What it is
SLU-PP-332 is not a peptide. Peptides are chains of amino acids. This is a synthetic small molecule with a molecular weight of 290.32 g/mol and the chemical formula C18H14N2O2. It sits alongside peptides on this site because the same vendors sell it.
It was developed at Saint Louis University in the early 2000s. It switches on a set of cell sensors called estrogen related receptors (ERRs). Despite the name, these have nothing to do with oestrogen — they do not bind oestrogen and switching them on does not change your oestrogen levels. The name only reflects a similarity in how the receptor proteins look. There are three types: ERR alpha, ERR beta and ERR gamma. SLU-PP-332 activates all three, which is why it is called a panagonist, and it is strongest at ERR alpha.
This page covers injection. That matters here more than with most compounds, because SLU-PP-332 does not dissolve in water at all. It is insoluble in water, sparingly soluble in DMSO (58 mg/mL) and only slightly soluble in ethanol (2 mg/mL). DMSO stands for dimethyl sulfoxide, a solvent that dissolves things water cannot. Every published study used a DMSO-based vehicle, and the common research mix is 5% DMSO, 40% PEG 300, 5% Tween 80 and 50% sterile water. If the powder is mixed with bacteriostatic water alone it does not go into solution — what gets injected is water with particles floating in it.
SLU-PP-332 is not FDA approved and has never been tested in humans in any clinical trial. Everything known about it in a living body comes from mouse studies. A 2025 pilot study used it on human muscle cells in a dish, which is not the same as giving it to a person. It is a research chemical only. WADA bans it under the S0 category for unapproved substances and under the metabolic modulator and exercise mimetic categories, so a tested athlete will be flagged. A 2026 study by the UCLA Olympic Analytical Laboratory identified 22 distinct metabolites specifically for doping control.
SLU-PP-332 is a synthetic small molecule — molecular weight 290.32 g/mol, formula C18H14N2O2 — not a peptide. It was developed at Saint Louis University in the early 2000s and acts as a pan-agonist of the estrogen-related receptors ERRα, ERRβ and ERRγ, orphan nuclear receptors named for structural homology with the oestrogen receptors rather than any shared ligand. ERRs do not bind oestrogen and activation has no effect on oestrogen levels. Potency is highest at ERRα.
Physicochemistry dictates the route. The molecule is hydrophobic: insoluble in water, sparingly soluble in DMSO (58 mg/mL), slightly soluble in ethanol (2 mg/mL). Every published in vivo study used intraperitoneal injection in a DMSO-based vehicle, and the common research formulation is 5% DMSO, 40% PEG 300, 5% Tween 80 and 50% sterile water — DMSO as the solubilising solvent, PEG 300 to maintain solubility, Tween 80 as surfactant. Reconstitution in bacteriostatic water alone does not produce a solution; it produces a particulate suspension, which is the most likely explanation for inconsistent reports from users injecting a water-only mix.
Regulatory and analytical status: not FDA approved, never administered to humans in a clinical trial, research chemical only, and WADA prohibited under S0 (unapproved substances) as well as the metabolic modulator and exercise mimetic categories. Avliyakulov, Sobolevsky and Ahrens (2026), from the UCLA Olympic Analytical Laboratory, characterised 22 distinct in vitro metabolites for doping-control purposes. A 2025 pilot study (Bonanni, Falvino, Matticari, et al.) applied the compound to primary human muscle cells in vitro; there is no human in vivo evidence of any kind.
How it works
Your cells make energy mainly in the mitochondria, the small power plants inside each cell. They turn nutrients from food into ATP, the energy currency the body runs on. More mitochondria, working better, means more energy available for endurance, fat burning, recovery and overall metabolic rate.
ERR alpha is sometimes called the master regulator of energy metabolism. It controls the genes for building new mitochondria (mitochondrial biogenesis), for burning fat as fuel (fatty acid oxidation), and for how efficiently cells produce energy through the electron transport chain. Exercise — especially endurance exercise — raises ERR alpha activity naturally, and that is part of how muscle adapts to training.
SLU-PP-332 switches on ERR alpha without the exercise. Researchers confirmed this by repeating their exercise experiment in mice bred without the ERR alpha gene: the effects disappeared completely, which showed the benefit came from ERR alpha and not something else.
What it does not do matters just as much. Exercise triggers hundreds of pathways — AMPK, mTOR, BDNF, IGF-1, myokines, signals to bone density and immune function, and more. SLU-PP-332 hits one. It copies one piece of a much bigger system and cannot replace training.
On timing: in mice given 30 mg/kg by injection, levels measured 0.2 micromolar in blood and 0.6 micromolar in muscle six hours after the injection. The estimated time for half the drug to clear the blood in rodents is roughly 8 to 10 hours, although no formal study has established that number. It does not cross into the brain well.
