AOD-9604 vs SLU-PP-332
AOD-9604 is a synthetic hexadecapeptide corresponding to the C-terminal lipolytic domain of human growth hormone, written in the older literature as hGH fragment 176-191. Its preclinical characterisation dates from 1993 to 2001, it entered human obesity trials whose pooled safety data were published in 2013, and its recent literature is dominated by anti-doping analytical chemistry. SLU-PP-332 is a synthetic small-molecule pan-agonist of the estrogen-related receptors ERRalpha, ERRbeta and ERRgamma, described as an exercise mimetic on the strength of rodent muscle transcriptomics, with an evidence base that is preclinical only. The two are paired because both are marketed as fat-loss compounds that work without appetite suppression, and because both now appear in sports drug-testing discussions. No published paper names both. Searches of PubMed and of Europe PMC across full text returned no shared record, including within the anti-doping literature that covers each of them separately.
No study has compared them directly.
Everything below is drawn from separate studies that used different models, endpoints and species. That is a real limit on what can be concluded, not a formality.
No study has administered or tested AOD-9604 and SLU-PP-332 together, and no publication names both. Searches were run against PubMed by title and abstract and against Europe PMC across full text, using AOD9604 and hGH fragment 176-191 for the first compound and pan-ERR agonist, estrogen-related receptor and exercise mimetic for the second. The most likely place for a shared citation is the anti-doping literature, since detection methods exist for each; the annual banned-substance reviews and the multi-analyte doping screens that cover AOD9604 were checked individually and none of them mentions SLU-PP-332, which entered that literature only in 2026. The comparison below is therefore indirect throughout, and it sets a peptide with a published human safety dataset against a small molecule that no human has received.
Side by side.
| AOD-9604 | SLU-PP-332 | |
|---|---|---|
| Evidence maturity | Early clinical | Preclinical only |
| Studies cited here | 17 | 13 |
| Published 2023 or later | 4 | 13 |
| Newest paper | 2026 | 2026 |
| Sequence and origin | A synthetic sixteen-residue peptide reproducing the C-terminal region of human growth hormone, so its sequence has a direct endogenous parent even though the fragment itself is manufactured. | A synthetic small molecule with no endogenous counterpart, developed through medicinal chemistry to activate a family of orphan nuclear receptors. |
| Mechanism as described in the literature | Rodent work reported increased lipolytic activity and decreased lipogenic activity in adipose tissue with increased fat oxidation, and binding experiments indicated no interaction with the growth hormone receptor. Effects persisted in beta3-adrenergic receptor knock-out mice, indicating the lipolytic action was not mediated directly through that receptor. | Pan-agonism at ERRalpha, ERRbeta and ERRgamma acting with PGC-1 coactivators, reported to drive mitochondrial biogenesis, fatty acid oxidation and an acute aerobic exercise-like transcriptional programme in mouse skeletal muscle, with the exercise-capacity effect dependent on ERRalpha. |
| Size of the evidence base | Seventeen studies in this library, spanning 1993 to 2026 and including one pooled human safety analysis, a non-clinical toxicology package, rodent and rabbit in vivo work, analytical chemistry and recent narrative reviews. | Thirteen studies in this library, all published from 2023 onward, consisting of rodent in vivo work, cell-based experiments, medicinal chemistry and doping-control metabolite characterisation. |
| Best-characterised finding | Reduced body-weight gain and increased fat oxidation in obese rodents. In one chronic oral study in genetically obese animals, weight gain fell by over 50% relative to controls, and chronic treatment was reported to produce no adverse effect on insulin sensitivity, in contrast to intact growth hormone. | Improved treadmill endurance and an acute exercise-like transcriptional signature in mouse skeletal muscle with an increase in type IIa oxidative fibres, plus increased energy expenditure, increased fatty acid oxidation and reduced fat mass in obese mice. |
| Human data | A pooled safety and tolerability analysis of six randomised, double-blind, placebo-controlled trials reported no effect on serum IGF-1, no negative effect on carbohydrate metabolism on oral glucose tolerance testing, and no detected anti-AOD9604 antibodies in the patients assayed. No efficacy trial has been published as a standalone peer-reviewed report. | None. The only human-derived work is a 2025 pilot study in which primary myoblasts from physically inactive women were treated in culture, and the authors stated that no participants were dosed with the compound. |
| Evidence maturity | Early clinical. Human trials were conducted and their pooled safety outcomes published, but body-composition efficacy has not been independently replicated in an indexed journal. | Preclinical only. A ClinicalTrials.gov query returned no studies, so human pharmacokinetics, dosing, efficacy and safety are entirely unestablished. |
| Recency of primary research | The efficacy literature is largely historical, concentrated between 1993 and 2001 with a single rabbit osteoarthritis study in 2015. Publications from 2022 onward are analytical methods and narrative reviews rather than new efficacy work. | Recent but preclinical. The 2026 output consists of structure-activity optimisation, work on the related oral analogue SLU-PP-915, and two independent in vitro metabolite studies performed to support doping-control detection. |
| Regulatory and anti-doping status | No approved medicine. A non-clinical package covering genotoxicity assays and chronic oral toxicology in rats and cynomolgus monkeys was published in support of a food-ingredient position, and the peptide is covered by validated urinary detection methods and by annual banned-substance reviews. | No approved product and no marketed formulation. Two 2026 laboratories independently characterised its metabolites specifically because the compound was judged to have doping potential, but it does not yet appear in the annual banned-substance reviews that cover AOD9604. |
And what it does not.
