SLU-PP-332: what the studies show, status and safety
Summary
SLU-PP-332 is not a peptide. It is a small synthetic molecule that switches on the estrogen-related receptors, which control how cells burn fuel, and it sits in this register because it is sold as a peptide. Not a single study in people exists. In mice it raised endurance and cut fat gain, but only when injected, because its developers state it is not absorbed when swallowed.
Key findings at a glance
- It is not a peptide, and not marginally so. The formula is C18H14N2O2, the mass 290.32 g/mol, and there is not one amino acid in it [1]. It was built at a chemistry bench by reshaping an older compound called GSK4716 [2].
- Zero human data. A registry search on 7 September 2026 found no trial of SLU-PP-332, of its successor, or of any other ERR agonist [3].
- Its developers state it does not work by mouth. Two papers say the substance lacks oral bioavailability. That means it does not pass from the gut into the blood [4], [5].
- Mice ran longer after injections. After a week of twice-daily abdominal injections, treated animals ran about 70 percent longer and about 45 percent further to exhaustion. Six animals per group [2].
- Fat gain almost stopped in mice. Over 28 days control animals gained about 5 grams of fat and treated animals under 0.5 grams. They ate the same amount [6].
- A heart model showed benefit and a limit. Survival rose after pressure overload, as did the share of blood the heart pushes out with each beat (the ejection fraction). The thickening of the heart muscle was not prevented [7].
- Banned in sport around the clock. Class S0 of the 2026 Prohibited List catches it through its wording rather than by name [8]. Two laboratories published detection work in 2026 [9], [10].
What it is
SLU-PP-332 is a small synthetic molecule that switches on three receptors known as ERR alpha, beta and gamma. Chemically it is an acylhydrazone: a naphthalene ring and a phenol ring joined by a short nitrogen bridge. Nothing like it occurs in the body [1], [2].
It was made by reshaping GSK4716, an older receptor activator. Swapping one side group for a naphthalene ring lifted its strength at ERR alpha more than fiftyfold [2]. The work came from academic groups around Thomas Burris and John Walker, hence the initials of Saint Louis University in the name [2].
Several authors of the core papers disclose that they co-founded or hold shares in companies developing ERR compounds. The papers say so themselves [2], [4]. That is their own declaration, not an allegation, and it matters because almost all the animal evidence comes from this one circle.
The name is a laboratory code. There is no approved drug name, no international nonproprietary name, and no entry in any medicines substance register [1], [11].
Quick facts
| Field | Value | Ref |
|---|---|---|
| Common name | SLU-PP-332, also written SR9861 or ERR pan-agonist 332 | [1] |
| Class | Small synthetic molecule, an acylhydrazone; a receptor activator | [1], [2] |
| Amino acid sequence | None. It is not a peptide | [1] |
| Formula and mass | C18H14N2O2, 290.32 g/mol | [1], [11] |
| Target | The receptors ERR alpha, beta and gamma | [2] |
| Strength at the target | Half the maximal effect at 98 nanomolar for ERR alpha, 230 for ERR beta and 430 for ERR gamma, measured in cells | [2] |
| How long it lasts in the body | Never measured in a person; no plasma half-life published at all | [5] |
| Water solubility | Poor. Fat-solubility measure 3.7; all animal work used solvent mixtures | [1], [2] |
| Status | Research chemical, approved nowhere | [11] |
| Developer | Academic groups at Saint Louis University and Washington University | [2] |
| CAS registry number | 303760-60-3 | [1] |
| PubChem CID | 5338394 for the E form; 5404083 is the mirror-image Z form | [1], [12] |
| ChEMBL | CHEMBL4208749; no clinical phase, no approval date | [11] |
| Catalogue listings | 33 laboratory chemical dealers list it, sold as research use only | [13] |
The peptide question is not a technicality. Bacteriostatic water dissolves peptides because they carry charged side chains, and this molecule has none. That is the subject of the separate guide on reconstituting SLU-PP-332.
How it works
The proposed mechanism runs through one small family of receptors. ERR alpha, beta and gamma sit on DNA and are permanently switched on, without needing a hormone. They control genes for building mitochondria and for burning fat [5].
- It binds and turns the dial up. In cells it activated all three receptors, most strongly ERR alpha, at 98 nanomolar. It did nothing at the classical estrogen receptors [2].
- These are not estrogen receptors. Despite the family resemblance, ERR receptors bind no natural estrogen at all. An estrogenic effect is therefore not the proposed route [5].