Mechanism is transcriptional. ERRα is a master regulator of oxidative metabolism, driving gene programmes for mitochondrial biogenesis, fatty-acid oxidation and electron transport chain efficiency. Endurance exercise raises ERRα activity as part of normal skeletal muscle adaptation; SLU-PP-332 engages the same receptor pharmacologically, which is the basis of the exercise-mimetic framing.
Target dependence is established rather than assumed. In the original exercise capacity work (Billon, Sitaula, Banerjee, et al., 2023), muscle-specific ERRα knockout mice showed no improvement, confirming the phenotype is ERRα-dependent and not off-target. In the heart failure model (Xu, Billon, Li, et al., 2024), ERRγ rather than ERRα was the principal mediator of cardioprotection, so the relevant isoform is tissue-dependent.
The ceiling on the concept is pathway breadth. Exercise recruits AMPK, mTOR, BDNF, IGF-1, myokine signalling, bone and immune adaptations and much else; ERR agonism reproduces one arm of that network.
Pharmacokinetics are thin. At 30 mg/kg intraperitoneally in mice, plasma exposure was 0.2 micromolar and muscle exposure 0.6 micromolar at 6 hours post-injection. Estimated plasma elimination half-life in rodents is approximately 8 to 10 hours, with no formal pharmacokinetic study published to establish it. Blood-brain barrier penetration is poor.
What it does
In mice, the effects are real and measurable. Treated mice ran 70% longer and 45% further than untreated ones, and had more of the oxidative type IIa muscle fibres and more mitochondrial DNA — meaning the muscle itself changed, not just performance on the day. Grip strength rose after 6 and 13 days of dosing.
In obese mice on a high fat diet, 28 days of treatment produced about 12% body weight loss. Glucose tolerance improved and fatty liver was reduced. Food intake did not change and activity level did not change — the mice were not eating less or moving more. Their metabolism was simply running hotter.
Older mice given eight weeks of treatment showed reversal of age-related kidney decline, including protein in the urine, loss of filtering cells and mitochondrial dysfunction. In mice with heart failure, treatment improved pumping function, reduced scarring and increased survival.
On human tissue, a 2025 pilot study treated muscle cells taken from inactive elderly women in a dish. The compound reduced oxidative stress, raised protective factors including SIRT1 and PGC-1 alpha, helped cells survive, pushed cells to fuse into mature fibres, and lowered ageing markers. Cells in a dish behave differently from cells in a person, so this is encouraging rather than proof.
There is no human data on what it does inside a living body. None.
All efficacy data is preclinical. In C57BL/6J mice, 50 mg/kg twice daily intraperitoneally for 7 to 15 days produced a 70% increase in run time and 45% increase in distance, with a shift towards type IIa oxidative fibres, higher mitochondrial DNA content, and increased grip strength after 6 and 13 days (Billon, Sitaula, Banerjee, et al., 2023).
In diet-induced obese mice, 50 mg/kg twice daily for 28 days produced approximately 12% body weight loss with minimal fat mass gain relative to controls, increased energy expenditure and fatty-acid oxidation, improved insulin sensitivity, and reduced hepatic steatosis, with no change in food intake or activity. Plasma total cholesterol, HDL cholesterol and triglycerides all fell; LDL was unchanged (Billon, Schoepke, Avdagic, et al., 2024).
In 21-month-old mice, 25 mg/kg daily for 8 weeks reversed age-related albuminuria, podocyte loss and mitochondrial dysfunction, and reduced profibrotic markers (TGF-beta, PAI-1, Col IV), macrophage markers and tubular injury markers; the investigators described the effect as essentially mimicking caloric restriction (Wang, Myakala, Libby, et al., 2023). In pressure-overload heart failure, 25 mg/kg twice daily improved ejection fraction, reduced fibrosis and increased survival, with ERRγ identified as the primary mediator (Xu, Billon, Li, et al., 2024).
In vitro on human myogenic cells from inactive elderly women, treatment reduced oxidative stress, enhanced SIRT1 and PGC-1α, promoted survival and myotube fusion, and decreased senescence markers (Bonanni, Falvino, Matticari, et al., 2025). Longest in vivo exposure in any species is 8 weeks. There is no in vivo human pharmacodynamic data.
Benefits
Evidence grades: what the labels mean
- Human trials Supported by randomised or placebo-controlled human trials.
- Limited human data Some human evidence, such as pilot studies, case reports or observational data, but no controlled trials.
- Animal or lab only Shown in animal or cell studies only; not yet tested in people.
- Anecdotal No published studies; based on user reports or theory.
Each grade reflects the strongest published support for that specific claim, not for the compound as a whole.
