SLU-PP-332: What It Is, Where to Get It Prescribed, and What It Costs

SLU-PP-332 is not a peptide. It is a small synthetic organic molecule, built around a naphthalene ring and a phenol, designed to bind a family of receptors called the estrogen-related receptors, or ERRs. It is listed alongside peptides because it is prescribed, compounded and injected through the same channels, but chemically it has more in common with a conventional drug than with BPC-157 or semaglutide: it is metabolised in the liver the way small-molecule drugs are, and the published work on it comes from pharmacology and medicinal chemistry rather than peptide biology.

The receptors it targets, ERRα, ERRβ and ERRγ, are "orphan" nuclear receptors. Despite the name they do not bind estrogen and have no known natural hormone that switches them on. They sit on DNA and control the genes that build mitochondria, run oxidative phosphorylation and oxidise fatty acids. In muscle, heart and kidney they are among the main switches the body uses to adapt to aerobic exercise.

SLU stands for Saint Louis University. The compound came out of a collaboration between medicinal chemists there and the pharmacology group of Thomas Burris, published in ACS Chemical Biology in 2023. That paper reported the first synthetic agonist with meaningful activity at ERRα, which had been considered hard to drug, alongside activity at ERRβ and ERRγ. The authors called it an "exercise mimetic" because, in mice, it switched on the same gene program that a bout of endurance exercise does. The number is its place in the lab's compound series; a later, orally active sibling is SLU-PP-915. A 2026 paper in the International Journal of Biological Macromolecules mapped how each part of the structure contributes to potency and selectivity, and describes SLU-PP-332 as the reference compound other ERR agonists are now measured against.

It is not a stimulant, a thyroid hormone or a thermogenic. It does not act on the brain to suppress appetite and it is not a GLP-1 medication. It is not a hormone, it does not bind an androgen or estrogen receptor, and it is not a substitute for exercise: the researchers who made it describe it as a candidate for people who cannot exercise adequately, not as a replacement for training in people who can.

It is also not a human-tested medication. Every efficacy finding on this page comes from mice or from cells in a dish.

ERRα and ERRγ, working with a coactivator protein called PGC-1α, control a large block of genes involved in mitochondrial biogenesis, the electron transport chain, the Krebs cycle and fatty acid oxidation. SLU-PP-332 binds all three ERR subtypes, with the highest potency at ERRα, and increases their transcriptional activity. In a mouse skeletal-muscle cell line, the 2023 ACS Chemical Biology paper reported increased mitochondrial function and cellular respiration after treatment: more mitochondrial machinery, more capacity to make energy aerobically.

A single session of endurance exercise changes which genes muscle expresses in the hours afterwards. The 2023 paper reported that a dose of SLU-PP-332 in mice induced a strikingly similar set of genes, and that the response depended on ERRα: mice engineered to lack it did not show the gene program and did not gain the endurance benefit. A 2026 paper in the Journal of Pharmacology and Experimental Therapeutics reported that one marker of that program, a gene called Ddit4, rose to levels matching or exceeding a treadmill run, depending on the muscle sampled.

Muscle fibres come in fast, glycolytic types that fatigue quickly and slower, oxidative types that keep going; endurance training shifts the balance toward the oxidative end. The 2023 work reported that treated mice had a higher proportion of type IIa oxidative fibres, the structural change the group proposed as the basis for the longer running times.

The 2024 paper in the Journal of Pharmacology and Experimental Therapeutics moved from muscle to whole-body metabolism. In diet-induced obese mice and in ob/ob mice, treatment was reported to raise energy expenditure and fatty acid oxidation, with less fat mass accumulated over the study. The authors' framing is that the compound shifts fuel preference toward fat, in the same direction regular aerobic exercise does.

Two groups outside the original lab have used SLU-PP-332 to ask what ERR activation does in other organs. A 2024 paper in Circulation reported that in a mouse model of pressure-overload heart failure, ERR agonists improved ejection fraction, reduced fibrosis and improved survival, with the effect tracing mainly to ERRγ in heart muscle cells. A 2023 paper in the American Journal of Pathology reported that eight weeks of treatment in 21-month-old mice moved several age-related kidney measures, including albuminuria and inflammatory signalling, back toward those of younger animals. Both are mechanism studies in animals; neither has been taken into people.

This is the founding result. Mice given SLU-PP-332 ran further and for longer on a treadmill than untreated mice, reported in the 2023 ACS Chemical Biology paper and reproduced in the 2026 JPET paper on its oral successor. The mechanism was tested with knockout animals, a higher standard than most compounds in this category meet. It remains a mouse result.

The 2024 JPET paper reported that in two mouse models of obesity, treatment increased energy expenditure and fatty acid oxidation and reduced fat mass gain, and that insulin sensitivity improved in the metabolic-syndrome model. These are the results behind the compound's "weight loss" categorisation. They were measured in animals with controlled diets, at doses that do not map directly onto a compounded vial.

