SLU-PP-332

SLU-PP-332 is not a peptide. It is a small synthetic drug-like molecule made in a university medicinal chemistry laboratory at Saint Louis University and named after it, even though it is sold next to peptides. Its job is to switch on three related proteins inside your cells called the estrogen-related receptors (ERR-alpha, ERR-beta and ERR-gamma) — despite the name these are not receptors for estrogen, they are orphan nuclear receptors that act as master switches for the genes controlling mitochondria, the tiny power plants in your cells, and for the genes that burn fat for fuel. Because aerobic exercise turns on many of those same genes, researchers describe SLU-PP-332 as an exercise mimetic. Everything published about it comes from mice, from liver enzyme preparations, and from muscle cells in a dish. As of today there is no published human trial, nothing registered on ClinicalTrials.gov, and no regulatory approval anywhere in the world.

• Endurance and aerobic capacity, based on treadmill running in mice
• Fat loss and reduced fat gain, based on diet-induced obese and ob/ob mouse models
• Insulin sensitivity and glucose tolerance in rodent metabolic syndrome models
• Heart failure research, where it improved ejection fraction in a mouse pressure-overload model
• Age-related muscle and kidney decline, studied in old mice and in muscle cells from sedentary women
• Marketed to consumers as exercise in a bottle, which is a claim about mice, not people

Imagine your muscle cells have a control panel with a dial labeled burn fuel aerobically. Real endurance training turns that dial up by activating the ERR switches, which tell the cell to build more mitochondria and pull more fat into them. SLU-PP-332 reaches in and turns the same dial without the running. The catch is that a dial is not a workout: the compound has not been shown to build tendon, bone, skill or cardiovascular fitness in any person, and everything known about the dial comes from animals.

1. First 2 hoursIn mice, a single dose lowered the respiratory exchange ratio within about two hours, meaning the animals shifted toward burning fat, and switched on the acute aerobic exercise gene Ddit4 in muscle (Billon 2024, Kim 2026). No human equivalent has been measured.
2. Days 1-12Twelve days of twice-daily injections reduced adiposity in genetically obese ob/ob mice (Billon 2024).
3. Weeks 1-4Twenty-eight days of twice-daily 50 mg/kg injections in diet-induced obese mice produced roughly 12 percent body weight loss, near-complete blockade of further fat gain, and about 25 percent higher fatty acid oxidation (Billon 2024).
4. Weeks 6-8Six weeks of 25 mg/kg twice daily improved ejection fraction and survival after cardiac pressure overload (Xu 2024); eight weeks in 21-month-old mice reversed age-related albuminuria and podocyte loss (Wang 2023).
5. In humansThere is no human timeline. No trial has ever dosed a person with this compound, so any schedule you are given is extrapolated from rodents.

• No adverse events have been reported in humans because no human has been studied under any published protocol — that is an absence of data, not a finding of tolerability.
• The rodent papers describe no overt toxicity at the doses and durations tested, and a 2026 systematic review of pan-ERR agonism likewise reports benefit without evident toxicity in preclinical models (Riquelme 2026). None of those studies were designed as toxicology studies.
• ERR-gamma is the receptor that drives the cardiac effects (Xu 2024), so the compound is directly altering heart gene expression. In mice this was protective under pressure overload; what sustained ERR-gamma activation does to a healthy human heart has never been measured.
• The compound shifts whole-body fuel use toward fat oxidation and away from carbohydrate within hours in mice (Billon 2024). Effects on blood glucose in a person who is fasting, training hard, or taking glucose-lowering medication are unstudied.
• Material sold to consumers is labeled research use only, is not made to pharmaceutical standards, and its purity and actual content are generally unverified.

• You are pregnant, trying to conceive, or breastfeeding — no reproductive or developmental toxicity data exists for this compound.
• You have any heart condition, arrhythmia, or history of heart failure; the cardiac work was done in mice and ERR-gamma activation changes cardiac metabolic gene expression directly.
• You have a current or past cancer diagnosis, since ERR-alpha is implicated in tumour metabolism and the consequences of activating it in a person are unknown.
• You have liver or kidney impairment — the compound is extensively metabolised by liver enzymes, with twenty-two metabolites identified in vitro (Sardela 2026), and none of that has been characterised in people.
• You are a tested athlete: anti-doping laboratories have already published detection methods aimed specifically at catching its use.
• You are not under the supervision of a physician who knows you are taking an unapproved research chemical.

• Taking it by mouth. The researchers who made it state plainly that SLU-PP-332 lacks oral bioavailability, which is why they went on to develop the orally active successor SLU-PP-915 (Kim 2026). An oral capsule, or a dose taken with a meal, is not the delivery route that produced any published result.
• Treating it like a peptide. It is a small molecule, so reconstitution, bacteriostatic water and cold-chain advice copied from peptide protocols does not necessarily apply, and it will not behave like a peptide in solution.
• Scaling the mouse dose by body weight. Published rodent work used 20 to 50 mg/kg intraperitoneally twice a day; that is not a human dose, and interspecies scaling for this compound has never been established.
• Assuming it replaces training. Every mouse study that measured endurance still put the animal on a treadmill to measure it, and the successor compound worked best combined with exercise training rather than instead of it (Kim 2026).
• Stacking it with other metabolic agents — GLP-1 drugs, thyroid hormone, stimulants, PPAR agonists — on the assumption that effects simply add. No interaction study of any kind exists.