- Endurance: mice treated by injection ran 70% longer and 45% further than untreated controls, with more oxidative type IIa muscle fibres and higher mitochondrial DNA content.Animal or lab only
- Strength: grip strength increased after 6 and 13 days of dosing in mice.Animal or lab only
- Fat loss: obese mice on a high fat diet lost about 12% of body weight over 28 days, with almost no fat mass gain, improved glucose tolerance and reduced fatty liver — and no change in how much they ate or moved.Animal or lab only
- Kidney: eight weeks of treatment in 21-month-old mice reversed age-related kidney decline, including protein in the urine, loss of filtering cells, mitochondrial dysfunction and inflammatory signals.Animal or lab only
- Heart: in mice with heart failure, treatment improved pumping function, reduced scarring and increased survival.Animal or lab only
- Human cells in a dish: a 2025 pilot study on muscle cells from inactive elderly women showed less oxidative stress, more SIRT1 and PGC-1 alpha, better cell survival, more fusion into mature fibres and fewer ageing markers.Animal or lab only
- Every one of these results is from mice or from cells in a dish. No human efficacy data exists, and using this compound is not recommended.Animal or lab only
- Exercise capacity: +70% run time, +45% distance at 50 mg/kg twice daily IP, with type IIa fibre shift and increased mitochondrial DNA; abolished in muscle-specific ERRα knockouts (Billon, Sitaula, Banerjee, et al., 2023).Animal or lab only
- Body composition and metabolic syndrome: ~12% body weight loss over 28 days at 50 mg/kg twice daily IP, increased energy expenditure and fatty-acid oxidation, improved insulin sensitivity, reduced hepatic steatosis, unchanged food intake and activity (Billon, Schoepke, Avdagic, et al., 2024).Animal or lab only
- Lipids in the same model: total cholesterol, HDL and triglycerides decreased; LDL unchanged. The HDL fall is a liability rather than a benefit.Animal or lab only
- Renal ageing: 25 mg/kg daily for 8 weeks in 21-month-old mice reversed albuminuria, podocyte loss and mitochondrial dysfunction, and lowered profibrotic, macrophage and tubular injury markers; human kidney tissue showed the same age-related ERR pathway decline, suggesting mechanistic conservation (Wang, Myakala, Libby, et al., 2023).Animal or lab only
- Cardiac: improved ejection fraction, reduced fibrosis and increased survival in pressure-overload heart failure at 25 mg/kg twice daily, mediated primarily by ERRγ, via cardiac fatty-acid metabolism and mitochondrial function (Xu, Billon, Li, et al., 2024).Animal or lab only
- Human myotubes in vitro: reduced oxidative stress, enhanced SIRT1 and PGC-1α, improved survival and fusion, reduced senescence markers (Bonanni, Falvino, Matticari, et al., 2025).Animal or lab only
- Evidence ceiling: no in vivo human data, longest exposure 8 weeks in any species, and use is explicitly not recommended.Animal or lab only
What to expect
There is no human clinical data, so there is no honest timeline. Nobody can say when effects appear, what they would be, or how long they last. What follows comes from external forums and is anecdotal, which does not carry the weight of published research.
Reports are extremely mixed, and that inconsistency is the most important thing to understand. Some users report more energy, better cardio endurance, a higher heart rate and feeling more out of breath during training in a way that suggests the metabolism is working harder, better focus in the gym, better recovery, and gradual fat loss over 4 to 8 weeks. One user reported losing 11 pounds over 4 weeks while looking leaner and more vascular, while combining SLU-PP-332 with other compounds.
Many users report feeling absolutely nothing. Some ramped from 250 mcg up to 1500 mcg per day without noticing any change. Others took it for over a month at 1000 mcg daily with no measurable results. Some took 8 capsules at once and felt nothing.
The pattern is not random. Positive reports cluster among people who take it with fats, use the sublingual route, or use higher doses. Negative reports come overwhelmingly from standard oral capsules. People injecting a bacteriostatic-water-only mix also report inconsistency, because the compound never actually dissolved. Expect unpredictability as the default outcome.
No human in vivo timeline exists. All experiential data is anecdotal, aggregated from external platforms including Reddit, AnabolicMinds, Canadian Brawn Forums and Eroids.
Positive reports describe elevated training heart rate, improved cardio endurance, a subjective sense of higher metabolic demand during exercise, better training focus, and gradual fat loss over 4 to 8 weeks when combined with training and diet; one report describes 11 pounds lost over 4 weeks alongside other compounds. Some users state the sublingual route is more consistent than swallowed capsules.
Null reports are at least as common. Dose ramps from 250 mcg to 1500 mcg daily with no perceived effect, over a month at 1000 mcg daily with no measurable change, and single large capsule loads with no response are all documented anecdotally.
