A synthetic small molecule, not a peptide, that activates ERR receptors and raised endurance and cut fat gain in mice. No human data.
Also called SLU-PP332, ERR pan-agonist 332, (E)-4-hydroxy-N'-(naphthalen-2-ylmethylene)benzohydrazide
SLU-PP-332 is not a peptide. It is a small lab-made molecule from Thomas Burris's group at Saint Louis University (the SLU in the name), designed to switch on the estrogen-related receptors ERR alpha, beta and gamma. Despite the name, these receptors do not respond to estrogen. They are switches in the cell nucleus that turn on the genes for building mitochondria and burning fat, the same genes endurance training turns on. It is grouped with peptides because it is sold by the same research-chemical vendors and is promoted as an exercise mimetic.
In sedentary mice, twice-daily injections of 50 mg/kg for a week made them run about 70% longer and 45% farther before exhaustion, and shifted their leg muscle toward fatigue-resistant type IIa fibers. In obese mice, four weeks of the same dosing raised energy expenditure and fat burning; the treated mice gained under half a gram of fat while untreated mice gained about 5 grams, with no change in food intake. Separate mouse studies found it improved heart function in a heart failure model and reversed some kidney aging markers.
None of this has been tested in a person. There is no human safety, dosing or pharmacokinetic data, no registered clinical trial, and its own developers wrote in 2025 that SLU-PP-332 lacks oral bioavailability, which matters because much of what is sold online is oral capsules. The researchers have since moved on to a related compound, SLU-PP-915, that can be taken by mouth. Anti-doping labs in Cologne and Los Angeles have already mapped how human liver enzymes break it down, so its breakdown products can be screened for in doping tests.
Not technically a peptide. SLU-PP-332 is listed here because it is discussed and used alongside peptides, but it is not built from amino acids joined by peptide bonds.
What it binds to, and what happens inside the body after that, step by step.
SLU-PP-332 binds and activates all three estrogen-related receptors, with the strongest effect on ERR alpha (EC50 about 98 nM, versus 230 nM for ERR beta and 430 nM for ERR gamma). These receptors control the genes for mitochondrial biogenesis, fatty acid oxidation and oxidative phosphorylation. In mice the endurance benefit depended on ERR alpha, and the heart benefit depended mainly on ERR gamma.
Human results and animal results are kept apart below. A result in rats tells you a mechanism is plausible. It does not tell you what happens in a person.
Mouse studies consistently show more endurance, more fat burning, less fat gain and better insulin sensitivity, plus heart and kidney benefits in disease models, mostly from the Saint Louis University developers and their collaborators. The only human tissue work treated muscle cells grown from biopsies of 10 inactive women in a dish. No person has been given SLU-PP-332 in any published study.
No human studies are among the key studies for SLU-PP-332. Everything known comes from animals or cells.
Sedentary mice, 50 mg/kg injected twice daily for 7 days; cultured muscle cells
Treated mice ran about 70% longer and 45% farther before exhaustion and had more type IIa oxidative fibers; the effect required ERR alpha.
Read the studyDiet-induced obese mice (7 per group) and ob/ob mice, 50 mg/kg twice daily for up to 28 days
Obese mice weighed about 12% less after 28 days and gained under 0.5 g of fat versus about 5 g on vehicle, with better glucose tolerance and unchanged food intake.
Read the studyMice with pressure-overload heart failure
SLU-PP-332 and SLU-PP-915 improved ejection fraction, reduced fibrosis and increased survival, mainly through ERR gamma.
Read the study21-month-old mice treated for 8 weeks; aging human and mouse kidney tissue
A pan-ERR agonist reversed age-related protein leakage in urine, podocyte loss and kidney inflammation in old mice.
Read the studyMuscle cells grown from biopsies of 10 inactive women having hip replacement
In the dish, SLU-PP-332 raised PGC-1 alpha, ERR alpha and SIRT1, lowered oxidative stress and improved myotube formation. The women were not given the drug.
Read the studyMice
The developers state SLU-PP-332 lacks oral bioavailability and introduce SLU-PP-915, which raises exercise capacity when taken by mouth.
Read the studyHuman liver S9 fraction and microsomes
Cologne doping lab identified nine SLU-PP-332 metabolites (six Phase I, three Phase II) for use in anti-doping tests.
Read the studyThese are questions the published research has not answered.
No product containing SLU-PP-332 is approved as a medicine by the FDA.
Not approved anywhere and no human trial was found on ClinicalTrials.gov. It is a preclinical research tool. It is not named on the WADA Prohibited List, but S0 bans any pharmacological substance with no current government approval for human therapeutic use, which covers it, and anti-doping labs have identified its metabolites for use in doping tests. The developers hold stock in companies working on ERR agonists (Myonid Therapeutics, Pelagos Pharmaceuticals).
No human half-life has been published for SLU-PP-332, so we do not draw a clearance curve. Half-lives quoted online for it are usually estimates from animal data.
No human study or approved label has published a dose for SLU-PP-332, so there is no table to show.
No dose of SLU-PP-332 has been tested in a published human study or approved on a label. Numbers that circulate online come from animal studies scaled up by guesswork or from sellers. We do not reproduce them.
Which symptoms are expected and which mean stop and get help: side effects and red flags.
Tap a claim to see what the studies found.
In mice it turned on exercise-related genes and raised endurance. Nobody has tested it in a person.
True for sedentary mice given 50 mg/kg injections twice daily for a week. There is no human figure.
Its own developers state it lacks oral bioavailability; every mouse result used injections into the abdomen.
It is a small acyl hydrazone molecule of about 290 g/mol with no amino acids.
ERRs got their name because their gene sequence resembles the estrogen receptor. They do not bind estrogen, and no study has shown an estrogen effect.
These pairings come up often. Almost none have been tested together in a trial, and the evidence note on each says so plainly.
Pairs two compounds promoted as exercise mimetics with different targets (ERR and AMPK).
EvidenceNever studied together; each has mouse data only.
Promoted online as a fat-loss pairing of an ERR agonist and an NNMT inhibitor.
EvidenceNo study of the combination exists.
The developers suggest ERR agonists may add to training adaptations.
EvidenceShown only for the related oral compound SLU-PP-915 in mice, where it added to gene changes from training.
Dry research powder; no pharmaceutical stability data. Vendors generally list cool, dry, dark storage.
No validated stability data. Mouse studies dissolved it in a DMSO, Tween and saline vehicle, not water.
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