This page requires a naming correction before anything else can be said about it. The compound described in the peer-reviewed literature is SLU-PP-332, developed in Thomas Burris's laboratory at Saint Louis University. The designation "SLU-PP-322" appears in vendor listings and search results but does not correspond to any published compound. Everything below refers to SLU-PP-332, and the discrepancy is flagged for manual review.
The second correction matters just as much: SLU-PP-332 is not a peptide. It is a synthetic small molecule — a designed pan-agonist of the estrogen-related receptors ERRα, ERRβ and ERRγ, with highest potency at ERRα. Those are orphan nuclear receptors that act as transcription factors inside the cell nucleus. A nuclear receptor ligand has essentially nothing in common, pharmacologically or structurally, with the receptor-binding peptides that make up the rest of this catalogue. It is listed here because it is sold alongside them, not because it belongs with them.
SLU-PP-332 is commonly described as an "exercise mimetic," a phrase that comes directly from the papers: in mice, it activates a transcriptional programme resembling the acute response to aerobic exercise. It increases type IIa oxidative muscle fibres, raises energy expenditure and fatty acid oxidation, reduces fat mass, and improves insulin sensitivity in obesity models. Two structurally distinct pan-ERR agonists from the same programme also improved ejection fraction and survival in a mouse model of pressure-overload heart failure.
All of that is mouse data. SLU-PP-332 has never been administered to a human being. There is no Phase 1 trial, no human pharmacokinetics, no human safety database, no established dose and no route of human administration. It is a chemical probe used to interrogate ERR biology in animals, and the published work is explicit that this is what it was designed to be.
SLU-PP-322 has never been given to a human. The only published figure is 10 mg/kg twice daily given intraperitoneally to mice — a weight-based amount, on a route not used outside a laboratory, that does not scale to people. There is no human amount, no human schedule and no human frequency to chart, and converting the mouse figure into one would be an invention rather than a conversion. The reconstitution figures above are arithmetic and are correct; what is missing is a human schedule to apply them to.
SLU-PP-322 has never been given to a human: there is no clinical trial, no human safety data and no human pharmacokinetics, so its half-life, clearance and toxicity in people are all unknown. The single published figure is 10 mg/kg twice daily by intraperitoneal injection in mice, from the 2023 characterisation of this ERR agonist — milligram-per-kilogram amounts in mice do not scale to humans, the route is one that is not used outside a laboratory, and no conversion of either is offered here, which is why that figure is recorded in this note rather than charted as a schedule. One further point needs checking before anything on this page is relied on: Athena lists this compound as SLU-PP-322, while the published literature and the available protocol references describe SLU-PP-332 — either the naming or the material needs confirming, and it has been flagged rather than assumed. Athena lists a single 50 mg vial, and its concentration arithmetic is exact — made up with 3 mL it comes to about 16.7 mg/mL; what is missing is a human schedule, not the arithmetic.
What this evidence establishes. SLU-PP-322 has never been given to a human. It is a recently described laboratory compound with no clinical trial, no human safety data and no human pharmacokinetics — the half-life, clearance and toxicity profile in people are all unknown. The one published mouse figure is recorded in the note above because it is the only figure that exists; milligram-per-kilogram doses in mice do not scale to humans and no conversion is offered.
Sources: Billon et al., 2023 — SLU-PP-322 preclinical characterisation
For educational and laboratory research purposes only. It does not provide medical advice, dosing recommendations, or instructions for human or veterinary use. Syringe units assume a U-100 syringe, on which 1 mL is 100 units and a 50-unit syringe holds 0.5 mL.
SLU-PP-332 works through gene transcription rather than through a cell-surface receptor. That is a slower, broader and less easily reversed kind of intervention than peptide receptor agonism, and it is worth understanding why before reading anything else about the compound.
Activates all three estrogen-related receptors — ERRα, ERRβ and ERRγ — with highest potency at ERRα. Designing a compound with ERRα agonist activity had been a long-standing difficulty in the field.
ERRs are orphan nuclear receptors that act as transcription factors. SLU-PP-332 is a small molecule that binds inside the cell and changes which genes are expressed.
In a skeletal muscle cell line it increased mitochondrial function and cellular respiration. In vivo it transcriptionally activated a broad set of genes governing fatty acid metabolism and mitochondrial function.
In mice it induced an ERRα-dependent acute aerobic exercise response, increased type IIa oxidative fibres and enhanced exercise capacity — the basis of the "exercise mimetic" description.
In diet-induced obese and ob/ob mice, administration increased energy expenditure and fatty acid oxidation, decreased fat mass accumulation and improved insulin sensitivity.
In pressure overload-induced heart failure, SLU-PP-332 and a second pan-ERR agonist improved ejection fraction, reduced fibrosis and increased survival, with ERRγ identified as the main dependency.