The variance is explicable rather than mysterious. Responders skew towards co-administration with fat, sublingual delivery or higher doses; non-responders skew towards plain oral capsules. Injectors using bacteriostatic water alone also report inconsistency, which is expected given the compound never enters solution in an aqueous vehicle. Treat unpredictable exposure as the baseline expectation for any route outside the published DMSO/PEG 300/Tween 80 formulation.
Reconstitution and dosing
This section is for educational context only and does not recommend using SLU-PP-332. No human dosing protocol has been established by any clinical trial.
What the mouse studies used. Every published study gave the compound by intraperitoneal injection in a DMSO-based vehicle, at 25 to 50 mg/kg daily. The exercise study used 50 mg/kg twice daily for 7 to 15 days. The fat loss study used 50 mg/kg twice daily for 28 days. The kidney study used 25 mg/kg daily for 8 weeks. The heart failure study used 25 mg/kg twice daily, duration not specified.
Scaling to a person. Converting the mouse doses by standard allometric scaling (dividing by 12.3) gives roughly 140 mg/day for a 154 lb adult from the 25 mg/kg dose, and roughly 560 mg/day from the 50 mg/kg twice daily dose. These are estimates using standard FDA conversion guidelines and they assume 100% absorption from intraperitoneal injection. What is actually sold contains anywhere from 100 mcg to a few milligrams per capsule — a tiny fraction of what worked in mice.
The vehicle is the whole problem. SLU-PP-332 does not dissolve in water. Bacteriostatic water alone does not work: the powder does not go into solution and you end up injecting water with particles in it. Every published study used DMSO to dissolve the compound, PEG 300 to keep it in solution, and Tween 80 as a surfactant. A common research formulation is 5% DMSO, 40% PEG 300, 5% Tween 80 and 50% sterile water. If it is going to be injected, that is the formulation that matches the research.
The protocol carried on this site. The 10 mg vial is mixed with 2 mL (200 units) of bacteriostatic water plus 0.5 mL (50 units) of DMSO, for 2.5 mL in the vial. "Units" means the marks on an insulin syringe: 100 units is 1 mL. With 10 mg in 2.5 mL, each millilitre holds 4 mg, so 1.25 mg is about 31 units and 2.5 mg is about 62.5 units. Weeks 1 to 4 use 1.25 mg daily and weeks 5 to 8 use 2.5 mg daily, once a day on 5 to 7 days per week, morning to early afternoon, no fasting needed, under the skin. Cycle length is 8 to 16 weeks with 4 to 8 weeks off. Note two gaps: the schedule stops at week 8 with no guidance for weeks 9 to 16, and this mix is bacteriostatic water plus DMSO rather than the full DMSO/PEG 300/Tween 80 research vehicle, so how much actually stays in solution is uncertain.
This section is educational only and does not recommend use; no human dosing protocol has been established by any clinical trial.
Published in vivo dosing. All studies used intraperitoneal injection in a DMSO-based vehicle at 25 to 50 mg/kg daily: exercise 50 mg/kg twice daily for 7 to 15 days; fat loss 50 mg/kg twice daily for 28 days; kidney 25 mg/kg daily for 8 weeks; heart failure 25 mg/kg twice daily, duration unspecified.
Allometric conversion. Dividing by 12.3 gives approximately 140 mg/day for a 154 lb adult from 25 mg/kg, and approximately 560 mg/day from 50 mg/kg twice daily. These are estimates under standard FDA conversion guidelines and assume 100% bioavailability from the intraperitoneal route. Oral bioavailability is unknown and likely far lower; claims of 40 to 50% oral bioavailability circulating online are unsupported by any study. Commercial products contain 100 mcg to a few milligrams per capsule, orders of magnitude below the scaled preclinical exposure.
Vehicle specification. The molecule is hydrophobic — insoluble in water, sparingly soluble in DMSO (58 mg/mL), slightly soluble in ethanol (2 mg/mL). Bacteriostatic water alone yields a suspension, not a solution. The research vehicle is DMSO as solvent, PEG 300 to maintain solubility and Tween 80 as surfactant, commonly 5% DMSO / 40% PEG 300 / 5% Tween 80 / 50% sterile water. Any injectable use that does not reproduce a co-solvent system delivers an unknown fraction of the labelled dose.
Protocol retained on this page. 10 mg vial reconstituted with 2 mL bacteriostatic water plus 0.5 mL DMSO, 2.5 mL final volume, 4 mg/mL, 40 mcg per insulin unit. Recomputed draws: 1.25 mg = 31.25 units (drawn as 31 units); 2.5 mg = 62.5 units (drawn as 62 units) — both within rounding. Weeks 1 to 4 at 1.25 mg daily, weeks 5 to 8 at 2.5 mg daily, once daily on 5 to 7 days per week, morning to early afternoon, fasting not required, subcutaneous. Cycle 8 to 16 weeks with a 4 to 8 week washout.