Nothing in the published record compares these two, and their evidence bases are unlike each other in kind rather than merely in size. AOD-9604 has been given to humans in randomised placebo-controlled trials and has a published pooled safety dataset, together with a non-clinical toxicology package; what it lacks is any peer-reviewed efficacy report, so the human body-composition claims made for it rest on data that were never published as a standalone study. SLU-PP-332 has the opposite profile: a recent, mechanistically detailed rodent and cell-culture literature with a clearly defined molecular target, and no human exposure at all. Neither compound has demonstrated fat loss in a published, controlled human trial, which is the claim that most often prompts the comparison. Both are of active interest to anti-doping laboratories, and for each the newest work concerns how to detect it rather than what it does.
Common questions.
- Has AOD-9604 ever been shown to cause weight loss in a published human trial?
Not in a standalone peer-reviewed efficacy report. The human data available in the literature are a pooled safety and tolerability analysis of six randomised, double-blind, placebo-controlled trials, which addressed tolerability, IGF-1 and carbohydrate metabolism rather than establishing a body-composition outcome. Body-composition results have not been independently replicated in an indexed journal. The weight and fat-oxidation findings that circulate for this peptide come from obese-rodent studies published between 1993 and 2001.
- Why is SLU-PP-332 described as an exercise mimetic when AOD-9604 is not?
The descriptions come from different kinds of measurement. SLU-PP-332 was reported to induce an acute aerobic exercise-like transcriptional signature in mouse skeletal muscle, to increase type IIa oxidative fibres and to improve treadmill endurance, so the term describes a resemblance to the gene-expression response to training. AOD-9604 was characterised on adipose-tissue endpoints instead, with reported increases in lipolysis and fat oxidation and decreases in lipogenesis, and no study has reported an exercise-like transcriptional response for it.
- Do either of them affect IGF-1 or the growth hormone axis?
For AOD-9604 the published position is that it does not. The pooled human analysis reported no effect on serum IGF-1, and rodent binding experiments indicated the fragment did not interact with the growth hormone receptor, with lipolytic effects persisting in beta3-adrenergic receptor knock-out mice. For SLU-PP-332 the question has not been addressed: its published pharmacology concerns nuclear receptor activation, mitochondrial biogenesis and fatty acid oxidation, and no study reports growth hormone or IGF-1 measurements.
- What is known about the safety of each compound?
The asymmetry is large. For AOD-9604 a non-clinical package reported no genotoxic activity across Ames, chromosomal aberration and micronucleus assays and described chronic oral administration in rats and cynomolgus monkeys as generally safe, alongside the pooled human tolerability analysis. For SLU-PP-332 a 2026 systematic review of preclinical studies reported no evident toxicity in the rodent models surveyed, but long-term toxicity, carcinogenicity and reproductive effects have not been characterised and no human safety data exist.
- Are both compounds detectable in sports drug testing?
Both have published detection work, at different stages of maturity. A validated urinary method for AOD9604 was reported in 2015 with six identified metabolites, one of which was substantially more stable than the parent peptide and proposed as a longer-window target, and the peptide appears in annual banned-substance reviews. For SLU-PP-332 two independent laboratories characterised in vitro metabolites in 2026 and proposed analytical targets, but this work is newer and the compound has not yet entered the banned-substance review literature.
For research purposes only. Not for human consumption, diagnosis, treatment, or prevention of any condition. Nothing on this page is medical advice, and no comparison here should be read as a recommendation of either compound.