The phrase is precise in its original context and misleading out of it. What the papers demonstrate is that a defined set of exercise-responsive genes can be switched on pharmacologically in mouse muscle, producing measurable changes in fibre type, respiration and endurance capacity. What they do not demonstrate — and do not claim — is that this reproduces the cardiovascular, musculoskeletal, neurological, immune and psychological effects of physical activity in a person. Exercise is a whole-organism stimulus. An ERRα agonist is a transcription-factor ligand. The overlap is real and partial and has been mapped only in rodents.
Pan-agonism at a nuclear receptor family also carries an inherent breadth problem. ERRα, β and γ are expressed in heart, skeletal muscle, brown adipose tissue, kidney, brain and elsewhere, and they regulate large transcriptional programmes. Activating all three systemically affects many tissues at once, and the off-target consequences of doing so over months or years in a human have not been studied because no human has taken it.
This is a well-conducted preclinical programme published in strong journals, and its limitations are the ordinary ones of preclinical work applied to a compound that people are buying and injecting anyway.
Every efficacy result is murine. Mouse metabolic physiology differs from human metabolic physiology in thermoregulation, basal metabolic rate, brown fat mass and fibre-type composition — all of which are directly relevant to an exercise-mimetic mechanism. The metabolic syndrome results come from genetically obese and diet-induced obese mice, models that respond to interventions that have repeatedly failed to translate.
Dose does not translate either. Milligram-per-kilogram doses in mice cannot be converted into human doses by simple scaling, and no allometric conversion is offered here because none would be meaningful without human pharmacokinetic data. The compound's own authors describe it as an in vivo chemical tool — a research instrument for asking whether ERR activation does something in an animal, not a candidate with a human dose.
Long-term consequences of sustained pan-nuclear-receptor agonism are entirely unstudied. The mouse experiments ran for weeks. ERRs regulate large transcriptional programmes across many tissues, and there is no dataset of any length in any species that would detect a slow-emerging problem.
There is no human safety data for SLU-PP-332. No contraindication list can be derived from clinical experience because there is none. The entries below describe the categories of risk that follow from the mechanism and from the absence of evidence.
| Condition / Factor | Risk Level | Rationale |
|---|---|---|
| Any human administration | NO EVIDENCE BASE | SLU-PP-332 has never been given to a human being in a published study. There is no Phase 1 trial, no pharmacokinetic data, no dose, no route and no safety database. |
| Injectable use | NOT SUPPORTED | This is a small molecule with no human formulation. No injectable schedule exists in any published source, and none is offered on this page. The dosing section is flagged accordingly. |
| Systemic pan-ERR activation | UNCHARACTERISED | ERRα, β and γ are expressed across heart, skeletal muscle, brown adipose tissue, kidney and brain and regulate broad transcriptional programmes. The tissue-level consequences of activating all three in a human are unknown. |
| Cardiac disease | UNKNOWN DIRECTION | ERRγ agonism improved outcomes in a mouse heart failure model. Whether the same intervention is beneficial, neutral or harmful in a human heart — healthy or diseased — has not been tested. |
| Malignancy | UNKNOWN | ERRα expression has been studied in relation to tumour metabolism in the oncology literature. Whether pharmacological ERR agonism affects tumour behaviour in either direction is not established, and no carcinogenicity study has been published for this compound. |
| Pregnancy and lactation | NOT ESTABLISHED | Nuclear receptor agonists acting on developmental transcriptional programmes are a category in which absence of reproductive toxicology data is a serious gap, not a neutral one. |
| Purity and identity of supplied material | HIGH | Material sold under the non-existent designation "SLU-PP-322" cannot be assumed to be SLU-PP-332, or to be any defined compound at all. Nothing sold under this name is manufactured to pharmaceutical standards. |
| Competitive athletes | PROHIBITED | Metabolic modulators, including agents that mimic the transcriptional effects of exercise on muscle, fall within WADA Prohibited List section S4. Non-approved substances are also covered by section S0. |
FDA: SLU-PP-332 is not approved for any indication, is not in clinical development that has reached a published trial, and has no investigational new drug programme in the public record. It is a preclinical chemical probe.
WADA: section S0 of the Prohibited List covers any pharmacological substance not currently approved by any governmental regulatory health authority for human therapeutic use, and section S4 covers metabolic modulators. A compound in this position is prohibited in sport regardless of whether it is named individually.
Items flagged for manual review on this page: first, the compound designation — the site lists "SLU-PP-322" while the published compound is SLU-PP-332, and the URL has been left unchanged pending a decision on how to handle that. Second, the category — this compound is a small-molecule nuclear receptor agonist listed under Single Peptides, which it is not. Third, the dosing section correctly carries no injectable schedule, and that flag should stand: there is nothing in the literature that could support one.
Test your understanding of what this compound is, what "exercise mimetic" means in the papers, and how much human data exists.
This profile is for educational and research purposes only. It is not medical advice, and nothing on it is a protocol, a recommendation, or an instruction for use in a person or an animal.
Athena Peptides Education does not prescribe, sell, or recommend any compound. Compounds discussed here are for laboratory research only and are not for human consumption. Always consult a qualified physician before making any decision about your health.