Two unresolved gaps. The stated cycle runs to 16 weeks while the schedule terminates at week 8, with no guidance for weeks 9 to 16; holding the week 5 to 8 dose is the conservative reading but has not been established. And this two-component vehicle is not the published DMSO/PEG 300/Tween 80 formulation, so solubility over the life of the vial is not assured. Where DMSO is used, the specification is pharma-grade, non-diluted.
Standard, 10 mg vial
Mix with 2.5 mL (250 units) of bacteriostatic water.
4 mg/mL · 40 mcg per unit
Cycle: 8–16 week cycle followed by a 4–8 week washout · Frequency: Once per day, 5–7 days per week; morning to early afternoon; fasting not required; subcutaneous. Reconstitution is 2 mL (200 units) bacteriostatic water plus 0.5 mL (50 units) pharma-grade DMSO; the published research vehicle is DMSO, PEG 300 and Tween 80.
| When | Dose | Draw | How often |
|---|---|---|---|
| Weeks 1–4 | 1.25 mg (≈31 units) | 31.25 units | 1×/day, 5–7 days per week |
| Weeks 5–8 | 2.5 mg (≈62 units) | 62.5 units | 1×/day, 5–7 days per week |
Alternative protocols
Alternative protocols reflect older community practice and are kept for reference.
Alternative, 10 mg vial
Mix with 2 mL (200 units) of bacteriostatic water AND 0.5 mL (50 units) of DMSO — 2.5 mL total in the vial. The DMSO is a required co-solvent, not an optional addition; use pharma-grade, non-diluted DMSO.
4 mg/mL · 40 mcg per unit
Cycle: 8–16 week cycle followed by a 4–8 week washout · Frequency: Once per day, 5–7 days per week; morning to early afternoon; fasting not required; subcutaneous
| When | Dose | Draw | How often |
|---|---|---|---|
| Weeks 1–4 (1.25 mg) | 1.25 mg | 31.25 units | 1×/day, 5–7 days per week |
| Weeks 5–8 (2.5 mg) | 2.5 mg | 62.5 units | 1×/day, 5–7 days per week |
10 mg in 2.5 mL is 4 mg/mL, or 40 mcg per unit. Draw 31.25 units (0.313 mL) for 1250 mcg.
Who should avoid it
- Anyone with active cancer or a tumour of any type should not use this. Anyone with a past cancer diagnosis should also avoid it. The reason is that the receptor this compound switches on, ERR alpha, is one that several cancers appear to use to grow.
- Anyone who has reacted badly to SLU-PP-332 or to anything in the mix should not use it.
- Tested athletes in any sport should not touch it. It is banned by WADA under the S0 category for unapproved substances and as a metabolic modulator and exercise mimetic. A 2026 laboratory study mapped 22 of its breakdown products specifically so that drug testers can find it.
- Extreme caution in pregnancy and breastfeeding — there is no safety data of any kind.
- Extreme caution with blood sugar problems or any medication that lowers blood sugar, because low blood sugar has been reported by users.
- Extreme caution if cholesterol is a concern: HDL, the so-called good cholesterol, went down in the mouse fat-loss study.
- Extreme caution with heart conditions, since the compound has effects on the heart, and with liver problems, because nobody knows how humans break it down.
- Earlier guidance for this compound listed no contraindications at all. That is missing documentation, not a clean safety record.
- It is not approved by the FDA, has never been tested in a human trial, and is classified as a research chemical only. Talk to a doctor before starting anything, and go through your full medication list with them.
- Absolute exclusions: active malignancy or tumours of any type, and any history of malignancy. ERR alpha is exploited by multiple tumour types — it is critical to the growth of oestrogen-receptor-negative breast cancer (Stein et al., 2008), promotes cancer stem cell characteristics (Muduli et al., 2023), induces VEGF expression (Stein et al., 2009), and drives proliferation, migration and invasion in A549 lung cancer cells via epithelial-to-mesenchymal transition (Huang et al., 2014). Chronic agonism of that receptor is an unquantified risk.
- Known hypersensitivity to SLU-PP-332 or any vehicle component.
- Tested athletes in any sport: WADA-prohibited under S0 (unapproved substances) and under the metabolic modulator and exercise mimetic categories. Avliyakulov, Sobolevsky and Ahrens (2026) characterised 22 in vitro metabolites via human liver microsomes expressly for doping control.
- Extreme caution: pregnancy and lactation (no safety data in any species), metabolic disorders or conditions affecting glycaemic control, concomitant glucose-lowering agents, dyslipidaemia or cholesterol concerns (HDL fell in the metabolic syndrome study), cardiovascular disease (the compound has direct cardiac effects), and hepatic impairment (human metabolic pathway unknown).
