Section 01
What it's used for
Fat Loss in Obese Mice
In a 2024 study (Billon et al.), obese mice given daily injections for 28 days gained 10 times less fat than untreated mice and lost 12% of body weight. It also reduced fatty liver buildup and improved blood sugar handling in these mice.
▸Clinical wording
In the primary preclinical study (Billon et al., 2024), administration of SLU-PP-332 to obese mice (50 mg/kg IP, twice daily, 28 days) resulted in 10-fold less fat mass accumulation compared to controls and 12% body weight reduction. The compound reduced hepatic steatosis and improved glucose tolerance in metabolic syndrome models.
Exercise-Mimicking Effect in Mice
Researchers describe it as an "exercise mimetic." In a mouse experiment, treated mice ran 70% longer and covered 45% more distance than untreated mice, with more endurance-type muscle fibers, mimicking real training adaptation.
▸Clinical wording
SLU-PP-332 is classified as an "exercise mimetic." Mice receiving the compound ran 70% longer and covered 45% greater distances compared to controls. Increased type IIa oxidative muscle fibers confirm direct muscle adaptation to endurance exercise.
Studied for Insulin Resistance
In obese mice on a high-fat diet, it improved blood sugar handling, lowered fasting glucose and insulin, and raised muscle glucose uptake — a lead for insulin resistance, though human data are lacking. GLUT4 involvement is unconfirmed.
▸Clinical wording
Improved insulin sensitivity and enhanced glucose utilization through increased GLUT4 expression make SLU-PP-332 a potential candidate for insulin resistance therapy. However, clinical data are lacking.
Reduces Fatty Liver in Mice
In mice, it significantly reduced fatty liver buildup and liver fat content, suggesting potential for fatty liver disease. Researchers link this to increased fat burning, but the exact cellular mechanism was not measured or confirmed.
▸Clinical wording
Significant reduction in hepatic steatosis in mice indicates potential for NAFLD/NASH treatment. The mechanism involves enhanced hepatocyte fatty acid oxidation and reduced de novo lipogenesis.
Studied for Age-Related Muscle Loss
A 2025 review (Frontiers in Physiology) is examining ERR-activating compounds like this one for age-related muscle loss. Researchers propose that activating ERR could counter declining muscle cell energy production seen with aging.
▸Clinical wording
Recent research (Frontiers in Physiology, 2025) explores ERR agonists for combating age-related muscle loss. ERR activation may counteract the decline in mitochondrial function characteristic of aging skeletal muscle.
Section 02
Mechanism of Action
Switching on energy-metabolism receptors
- The compound binds a family of receptors inside the cell nucleus that govern energy metabolism.
- It activates all three family members, with the strongest effect on the first one (ERRα).
- Despite the name, these receptors do not carry oestrogen signalling directly.
- They are most abundant in energy-hungry tissue: skeletal muscle, heart and brown fat.
▸Clinical wording
ERR Receptor Activation
SLU-PP-332 binds to nuclear receptors of the ERR family (Estrogen-Related Receptors) — ERRα, ERRβ, and ERRγ, acting as a pan-agonist with preferential activity at ERRα. These receptors are not directly involved in estrogen signaling but are key regulators of energy metabolism. ERRα is highly expressed in energy-demanding tissues — skeletal muscle, heart, and brown adipose tissue.
Switching on the exercise gene program
- Binding the receptor turns on hundreds of genes normally associated with physical exercise.
- Key targets include the master switch for building mitochondria and a glucose transporter.
- The result is muscle shifting toward oxygen-based metabolism without the mechanical strain of training.
▸Clinical wording
Activation of Aerobic Exercise Transcriptional Program
Upon binding to ERRα, SLU-PP-332 triggers expression of hundreds of exercise-associated genes. Key targets include PGC-1α (master regulator of mitochondrial biogenesis) and GLUT4 (glucose transporter upregulated by insulin and exercise). This shifts skeletal muscle toward oxidative metabolism without the mechanical stress of actual training.
More output from cellular power plants
- The compound strongly increases mitochondrial respiration and fatty acid burning in muscle cells.
- Those measurements came from a cultured muscle cell line, not from whole animals or people.
- It also raises the share of endurance-type muscle fibres, a hallmark effect of aerobic training.
▸Clinical wording
Mitochondrial Function Enhancement
SLU-PP-332 significantly enhances mitochondrial respiration and fatty acid oxidation in skeletal muscle cells (C2C12 myocytes). The compound increases the proportion of type IIa oxidative fibers in skeletal muscle — a hallmark effect of aerobic training.
Burning more energy at rest
- The compound raises resting energy expenditure and speeds up the breakdown of fats.
- It reaches this without changing appetite, food intake or physical activity levels.
- The source describes it as making the body behave as though it were exercising.
▸Clinical wording
Increased Energy Expenditure
The compound increases resting energy expenditure by accelerating fat metabolism. This effect occurs without affecting appetite, food intake, or locomotor activity — the drug makes the body function as if it is exercising, resulting in enhanced fat burning.
