug arms; the investigator considered none related to study medication, and IGF-1 had not changed. We report that alongside FDA's language without asserting a connection, because no public document establishes one.Finally, every reassuring datapoint above comes from supervised intravenous or oral dosing of cGMP-manufactured material, not from subcutaneous injection of an unverified research chemical.

### What is LAT8881, and is it the same thing?
The same peptide under a later code. A 2023 paper states LAT8881 was formerly identified as AOD9604. It is why a ClinicalTrials.gov search for AOD9604 returns nothing while three registered trials of the molecule exist.

Yes, it is the same peptide under a later development code. After the obesity program ended, the molecule was picked up by Lateral Pharma Pty Ltd of Melbourne and developed as LAT8881. A 2023 peer-reviewed paper states it directly: LAT8881, formerly identified as AOD9604, with the same 16-amino-acid disulfide-bridged sequence YLRIVQCRSVEGSCGF.That second life produced three registered human trials with posted results, in neuropathic pain, acute migraine and lumbar radicular pain, plus preclinical work identifying lanthionine synthetase C-like protein 1 as a binding target in the spinal cord and mouse influenza studies.This matters for two practical reasons. It is why a ClinicalTrials.gov search for AOD9604 returns zero studies while three trials of the molecule exist. And it means the compound's human record includes three additional pain trials whose posted primary results did not separate from placebo.

### Does AOD-9604 raise IGF-1 or affect blood sugar?
No, in humans. IGF-1 did not change significantly in any trial, including 24 weeks of daily dosing (p = 0.50844 and p = 0.75754), and oral glucose tolerance was unchanged. Some older rat work on the same sequence did show insulin antagonism.

In humans, no on both counts, and this is the compound's most reproducible human finding.IGF-1 was measured across the program because raising it is the mechanism behind growth hormone's long-term risks. No human trial found a significant change. In the 24-week trial, mean IGF-1 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 placebo.Glucose handling was likewise unchanged: no significant oral glucose tolerance test differences in any trial or group, with one isolated 8 percent glucose rise at a single timepoint in one subject on the highest oral dose.The animal picture is less uniform, and it deserves a mention rather than burial. The same C-terminal sequence caused hyperglycaemia and insulin resistance in normal rats in 1982 and reduced insulin-stimulated glucose uptake in isolated rat fat cells, while AOD9604 itself showed no adverse effect on insulin sensitivity by euglycemic clamp in obese rats.

### Why is it sold as an injection when the trials used capsules?
The program moved the opposite way, toward oral dosing: four of six obesity trials used capsules or tablets and the peptide is orally bioavailable in animals. No human study of this molecule ever used subcutaneous injection.

A fair question with no published answer, so here is what is documented.The development program deliberately moved to oral dosing. Only the phase 1 and the first phase 2a study used intravenous infusion; the four later obesity trials used capsules or tablets, and the sponsor's own kinetics work established that the peptide is orally bioavailable in animals, appearing in plasma with its degradants after oral dosing. Two of the three later pain trials also used oral capsules.The gray market sells subcutaneous vials, and forum protocols in the peer-reviewed literature describe 250 to 500 mcg per day subcutaneously. Note the size of the gap: the 24-week trial gave 1 mg by mouth once daily.What can be said with confidence is that no human study of this molecule used subcutaneous injection, so nobody, seller or buyer, has human data for the product actually being sold.

### Was AOD-9604 approved as a food ingredient?
No. The sponsor's papers record a GRAS determination by a convened expert panel, which is the self-affirmation route, not an FDA approval. Neither paper cites an FDA GRAS notice number, and the drug-side status remains unapproved.

Not approved, and the distinction matters. After the drug program ended, the sponsor's authors published the compound's non-clinical safety data under the title of a nutraceutical ingredient for improved metabolic health, and the 2013 clinical safety paper records that AOD9604 was determined by an appropriately qualified GRAS panel of experts to be Generally Recognized As Safe under conditions of intended uses in foods.Read that carefully. It describes a determination made by a panel convened for the purpose, which is the self-affirmation route. Neither paper cites an FDA GRAS notice number, and no corresponding entry was retrievable from FDA's GRAS Notice Inventory when this page was built. A GRAS self-affirmation is not an FDA approval, and it says nothing about efficacy for anything.Meanwhile the compound's regulatory position on the drug side is unchanged: not approved, and listed by FDA among bulk substances that may present significant safety risks.

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