- Muscle may read it as a short run, but a weaker one. In mouse muscle the gene Ddit4 rose about threefold after an injection. Forty minutes of treadmill running raised it about sixfold, and the two together about elevenfold. A second gene, Slc25a25, rose about elevenfold under either. Both were back to baseline after three hours [2].
- Fuel choice may shift towards fat. In mice the respiratory quotient, a measure of which fuel is being burned, fell within two hours of the first injection [6].
- The heart uses a different member of the family. In the heart model the protection disappeared in animals lacking ERR gamma. The muscle effects, by contrast, needed ERR alpha [2], [7].
- Cell recycling may be involved. In heart and muscle cells, ERR activation raised TFEB, a master switch for the cell's disposal system [14].
Every one of these steps comes from cells or from rodents. The authors of the first paper add that the compound is not selective enough to separate the individual receptors [2].
The phrase "exercise mimetic" needs care. It describes copying single molecular responses, not replacing training. A 2026 review argues directly that exercise pills cannot reproduce the whole body-wide state that exercise creates [15].
Cell-based reporter assays in HEK293 cells, not a measurement in animals or people. Source [2].
What the studies found
Every result below comes from a mouse, a rat cell or a dish of cells. Nobody has given this substance to a person in any study, of any size, for any purpose [3].
Endurance in mice
Animal data Sedentary mice received twice-daily abdominal injections for six to seven days, then ran on a treadmill to exhaustion. Treated animals ran about 70 percent longer and about 45 percent further than controls, with 6 animals per group [2].
Animal data The effect was traced to one receptor. In mice engineered to lack ERR alpha in muscle, treated animals performed exactly like untreated ones, with 5 animals per group [2].
Sedentary C57BL/6J mice, twice-daily abdominal injection for six to seven days, 6 animals per group. Mouse results, injected, and they do not transfer to people. Source [2].
Muscle tissue
Animal data After 15 days of treatment, thigh muscle held more of the fatigue-resistant fibres that burn fuel with oxygen (type IIa fibres). It also held more mitochondria under the electron microscope and more mitochondrial DNA, with 8 animals per group. Grip strength rose over two weeks [2].
Body fat and blood sugar
Animal data In normally fed mice treated for 28 days, total body weight did not differ from controls. Fat gain did: about 5 grams in controls against under 0.5 grams in treated animals, with 8 animals per group. Food intake and movement were unchanged [6].
Animal data In two obesity models, treated animals lost weight progressively, had smaller fat cells and showed lower fasting glucose and insulin. The obese mice stayed on their high-fat diet throughout, with 7 to 8 animals per group [6].
The heart
Animal data Mice had the aorta narrowed surgically, then received injections twice daily for six weeks. The pumping fraction improved from week four, scarring fell and survival rose [7].
The ageing kidney
Animal data In 21-month-old mice treated daily for eight weeks, age-related protein loss in the urine fell and mitochondrial function improved. The authors compare the pattern to lifelong calorie restriction [16].
Human cells in a dish
In vitro Twenty women having hip replacements gave muscle samples during surgery. Cells grown from the ten least active women were treated in the dish for 48 hours, at the concentration listed in the doses table. Ageing markers fell and muscle-building markers rose [17].
No participant received the substance. This is a cell study using human material, and the authors call it a pilot study [17].
Negative and unwelcome findings
Animal data In the heart model the thickening of the heart muscle was not prevented. Wall thickness and cell size stayed as in untreated animals [7].
Animal data In mice made obese by a genetic defect (the ob/ob strain) the planned 28 days were cut to 12. The animals tolerated twice-daily abdominal injection poorly [6].
Animal data In the same metabolic study the insulin tolerance test did not improve, and the authors describe their own data on insulin sensitivity as conflicting [6].
What is still unknown
- Whether anything seen in mice happens in a person. No human study of any kind exists [3].
- What a safe amount would be. There is no toxicology programme to argue one from [18].
- Whether the substance can reach the blood at all when swallowed. Two papers say it cannot [4], [5].
- Whether long-term switching on of ERR alpha carries a cancer risk. The same receptor family is targeted in oncology by blocking it, and no cancer study exists [19].
- Whether what is sold is what the label says. No independent analysis of market samples has been published [13].
Side effects and safety
There is no side-effect profile for SLU-PP-332, because there is no documented human use to build one from. Empty databases are not a clean bill of health.
- No reports of harm anywhere. The FDA adverse-event database returned no matches for either spelling on 7 September 2026 [20]. Substances traded outside the medicines system rarely generate reports at all.
- "No overt toxicity" is a short observation, not a study. Mice on twice-daily injections for 10 days had normal blood counts, electrolytes and a normal muscle enzyme [2]. Ten days of three measurements is not toxicology.