Section 03
Biological Pathways
- ERRα/PGC-1α Transcriptional CascadeERRα, coactivated by PGC-1α, drives transcription of oxidative-phosphorylation genes, mitochondrial biogenesis, and fatty acid β-oxidation, activating electron transport chain gene promoters and citrate synthase.
- PGC-1α/NRF/TFAM Mitochondrial BiogenesisThrough the PGC-1α to NRF-1/NRF-2 to TFAM cascade, the compound stimulates mitochondrial DNA replication and new mitochondria assembly, shifting muscle metabolism from glycolytic to oxidative.
- AMPK/SIRT1 Energy SensingERR-driven metabolism raises the AMP/ATP ratio, activating AMPK, which stimulates catabolic processes such as fatty acid oxidation and autophagy while suppressing fat and protein synthesis via mTORC1 inhibition.
- Calcineurin/NFAT/MEF2 Fiber RemodelingActivation of calcineurin/NFAT and MEF2-dependent transcription shifts skeletal muscle fiber composition toward oxidative type IIa fibers, mirroring adaptation to aerobic endurance training.
Section 04
Dosage Information
| Route / system | Context | Range studied | Limitation |
|---|---|---|---|
| Intraperitoneal — mouse studies | Obese mice, diet-induced and genetic, 12–28 days | 50 mg/kg twice a day for 12–28 days, or 25 mg/kg once a day for 15 days, into the abdomen. For a 70–90 kg adult: 3.5–4.5 g a shot. | A laboratory route, never used in people; the gram figure is arithmetic. No conversion to a human dose and no human measurements exist. |
| Any route in humans | Trials, regulatory filings, published data | None. No study in a person is registered or published, by any route. The compound is approved nowhere and in development nowhere. | Every dose ever measured for this molecule is a mouse dose. It has never been given to a person, so there is no human dose to be too high or too low. |
| Oral — self-administration | Tablets sold as a research chemical | 25, 50 and 100 mg a day circulate, sold as 50 mg tablets. Nothing ties these figures to the mouse work or to any person. | A small molecule, not a peptide: how much of a swallowed tablet reaches the blood was never measured in a person. Sellers picked the strengths. |
| Subcutaneous — self-administration | Reconstituted vials sold for injection | 250 µg to 1.5 mg a day — roughly 3–20 µg/kg for a 70–90 kg adult, several thousand times less per kilogram than the mice got. | It does not dissolve in water; the animal work used DMSO. No injectable human form, no measurement of what reaches the blood, no reason for these amounts. |
Results
Syringe Fill Level (100u syringe)
Set positive values for: Recommended dose per kg.
Research Use Only. This information is for educational and research purposes only. Not intended for medical advice or self-medication.
Section 05
Protocols
- Protocol 01
SLU-PP-332 — Metabolic Enhancement
Experimental protocol based on the exercise mimetic SLU-PP-332 (ERRα/β/γ agonist) for enhancing fat oxidation, increasing endurance, and improving metabolic profile. For preclinical research only.
- Focus
- Weight Loss
- Level
- Advanced
- Duration
- 28 days
Section 06
Stability & Storage
Lyophilised powder
SLU-PP-332 powder is stable at −20°C for up to 3 years when sealed and protected from light and moisture. It is freely soluble in DMSO (58 mg/mL), only slightly soluble in ethanol (2 mg/mL), and insoluble in water, so DMSO is the standard solvent for research use.
After reconstitution
Stock solutions prepared in DMSO remain stable at −80°C for up to a year, or at −20°C for up to a month. For research use, they are typically diluted into an appropriate vehicle just before administration.
Section 07
Side Effects & Precautions
All safety data on SLU-PP-332 come from short-term mouse studies; no clinical, long-term, or human safety data exist yet.
What The Standard Mouse Study Found
In the primary study (Billon et al., 2024), only minor changes in plasma cholesterol levels and liver enzymes were noted. No significant liver, kidney, or cardiovascular toxicity was identified within the 28-day protocol.
Obese Mice Tolerated It Worse
In genetically obese (ob/ob) mice, treatment duration was cut to 12 days because of tolerability issues. The publication does not detail what those issues were, but this may point to more pronounced side effects in severe obesity.
Why The Mechanism May Lower Endocrine Risk
- SLU-PP-332 works through gene transcription and nuclear receptor activation, not hormonal axes, and does not suppress the body's own (endogenous) hormones.
- It does not stimulate appetite or act as a CNS stimulant; skipping the hypothalamic-pituitary axis may lower the risk of hormone-related side effects.
What Nobody Has Studied Yet
- No data exist on long-term toxicity, carcinogenicity (cancer-causing potential), or teratogenicity (risk of birth defects).
- No data exist on drug interactions or safety in humans; until full toxicological studies and Phase I trials are run, the safety profile stays uncertain.
Section 08
Regulatory Status
It has not been tested in humans: every published result, including its metabolism, comes from mouse studies and in-vitro liver assays.
FDA / EMA
Not approved
No regulator has cleared SLU-PP-332 for any use, and no public clinical trial application exists for it.
WADA
Prohibited as a metabolic modulator
A February 2026 peer-reviewed doping-control study treats it as an exercise-mimetic substance under the hormone-and-metabolic-modulator class (S4), the same category covering other exercise mimetics.
