Biohacking Kompakt

Peptide & experimental

SLU-PP-332

ERR (estrogen-related receptor) α/β/γ agonist · “Exercise mimetic”

SLU-PP-332 is a small molecule designed in the laboratory that switches on those energy switches of the cell that are otherwise activated by endurance training. In mice it increased endurance and fat burning without the animals having trained. It has not yet been studied in humans.

In short

SLU-PP-332 activates the estrogen-related receptors ERRα, ERRβ and ERRγ, master regulators of mitochondria and fat burning. In mouse studies, treated animals ran around 70 percent longer and 45 percent farther after a single dose, and overweight mice barely put on fat even though they ate the same amount. This is clean basic research, and the mechanism of action is genetically confirmed in animals. The catch: there is no study in humans, no safety data, and according to its developers the substance is not sufficiently available when taken by mouth.

What it is

SLU-PP-332 is not a peptide but a synthetic small molecule. It was developed by the research group of pharmacologist Thomas Burris; the abbreviation SLU stands for Saint Louis University, where the early work took place. In 2023 the team presented the substance as an agonist that switches on all three ERR receptors, most strongly ERRα. For research this was a step forward, because until then there were hardly any tools to activate these receptors selectively in the living animal.

In the scene, SLU-PP-332 is known as an exercise mimetic, that is, an exercise imitator, sometimes under the nickname “exercise in a syringe”. The interest comes from three directions: endurance athletes who want to amplify the training effect, people concerned with body composition and fat burning, and the longevity scene, for which healthy mitochondria are a central aging topic.

How it is supposed to work

The ERR receptors are called estrogen-related, but they do not bind the body’s own estrogen. They are transcription factors that control genes for new mitochondria, cellular respiration and fat burning, above all in the heart, skeletal muscle and liver. Their most important partner is the coactivator PGC-1α. You can think of PGC-1α as the conductor and the ERR receptors as musicians who translate its instructions into gene activity. Endurance training raises the baton; SLU-PP-332 makes the musicians play directly.

The research group examined this mechanism closely. In muscle cells, the substance increased cellular respiration and mitochondrial function. In mouse muscle it switched on a gene program similar to that after an acute bout of endurance exercise, led by the gene Ddit4, which is also activated during training. Mice genetically lacking ERRα in muscle did not benefit: their endurance stayed at the level of untreated animals. The effect therefore really does depend on the target receptor.

More than a sports topic

The medical vision goes far beyond sport. Exercise is one of the most effective means against metabolic diseases, but not everyone can train, for example after injuries, in severe illness or in old age. For these people, a molecule that delivers part of the training stimulus would be of interest. In a mouse model of heart failure, SLU-PP-332 and the sister compound SLU-PP-915 improved pumping function and survival. In 21-month-old mice, that is, animals of advanced age, an 8-week treatment reversed age-related kidney changes such as protein in the urine, mitochondrial weakness and inflammatory messengers.

There is also a first study with human cells. In 2025, researchers treated muscle precursor cells from physically inactive women receiving a hip replacement with SLU-PP-332 in the laboratory. The cells formed more PGC-1α and ERRα, showed less oxidative stress and formed abundant myotubes, the precursors of muscle fibers. This suggests that the mechanism also works in human tissue. It is not yet an effect in living humans.

What users report

The substance is sold as a research product and in the scene is sometimes injected, sometimes taken as a tablet. A rapidly noticeable endurance effect is consistently reported; some measure it by their own running or cycling times. That an effect appears quickly does not contradict the biology, because in the animal experiment a single dose one hour before running was already effective.

It remains open whether the amounts and routes common in the scene even reach active levels like those in the animal experiment. Nobody has measured this. Such reports are observations without a control group; expectation and normal fluctuations in training cannot be factored out. They are interesting, but not proof of efficacy.

What is well supported

What is well supported is the effect in animals, and from several angles. After a single dose, untrained mice ran around 70 percent longer and 45 percent farther than control animals. After repeated dosing, the proportion of enduring, oxidative type IIa fibers in muscle increased, and the amount of mitochondrial DNA rose. In normal-weight mice, energy production shifted toward fat within the first hours; fat oxidation was 25 percent higher. Overweight mice used more energy, lost weight and became more insulin-sensitive without eating less. That the endurance effect fails to appear without ERRα in muscle makes the mechanism more robust than for many other substances in the scene.

What the studies show

Endurance in the mouse experiment (Billon, 2023)

The paper in ACS Chemical Biology introduced SLU-PP-332. Untrained mice received a single dose one hour before a treadmill test to exhaustion, with 6 animals per group. They ran around 70 percent longer and 45 percent farther. After longer dosing, grip strength and the proportion of oxidative type IIa fibers increased. Mice without ERRα in muscle showed no endurance gain after 14 days of treatment. The groups were small, and the animals received the substance into the abdominal cavity.

Overweight and metabolism (Billon, 2024)

In the Journal of Pharmacology and Experimental Therapeutics, the same group tested the substance in mice with diet-induced obesity and in genetically obese ob/ob mice. After 28 days, the treated overweight animals weighed around 12 percent less. The control animals gained about 5 grams of fat, the treated ones less than 0.5 grams. Food intake remained the same, the additional expenditure came from metabolism, and insulin sensitivity improved.