- One tolerance problem is on record. The shortened ob/ob study is the clearest safety-relevant note in the literature, and the authors attribute it to the injection route [6].
- Nothing has been tested formally. No repeated-dose toxicity study, no test for genetic damage, no fertility or development study, no cancer study, no heart-rhythm screen [18].
- The longest exposure is eight weeks. That is the ageing-kidney study in mice. The heart study ran six weeks [7], [16].
- The breakdown products in people are unmapped. Laboratories found 22 and 9 breakdown products in human liver preparations, but only in test tubes. Which ones form in a living person is unknown [9], [10].
One point deserves care. SLU-PP-332 appears on no FDA list of substances that may pose a serious safety risk in compounding [21]. That is not a clearance. Those lists cover substances somebody nominated for assessment, and this one was never nominated.
Chemistry adds a further open question. A review from the developers' own circle calls the molecule metabolically unstable, and not stable enough to be a drug candidate without further work [5].
The numbers around it show the same weakness. GSK4716, the building block it was made from, survived only 6.4 minutes in human liver preparations. The successor compound built to fix that lasted more than 60 minutes [5], [22].
Doses used in studies
These are the doses used in the cited studies, listed for reference. They are not a recommendation.
Every line below comes from a mouse or from cells in a dish. The route matters more here than almost anywhere else in this register. Everything that showed an effect was injected into the abdomen, dissolved in a mixture built around the laboratory solvent DMSO.
| Study | Model | Dose | Route | Duration | Ref |
|---|---|---|---|---|---|
| Billon 2023, uptake and tissue levels | Mouse, 3 months old, 3 animals | 30 mg/kg once | Abdominal injection, DMSO mixture | Measured to 6 hours | [2] |
| Billon 2023, muscle physiology | Mouse, 3 months old, 8 animals per group | 50 mg/kg, twice daily | Abdominal injection | 15 days | [2] |
| Billon 2023, treadmill test | Mouse, 12 weeks old, 6 animals per group | 50 mg/kg, twice daily | Abdominal injection | 6 to 7 days | [2] |
| Billon 2023, acute gene response | Mouse, 3 months old, 6 animals per group | 50 mg/kg once | Abdominal injection | Tissue taken at 1, 3 and 6 hours | [2] |
| Billon 2023, receptor knockout comparison | Mouse, 20 to 24 weeks old, 5 animals per group | 25 mg/kg daily | Abdominal injection, DMSO mixture | 15 days | [2] |
| Billon 2024, metabolism | Mouse, 12 weeks old, 8 to 10 animals per group | 50 mg/kg, twice daily | Abdominal injection | 28 days | [6] |
| Billon 2024, ob/ob obesity model | Mouse, 3 months old, 8 animals | 50 mg/kg, twice daily | Abdominal injection | 12 days, cut short from 28 | [6] |
| Xu 2024, heart failure | Mouse, 8 weeks old, aorta narrowed | 25 mg/kg, twice daily | Abdominal injection, DMSO mixture | 6 weeks | [7] |
| Wang 2023, ageing kidney | Mouse, 21 months old, male | 25 mg/kg daily | Abdominal injection, 3 percent DMSO | 8 weeks | [16] |
| Bonanni 2025, human muscle cells | Human cells in a dish | 10 micromolar | Added to the culture medium | 48 hours | [17] |
| Billon 2023, muscle cell line | Mouse cells in a dish | 1 to 10 micromolar | Added to the culture medium | 2 to 24 hours | [2] |
Three things make it impossible to carry these numbers across to a person. Every effective dose was injected into the abdominal cavity, a route almost unknown in human medicine.
The substance is also stated to lack oral bioavailability, so a swallowed form does not reproduce these conditions [4], [5]. And no measurement of blood levels in a person exists, so any conversion from milligrams per kilogram of mouse would be guesswork.
The only exposure measurement anywhere is the first line of the table. Two hours after that single injection, mice carried about 0.6 micromolar in muscle against about 0.2 micromolar in blood, so the substance gathers in the tissue it acts on. Three animals [2].
Development and approval status
From an older receptor activator to the 2026 doping laboratories
- Before 2023GSK4716 is the starting pointAn older ERR activator, reshaped into this molecule, ref [2]
- 2023First description and the endurance resultMice run about 70 percent longer after injections, ref [2]
- 2023Successor series published, SLU-PP-915 identifiedBuilt for stability the parent lacks, ref [22]
- 2024Obesity model and heart failure model publishedFat gain almost stopped; pumping fraction improved, refs [6], [7]
- 2026Two anti-doping laboratories map its breakdown products22 products at UCLA, 9 in Cologne, refs [9], [10]
- 2026Registry search still finds no trial in peopleSix search terms on 7 September 2026, ref [3]
- 2023 — the first description appears, with the endurance and muscle results in mice [2].