- The vehicle itself is a consideration on this route. The published studies use a compounded formulation — DMSO, PEG 300, Tween 80 and sterile water — and handling those materials safely and sterilely is beyond most non-laboratory settings.
- Regulatory position: not FDA approved, never administered to a human in a clinical trial, research chemical only, not legal for sale as a drug, food or dietary supplement. The earlier reconstitution-and-dosing material circulating for this compound carried no contraindication list; treat that as absent documentation.
Side effects
- In the mouse fat-loss study, HDL cholesterol went down. Total cholesterol and triglycerides also went down, and LDL did not change. The HDL drop matters because HDL is thought to protect the heart.
- No other adverse effects were reported in the published mouse studies. But the longest study ran only 8 weeks, and none of them were built to catch slow problems such as cancer.
- The cancer question is the big unknown. No study has shown that SLU-PP-332 causes cancer. The worry is that ERR alpha, the receptor it switches on, is one that cancer cells appear to rely on. Blocking that receptor slows tumour growth in several cancer types. Switching it on for months or years has never been studied. That is an unknown risk, not a proven harm.
- Users on forums report low blood sugar at higher doses, disturbed sleep, mild stomach discomfort, and tiredness. These reports are sparse and unverified. Low blood sugar is plausible because the compound raises metabolic rate and fat burning, so it is more of a concern for anyone fasting, eating too little, or taking other things that lower blood sugar.
- No long-term safety data exists in any species — no multi-month and no multi-year data.
- On the injection route specifically: injecting under the skin can cause redness, swelling or itching at the site with any compound, and the solvents needed to dissolve this one add their own local irritation risk. This is not something the published studies address in humans.
- Observed in mice: HDL cholesterol decreased in the metabolic syndrome study (Billon et al., 2024), alongside decreases in total cholesterol and triglycerides; LDL was unchanged. The HDL reduction is the notable signal given its cardioprotective association.
- No other adverse effects were reported in the published mouse work. The longest exposure in any study was 8 weeks (kidney study), and none were powered or designed to detect long-latency toxicity.
- Oncological risk remains unresolved rather than excluded. ERR alpha dependence has been documented across tumour types, and pharmacological inhibition with the inverse agonist XCT-790 slows tumour growth in multiple models. Chronic pan-ERR agonism in a host with occult neoplasia, or over years in healthy tissue, has never been examined with this compound. The distinction between "causes cancer" and "long-term safety unknown" should be held precisely.
- User-reported, sparse and unverified: hypoglycaemia at higher doses, sleep disturbance, mild gastrointestinal discomfort, fatigue. Hypoglycaemia is mechanistically plausible given increased metabolic rate and fatty-acid oxidation, particularly during fasting, energy restriction, or co-administration of glucose-lowering agents.
- Route-specific: subcutaneous or intraperitoneal delivery requires a mixed-solvent vehicle, and local tolerance of DMSO, PEG 300 and Tween 80 is an additional consideration no human data addresses. Injection-site reactions are plausible on any parenteral route.
- Unknown long-term effects generally: no multi-month or multi-year safety dataset exists in any species, and the interaction between chronic ERR activation and cancer risk has never been tested directly with SLU-PP-332.
What the evidence shows
There are no human trials. Not one. Five published studies have looked at SLU-PP-332 directly, plus one doping-analysis study, and every study of whether it works was done in mice or on human cells in a dish.
In the 2023 exercise study, mice given 50 mg/kg twice daily by injection for 7 to 15 days ran 70% longer and 45% further than untreated mice. When the same experiment was repeated in mice bred without the ERR alpha gene, the effect vanished, which showed the benefit really did come from that receptor. Published by Billon, Sitaula, Banerjee, et al. in ACS Chemical Biology, 2023.
In the 2024 fat-loss study, obese mice on a high-fat diet given 50 mg/kg twice daily for 28 days lost about 12% of their body weight. They did not eat less or move more. Glucose tolerance improved and fatty liver was reduced. Published by Billon, Schoepke, Avdagic, et al. in Journal of Pharmacology and Experimental Therapeutics, 2024.
In a 2023 kidney study, 21-month-old mice given 25 mg/kg daily for 8 weeks showed reversal of age-related kidney decline. In a 2024 heart study, mice with heart failure given 25 mg/kg twice daily had better pumping function, less scarring, and better survival. A 2025 pilot study treated human muscle cells in a dish and saw less oxidative stress and better cell survival — encouraging, but cells in a dish are not a person.
Two things matter most. Every single mouse study used injection into the abdominal cavity with a DMSO-based vehicle; no study has ever tested swallowing it. And the longest treatment in any study was 8 weeks, so there is no long-term safety data in any species.
Five published studies examine SLU-PP-332 directly, plus one doping-control analysis. All efficacy work is murine in vivo or human in vitro; no human clinical trial exists at any phase.