Development stage
Preclinical only
The compound is still being optimised for oral dosing and wider toxicology, with no Phase I filing yet prepared.
Availability
Sold as a lab reagent only
Suppliers including Sigma-Aldrich, Selleck, Tocris and Cayman Chemical list it at ≥98% purity for laboratory research, not human use.
WADA's ban applies to competing athletes regardless of a compound's regulatory approval status elsewhere, and rules can change with each annual Prohibited List update — verify current sources before relying on this.
Section 09
Research Studies
- [1]Synthetic ERRα/β/γ Agonist Induces an ERRα-Dependent Acute Aerobic Exercise Response and Enhances Exercise CapacityBillon C, Sitaula S, Banerjee S, Welch R, Elgendy B, Hegazy L, et al. · ACS Chemical Biology · 2023
- [2]A Synthetic ERR Agonist Alleviates Metabolic SyndromeBillon C, Schoepke E, Avdagic A, Chatterjee A, Butler AA, Elgendy B, et al. · The Journal of Pharmacology and Experimental Therapeutics · 2024
- [3]Novel Pan-ERR Agonists Ameliorate Heart Failure Through Enhancing Cardiac Fatty Acid Metabolism and Mitochondrial FunctionXu W, Billon C, Li H, Wilderman A, Qi L, Graves A, et al. · Circulation · 2024
- [4]Estrogen-Related Receptor Agonism Reverses Mitochondrial Dysfunction and Inflammation in the Aging KidneyWang XX, Myakala K, Libby AE, Krawczyk E, Panov J, Jones BA, et al. · The American Journal of Pathology · 2023
- [5]Targeting ERRs to counteract age-related muscle atrophy associated with physical inactivity: a pilot studyBonanni R, Falvino A, Matticari A, Rinaldi AM, D'Arcangelo G, Cifelli P, et al. · Frontiers in Physiology · 2025
- [6]An orally active estrogen receptor-related receptor agonist, SLU-PP-915, enhances aerobic exercise capacityBillon C, Appourchaux K, Cote I, Burris TP. · The Journal of Pharmacology and Experimental Therapeutics · 2026
- [7]Chemical optimization of the exercise mimetic SLU-PP-332 enables insight into estrogen-related receptor signalingOkda HE, Zhao P, Hayes M, Duvall C, Quillin E, Fang H, et al. · International Journal of Biological Macromolecules · 2026
- [8]Transcriptional Control of Energy Homeostasis by the Estrogen-Related ReceptorsGiguere V. · Endocrine Reviews · 2008
- [9]Estrogen-Related Receptor α Directs Peroxisome Proliferator-Activated Receptor α Signaling in the Transcriptional Control of Energy Metabolism in Cardiac and Skeletal MuscleHuss JM, Torra IP, Staels B, Giguere V, Kelly DP. · Molecular and Cellular Biology · 2004
- [10]In Vitro Metabolism and Analytical Characterization of SLU-PP-332 and SLU-PP-915: Novel Pan-ERR Agonists With Doping PotentialMoller T, Krug O, Thevis M. · Rapid Communications in Mass Spectrometry · 2026
Section 10
Frequently Asked Questions
Only in mice. In obese mice dosed for 28 days it produced a 12% reduction in body weight and roughly tenfold less fat accumulation than untreated controls, and separately increased running endurance by about 70% and distance by about 45%. No human trial of any kind has been registered or published, so whether any of this applies to a person is unknown.
No — every measurement of this compound comes from mouse studies, and it has never been given to a person in any published or registered trial. It is not approved by any regulator anywhere and is sold only as a research chemical for laboratory use; WADA may in future classify it under its S4 metabolic-modulator category because of its exercise-mimetic effects, but that has not happened yet.
All safety data are short-term and rodent-only. The 28-day mouse study found only minor changes in cholesterol and liver enzymes and no major organ toxicity, but in genetically obese mice the treatment period had to be shortened to 12 days for unspecified tolerability problems. No study has examined long-term toxicity, carcinogenicity, teratogenicity or drug interactions in any species.
This has not been measured in any species. SLU-PP-332 is essentially insoluble in water, and the mouse studies dissolved it in DMSO for injection rather than dosing it orally. Oral tablets sold as a research chemical have no bioavailability data behind them in mice, let alone in people.
The only studied dose is 50 mg/kg injected into the abdomen of mice twice daily — scaled arithmetically, that would be several grams for an adult human, but that conversion has never been tested. Doses circulating for self-administration (25–100 mg oral, 250 µg–1.5 mg injected) are thousands of times lower per kilogram than the mouse dose and are not derived from any measurement in a person.
There is no established answer in humans. The mouse studies measured outcomes after 12 to 28 days of twice-daily dosing; no human pharmacokinetic or effect-timeline data exist for this compound at all.
No — it is a small synthetic molecule (molecular weight 290 Da) that activates estrogen-related receptors, not a chain of amino acids. It is often grouped with peptide exercise mimetics in vendor marketing, but chemically and pharmacologically it belongs to a different class of compound.