- 2023 — a successor series is published, and SLU-PP-915 is identified as the stable, orally active candidate [22].
- 2023 — the ageing-kidney study appears, comparing the effect to calorie restriction [16].
- 2024 — the obesity study and the heart failure study are published [6], [7].
- 2025 — an Italian group reports effects in human muscle cells in a dish. It is the only work outside the founding circle with its own experiments [17].
- 2026 — a structure-activity study still treats the molecule as a research tool rather than a candidate [23].
- 2026 — two anti-doping laboratories publish detection work, and the registry search still returns nothing [3], [9], [10].
| Market | Status | Note | Ref |
|---|---|---|---|
| United States | Not approved | Never nominated for compounding, so never assessed | [11], [21] |
| European Union | Not approved | No pharmacopoeia entry; not a permitted food ingredient | [11] |
| Germany | Not approved | Not named in any substance-specific rule | [11] |
| United Kingdom | Not approved | Not separately checked | [11] |
| Australia | Not classified | Not named in the Poisons Standard | [24] |
| Canada | Not approved | Not separately checked | [11] |
| Switzerland | Not approved | Not separately checked | [11] |
All of this was checked on 7 September 2026. Where the table says not separately checked, that rests on the worldwide absence of any approval, not on a search of that register [11].
Anti-doping
SLU-PP-332 is banned in sport at all times, in and out of competition. It is not printed on the 2026 Prohibited List by name.
It falls instead under class S0, which covers "any pharmacological substance which is not addressed by any of the subsequent sections of the List and with no current approval by any governmental regulatory health authority for human therapeutic use". The class names compounds in preclinical development as an example [8].
The filing matters. The metabolic modulator class S4.4.1 names AMPK activators, PPAR delta agonists and Rev-erb alpha agonists, and ERR agonists are none of those [25].
Substances caught by S0 count as specified substances, while those in S4.4 do not. Specified means an athlete has more room to argue that the substance was taken without intent to cheat, which can shorten a ban [8], [25].
The college sports association in the United States does not name it either, and states that its list is neither complete nor exhaustive [26]. Detection is already prepared, since two laboratories published breakdown profiles in 2026 [9], [10]. Further detail sits under peptides banned in sport.
Compared with related peptides
| Substance | What it is | Point of attack | Human studies | Anti-doping status |
|---|---|---|---|---|
| SLU-PP-332 | Small synthetic molecule, 290.32 g/mol [1] | Switches on ERR alpha, beta and gamma [2] | None at all [3] | Caught by class S0 as a catch-all [8] |
| 5-Amino-1MQ | Small synthetic molecule, also not a peptide [27] | Blocks the enzyme NNMT [27] | None at all [27] | Caught by class S0 as a catch-all [27] |
| MOTS-c | A peptide encoded in mitochondrial DNA [25] | Activates AMPK [25] | Not assessed on this page | Named in class S4.4.1 by name [25] |
| Cardarine, GW501516 | Small synthetic molecule [25] | PPAR delta agonist [25] | Not assessed on this page | Named in class S4.4.1 by name [25] |
The most useful comparison is with 5-Amino-1MQ, because the two share a situation rather than a mechanism. Both are bench chemicals sold through peptide channels, both have no human data, and both are banned through wording rather than by name.
MOTS-c is the one that is genuinely a peptide, and it shows what the label on the shelf is worth. It is named on the Prohibited List, while SLU-PP-332 is not, yet both are banned [8], [25].
Cardarine is the substance SLU-PP-332 is most often confused with. Both circulate as endurance compounds, but they act on different receptors, and only Cardarine is printed on the list by name [25].
One more name deserves a warning. SLU-PP-1072 comes from the same laboratory series, and it does the opposite: it switches the same receptors off, and was built to study prostate cancer cells [19]. The numbers in the series are a counting system, not a statement about what a compound does.
Common misconceptions
- "SLU-PP-332 is a peptide." It has no amino acids and no sequence. It is a three-ring molecule of 290.32 g/mol that ended up in peptide catalogues because it moves through the same channels [1], [2].
- "It is exercise in a pill." The term exercise mimetic describes copying single molecular responses. A 2026 review sets out why a pill cannot reproduce the body-wide state that training creates [15].
- "Swallowing it does what the studies did." Every effective study injected it into the abdomen. Two papers state that the substance lacks oral bioavailability, and that was the stated reason for building a successor [4], [5].