Exercise capacity (2023): male C57BL/6J mice, 50 mg/kg twice daily intraperitoneally for 7 to 15 days, ran 70% longer and 45% further than controls, with increased type IIa oxidative fibres and higher mitochondrial DNA content, plus grip strength gains at 6 and 13 days. Muscle-specific ERR alpha knockouts showed no improvement, confirming mechanism; 25 mg/kg for 15 days was also tested in the knockout model. Billon, Sitaula, Banerjee, et al., ACS Chemical Biology, 2023.
Metabolic syndrome (2024): diet-induced obese mice, 50 mg/kg twice daily for 28 days, lost approximately 12% of body weight with minimal fat mass accrual, increased energy expenditure and fatty-acid oxidation, improved insulin sensitivity, and no change in food intake or activity. Plasma total cholesterol, HDL and triglycerides all fell; LDL unchanged. Billon, Schoepke, Avdagic, et al., JPET, 2024.
Renal ageing (2023): 21-month-old mice, 25 mg/kg daily intraperitoneally for 8 weeks, with reversal of albuminuria, podocyte loss and mitochondrial dysfunction, and reductions in TGF-beta, PAI-1, Col IV, macrophage and tubular injury markers. Human kidney tissue showed parallel age-related ERR pathway decline. Wang, Myakala, Libby, et al., American Journal of Pathology, 2023.
Heart failure (2024): pressure-overload model, 25 mg/kg twice daily, improved ejection fraction, reduced fibrosis and increased survival, with ERR gamma rather than ERR alpha identified as the principal mediator of cardioprotection. Xu, Billon, Li, et al., Circulation, 2024.
Muscle atrophy pilot (2025): muscle from 20 women undergoing hip replacement, split active (n=10) and inactive (n=10); myocytes from the inactive group treated in vitro showed reduced oxidative stress, enhanced SIRT1 and PGC-1 alpha, improved survival and myotube fusion, and decreased senescence markers. Bonanni, Falvino, Matticari, et al., Frontiers in Physiology, 2025.
Doping detection (2026): UCLA Olympic Analytical Laboratory identified 22 distinct metabolites using human liver microsomes. Avliyakulov, Sobolevsky and Ahrens, Drug Testing and Analysis, 2026.
Pharmacokinetics are thin: at 30 mg/kg intraperitoneally in mice, plasma exposure was 0.2 micromolar and muscle exposure 0.6 micromolar at 6 hours. Rodent plasma elimination half-life is estimated at approximately 8 to 10 hours, with no formal pharmacokinetic study establishing it. Blood-brain barrier penetration is poor.
Bottom line: preclinical signal is consistent across muscle, adipose, kidney and heart, every study used intraperitoneal dosing in a DMSO-based vehicle, no study has tested oral administration, no in vivo human data exists, and the longest exposure in any species was 8 weeks.
User reports
From public forums
Reports gathered from outside platforms including Reddit, AnabolicMinds, Canadian Brawn Forums and Eroids are extremely mixed, and that inconsistency is the single most important thing to understand. None of this is published research.
On the positive side, some users report higher heart rate during workouts, better cardio endurance, feeling more out of breath during exercise in a way that suggests the body is working harder, better focus in training, better recovery, and gradual fat loss over 4 to 8 weeks when training and diet are in place. One user reported losing 11 pounds over 4 weeks and looking leaner and more vascular while combining SLU-PP-332 with other compounds.
On the negative side, many users report feeling nothing at all. Some ramped from 250 mcg up to 1500 mcg a day without any change. Others took 8 capsules at once and felt nothing. One user took 1000 mcg daily for over a month with no measurable result.
There is a pattern. The positive reports tend to come from people taking it with fats, using it under the tongue, or using higher doses. The negative reports come overwhelmingly from people swallowing standard capsules. People injecting it after mixing with bacteriostatic water also report inconsistent results, because the powder does not actually dissolve in water — the syringe holds water with particles floating in it. The mixed reviews are most likely an absorption problem rather than a mystery about whether the compound works.
The questions asked most often are how to reconstitute it, whether to swallow it or inject it, what dose to use, whether it stacks with retatrutide or other compounds, and whether it causes cancer. Published research answers none of them.
Anecdotal reports aggregated from external platforms (Reddit, AnabolicMinds, Canadian Brawn Forums, Eroids) are bimodal and carry no weight comparable to published work.
Positive reports: elevated exercise heart rate, improved cardio endurance, subjectively greater ventilatory demand consistent with raised metabolic rate, improved training focus, better recovery, and gradual fat loss over 4 to 8 weeks. One user reported an 11 lb loss over 4 weeks with improved leanness and vascularity while stacking with other compounds. Some describe sublingual administration as more consistent than swallowed capsules.
Null reports: many users report no discernible effect at any dose, including ramps from 250 mcg to 1500 mcg daily, single administrations of 8 capsules, and over a month at 1000 mcg daily.