The Circulation paper is the most rigorous single study of the compound: a pressure-overload model with functional, genetic and multi-omics readouts. It says nothing about the heart of a healthy person taking the compound for a metabolic reason, which has not been studied.

The American Journal of Pathology paper is one of the few long-duration treatment studies, eight weeks in old animals, and reported no obvious harm alongside the kidney findings. It is a study of ERRs as a caloric-restriction mimetic, not of SLU-PP-332 as a product.

This is the honest part, and it is shorter than it is for most peptides on this site. There are no randomised controlled trials of SLU-PP-332 in humans. There are no published human trials of any kind, at any phase, and no human pharmacokinetic data. The nearest thing is a 2025 pilot study in Frontiers in Physiology, in which muscle cells taken from inactive women during hip surgery were treated with SLU-PP-332 in culture and showed changes in mitochondrial and stress-response proteins. That is human tissue in a dish, and the authors call for further work before drawing conclusions.

The other human-relevant literature is anti-doping science. Two 2026 papers, in Drug Testing and Analysis and Rapid Communications in Mass Spectrometry, mapped how human liver enzymes metabolise it so that testing labs can detect it. Those exist because the World Anti-Doping Agency prohibits exercise mimetics and metabolic modulators as a class, not because anyone has measured what the compound does in a person.

So the accurate framing is: a well-characterised mouse pharmacology tool, with no human evidence in either direction. Any source describing it as proven in people is describing something that has not been published.

• It does not establish that any effect seen in mice occurs in humans. Exercise mimetics have a history of working in rodents and failing to translate; that question is open here.
• It does not establish a human dose. The mouse doses were set by body weight and given intraperitoneally; the compounded directions are a physician's judgement, not a trial-derived figure.
• It does not establish a timeline. There are no human endpoints to anchor one.
• It does not establish safety in humans over any duration.
• It does not establish efficacy for any condition as an approved treatment. It is not approved for anything.

The mouse gene-expression changes are rapid, within hours of a dose, but that says nothing about what a person notices. Prescribers most often describe steadier energy through the day as the earliest report, if anything is reported at all. Injection-site redness in this window is normal. Noticing nothing is also normal.

This is the window prescribers point to for any change in stamina or body composition, on the reasoning that the animal fibre-type and fat-mass changes took weeks rather than days. Whether those changes occur in humans at the compounded dose is exactly the thing nobody has measured. Anyone who tells you what to expect by week six is guessing.

The compound was designed around the exercise response. The 2026 JPET paper reported that its oral successor's effect on mitochondrial gene expression was larger combined with exercise training than with either alone. Whatever it does, the honest expectation is that it does more in someone who is also training.

Refills run on a 28-day cycle and a physician reviews each one. There is no described withdrawal, because nothing about stopping it has been studied in people. The longest animal treatment on file is eight weeks. Whether continuous use over months is appropriate is your physician's judgement, and one the research cannot make for them.

The directions are written in millilitres and insulin-syringe units because that is what you can read off the barrel. 0.25 mL is 25 units on a U-100 syringe. You are not calculating anything; the number is printed on your medication.

Subcutaneous means into the fat layer, not the muscle. Abdomen and thigh are the usual sites, rotated so the same spot is not used repeatedly. It is injected rather than swallowed because the published pharmacology reports that SLU-PP-332 lacks oral bioavailability; the Burris group's 2026 paper describes developing SLU-PP-915 for exactly that reason. The mouse studies gave it by intraperitoneal injection, which has no equivalent in routine care, so subcutaneous is the practical route.

20 doses at once daily Monday through Friday is four weeks, which is why refills run on a 28-day cycle. The weekend gap is part of the directions, not an omission. One vial per fill, always; not a stockpile.

Refrigerated, and it ships that way in insulated packaging with ice packs. Beyond-use dating runs from first puncture and is on the label. Do not freeze it.

Different mechanisms and, more importantly, different evidence. Semaglutide and tirzepatide act on gut-hormone receptors to reduce appetite and are approved drugs in their branded forms, with large human trials. SLU-PP-332 acts inside muscle and other cells on how fuel is used, has no appetite mechanism, and has no human trials. They are not interchangeable.

Both are described around mitochondrial metabolism and both are animal-evidence products. MOTS-c is a peptide encoded in mitochondrial DNA, described as acting through AMPK signalling; SLU-PP-332 is a synthetic molecule acting through the ERR nuclear receptors upstream of mitochondrial gene expression. The MOTS-c literature is older and broader; the SLU-PP-332 literature is newer and more mechanistically precise. Neither has human trial data.

5-Amino-1MQ inhibits an enzyme called NNMT in fat cells and is described around cellular NAD+ and fat-cell metabolism. SLU-PP-332 is aimed at muscle first and fat second. Both rest on mouse work.