Heart failure in the animal model (Xu, 2024)

In Circulation, SLU-PP-332 and SLU-PP-915 improved ejection performance, reduced fibrotic remodeling and prolonged survival in mice with pressure-induced heart failure. This was mediated mainly via ERRγ and improved fat and energy metabolism of the heart muscle. The thickening of the heart muscle itself remained unchanged.

Where the data stop

All efficacy research comes from animals and cell cultures. A 2026 systematic review on SLU-PP-332 and SLU-PP-915 found exclusively preclinical studies and considers clinical trials necessary before anything can be said about efficacy and safety in humans. The efficacy data come predominantly from a research network around the same group; independent replications are rare.

Then there is absorption by mouth. The developers themselves write in 2026 that SLU-PP-332 is not orally bioavailable, and therefore presented the successor SLU-PP-915, which also works when swallowed. Tablets containing SLU-PP-332 therefore lack a basis. A review in Trends in Endocrinology and Metabolism also points out that training is far more than mitochondria: blood vessels, the autonomic nervous system, inflammation and messenger substances from muscle change as well. A pill that operates a single switch does not reproduce this overall package.

Status, approval and legal

SLU-PP-332 is not approved as a medicine anywhere and is in early preclinical research; no clinical trials have been published. It is sold as a research chemical without pharmaceutical quality control. In sport, as a non-approved, pharmacologically active substance, it falls under class S0 of the WADA Prohibited List 2026, which prohibits such substances at all times, including out of competition. It is not named there, but in 2026 doping laboratories already described its metabolites in human liver preparations in order to be able to detect misuse. We do not give doses for non-approved substances.

Safety

There are no safety data in humans. In animals, the research group found no obvious toxicity after 10 days of dosing; blood count, electrolytes and the muscle marker creatine kinase remained unremarkable. This is a short-term finding in a few mice and says nothing about months or years in humans. Because ERR receptors broadly reprogram the metabolism of the heart, liver, kidney and muscle, long-term consequences are difficult to predict. On interactions, pregnancy, and pre-existing conditions of the heart, liver or kidney, there are no data whatsoever. With research products, unclear purity and unclear content come on top.

BK-Score Not studied in humans

Human evidence0
Mechanism5
Safety data1
Hype gap1
Track record of use3

What applies here is not “tested and refuted” but “not tested”: there is no human study, only animal and cell studies. These, however, are solid. After a single dose, mice ran around 70 % longer and 45 % farther; overweight mice weighed around 12 % less after 28 days (Billon 2023, 2024). Mechanism 5, because the dependence on the target receptor has been shown genetically – without ERRα in muscle, no endurance gain – and first data on human muscle precursor cells are available (Bonanni 2025); confirmation in living humans is missing. Evidence 0 and safety 1, because there are neither clinical efficacy nor safety data, in animals only short-term findings over 10 days. The developers themselves state that SLU-PP-332 is not orally bioavailable, and therefore developed SLU-PP-915 (Billon 2026) – tablets sold therefore have no basis. Hype 1, because “exercise in a syringe” appears as a promise for humans, although the data come only from mice. Use 3: in circulation in a niche as a research product, without studies in humans.

The score rates the state of knowledge, not the substance. “Safety data 9” means well studied – not harmless.
Subjective assessment by Biohacking Kompakt based on published scoring rules – not a scientific rating and not a medical recommendation. Rules and all ratings (German)

Frequently asked questions about SLU-PP-332

What is SLU-PP-332?

A synthetic small molecule that activates the estrogen-related receptors ERRα, ERRβ and ERRγ. These switches control the formation of mitochondria and fat burning and are also stimulated by endurance training. That is why SLU-PP-332 is considered an exercise mimetic.

Does SLU-PP-332 work in humans?

That has not been studied. All efficacy data come from mice and cell cultures, including one laboratory study with human muscle precursor cells. There is no clinical trial.

Can SLU-PP-332 replace training?

No. In animals it mimicked part of the training adaptation in muscle. Training, however, also acts on blood vessels, the nervous system, inflammation and messenger substances from muscle, and a single molecule does not reproduce this overall package.

Does SLU-PP-332 help with weight loss?

In overweight mice, weight fell by around 12 percent after 28 days without the animals eating less. Whether this would be similar in humans, nobody knows, because there is no human study.

Is SLU-PP-332 safe?

The data for that are missing. In animals there was no obvious toxicity over 10 days; long-term and human data do not exist. Research products are also not tested for purity and content.

Is SLU-PP-332 legal and permitted in sport?

It is not approved as a medicine and is sold as a research chemical. In sport it falls under class S0 of the WADA list and is prohibited at all times; doping laboratories are already working on detection methods.

The podcast episode (in German)

Episode 5

AI podcast: SLU-PP-332 – “Exercise in a syringe”?

The podcast by Paul Höser (Episode 5) · with Paul & Paula. Fresh, positive AI dialogue episode on SLU-PP-332, the “exercise mimetic”: a small molecule that mimics the adaptation to endurance training via the ERR switches – more mitochondria, more fat burning, more endurance. What the 2024 Nature Metabolism study (Billon et al.) showed in mice, the medical vision of “exercise in tablet form” and the honest framing: so far only animal data. Information only, no dosage or usage recommendation.

Listen on Spotify

To the episode page with summary and sources (German)

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Sources

Open in the database – with search, filters and comparison (German app)

Information only, not medical advice and not a usage or dosage recommendation. Prescription-only and unapproved substances belong in the hands of a physician. Last updated: 2026-09-27.