- "It is basically Cardarine." Different receptor, different listing. Cardarine is a PPAR delta agonist printed on the Prohibited List by name; this one is an ERR agonist caught by the catch-all class [25].
- "Not on the WADA list means allowed." The reverse. Class S0 exists precisely to catch substances without approval, and names preclinical compounds as its example [8].
- "You can reconstitute it like a peptide." Bacteriostatic water will not dissolve it. The molecule is oily, with a fat-solubility measure of 3.7 and no charged side chains, and every study used solvent mixtures [1], [2].
- "There is human evidence, because a study used human cells." Twenty women donated muscle tissue during hip surgery. The cells were treated in a dish, and no participant received anything [17].
Frequently asked questions
Is SLU-PP-332 a peptide?
No. A peptide is a chain of amino acids, and SLU-PP-332 contains none. It is a small synthetic molecule of three rings weighing 290.32 g/mol, sold beside peptides because it travels through the same shops. The difference is practical: bacteriostatic water will not dissolve it, and anti-doping rules file it outside the peptide class.
Has SLU-PP-332 ever been tested in people?
No. A search of the ClinicalTrials.gov registry on 7 September 2026 found no registered study of SLU-PP-332, of its successor SLU-PP-915, or of any other ERR agonist. There are no published case reports and no measurement of what the substance does in a human body.
What does SLU-PP-332 do in the body?
In mice and in cells it switches on three receptors called ERR alpha, beta and gamma, which control genes for mitochondria and for burning fat. Muscle then behaves in some ways as it does after aerobic exercise. None of this has been measured inside a person.
Does SLU-PP-332 work if you swallow it?
The published record says no. Two papers state in plain words that SLU-PP-332 lacks oral bioavailability, meaning it does not reach the bloodstream from the gut. That finding was the stated reason for building a successor compound, SLU-PP-915, that survives the trip.
What did the animal studies of SLU-PP-332 find?
Mice given abdominal injections for a week ran about 70 percent longer and about 45 percent further before exhaustion. Over 28 days they gained under 0.5 grams of fat while controls gained about 5 grams. In a heart failure model the pumping fraction improved and survival rose.
Is SLU-PP-332 safe?
Nobody knows, because the work that would answer it has never been done. There is no repeated-dose toxicity study, no test for genetic damage, no fertility study and no cancer study. The longest exposure anywhere in the literature is eight weeks, in mice.
Is SLU-PP-332 approved anywhere?
No. As of 7 September 2026 no medicines authority anywhere has approved it, and the ChEMBL database records neither a clinical phase ever reached nor a first approval date. It is traded as a laboratory chemical under catalogue numbers, which is a research supply route rather than a medical one.
Is SLU-PP-332 banned in sport?
Yes, at all times. Class S0 of the 2026 Prohibited List covers any drug-like substance that no health authority approves for human use, and names substances in preclinical development as an example. Two anti-doping laboratories published detection work on SLU-PP-332 in 2026.
Is SLU-PP-332 the same thing as Cardarine?
No. Both circulate as endurance substances, but they hit different receptors. Cardarine, also called GW501516, is a PPAR delta agonist and is printed on the Prohibited List by name. SLU-PP-332 works on the ERR receptors and is caught by the catch-all class instead.
Why does SLU-PP-332 not dissolve in bacteriostatic water?
Because it is an oily, ring-shaped molecule with nothing for water to grab. Its fat-solubility measure is 3.7, and it carries no charged side chains. Every animal study dissolved it in solvent mixtures containing DMSO instead. That is why the reconstitution guide on this site treats it as a special case.
Sources
- PubChem. Compound CID 5338394, 4-hydroxy-N-(E)-naphthalen-2-ylmethylideneaminobenzamide. Formula C18H14N2O2, 290.3 g/mol, CAS 303760-60-3, XLogP 3.7, InChIKey RNZIMBFHRXYRLL-XDHOZWIPSA-N. Retrieved 7 September 2026. https://pubchem.ncbi.nlm.nih.gov/compound/5338394
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Cite this page
The facts on this page were checked on 7 September 2026, and every register search behind the status table was run on that date. This is a substance with no human data at all, so the date of the check matters as much as the text.
myPeptides Research & Editing. (2026). SLU-PP-332: what the studies show, status and safety. Version 1.0, 7 September 2026. myPeptides Peptide Register. Retrieved from https://mypep.app/peptides/slu-pp-332
How pages in this register are compiled and graded is described under methodology; the full register is at peptides.
| Version | Date | Note |
|---|---|---|
| 1.0 | 7 September 2026 | Initial publication |