The distribution is not random. Positive responders cluster among those co-administering fats, using sublingual delivery, or dosing higher; null responders cluster among standard oral capsule users. Parenteral users who reconstitute in bacteriostatic water alone also report inconsistency, which is expected — the compound is insoluble in water and does not enter solution, so the syringe contains a suspension of undissolved particulate rather than a solution. The variance maps onto delivery and dissolution, not onto whether ERR agonism does anything.
Recurring unanswered questions concern reconstitution vehicle, oral versus injected route, dose selection, combination with retatrutide and other metabolic agents, and carcinogenic risk. None has a published answer.
User reports are individual experiences submitted by site visitors. They are not medical advice, are not verified for accuracy, and do not reflect Amino Reference's views. Read the evidence section above and talk to a clinician. Full disclaimer.
Stacking
The same compound in capsule form, and the route with the biggest problem. SLU-PP-332 does not dissolve in water, so how much gets absorbed from a dry powder capsule is unpredictable. Read that page before switching routes, and do not run both at once.
Same molecule, oral route. Hydrophobic and water-insoluble, so intestinal absorption across the roughly 100 micrometre aqueous boundary layer is erratic and dependent on bile secretion, meal fat content and individual gut variation. No formal oral bioavailability study has been published, and claims of 40 to 50% oral bioavailability are unsupported. Route alternative, not an addition.
A completely different mechanism, and one of the most frequently asked-about combinations. In theory SLU-PP-332 raises how much energy the body burns while a GLP-1 type drug reduces appetite and improves blood sugar control. Whether putting them together adds anything is unknown, and no published study has tested the pair.
Non-overlapping mechanisms with no known interaction. ERR-driven increases in energy expenditure and fatty-acid oxidation versus incretin-mediated appetite suppression and glycaemic improvement. Theoretically additive, entirely unstudied in combination. Note the compounded hypoglycaemia consideration, since both limbs can lower blood glucose.
Another GLP-1 type option with a different mechanism. No known interaction, but no study has looked at the combination either. Watch blood sugar, since both can push it down.
Same rationale as the retatrutide pairing: incretin agonism for appetite and glycaemic control alongside ERR-mediated energy expenditure. No published combination data supports or warns against it; additive hypoglycaemic potential is the main practical caution.
A third GLP-1 type option. Different mechanism, no known interaction, and no published data on running it with SLU-PP-332.
Dual incretin agonism paired with pan-ERR agonism. Mechanistically distinct, theoretically complementary for body composition, and never formally studied together.
Both aim at the energy factories inside cells, but by different routes. MOTS-c works through a sensor called AMPK; SLU-PP-332 works through the ERR receptors. In theory they complement each other, though the pair has never been studied. MOTS-c is also one of the better-understood alternatives if the goal is mitochondrial support rather than this specific compound.
Both converge on mitochondrial function through separate upstream nodes: AMPK activation for MOTS-c, ERR agonism for SLU-PP-332. Theoretically complementary, never studied in combination. MOTS-c is also a substitution candidate, carrying a better-characterised mechanism and actual safety data.
SS-31 helps stabilise the inner membrane of the mitochondria; SLU-PP-332 switches on the genes that build new ones. That sounds complementary, but the pair has never been tested together. SS-31 is also a reasonable alternative on its own for mitochondrial goals.
Cardiolipin-targeted inner-membrane stabilisation alongside transcriptional mitochondrial biogenesis. Theoretically complementary, no combination data. Also a substitution candidate for mitochondrial support with a better-defined safety profile.
Another option aimed at cellular energy through a pathway that is better understood, with real safety data behind it. Often used as a substitute for SLU-PP-332 rather than an addition to it.
Substrate-level support for NAD-dependent signalling, including sirtuin activity, versus direct nuclear receptor agonism. Frequently positioned as a replacement for SLU-PP-332 in metabolic and mitochondrial protocols on the grounds of better-characterised pharmacology. Berberine and niacin are sometimes added for additional metabolic support.
A different route to the same general goals — fat oxidation and metabolic improvement — through a pathway that is better understood. Usually considered instead of SLU-PP-332, not alongside it.
NNMT inhibition raising intracellular NAD availability, as an alternative approach to fat oxidation and metabolic improvement with a clearer mechanism than pan-ERR agonism. Positioned as a substitution rather than a co-administration.
Common questions
Is SLU-PP-332 a peptide?
No. It is a manufactured small molecule with a molecular weight of 290.32 g/mol and the formula C18H14N2O2. Peptides are chains of amino acids; this has a completely different structure. It gets grouped with peptides because the same vendors sell it and the same circles discuss it.
No. It is a synthetic small molecule, 290.32 g/mol, C18H14N2O2, developed at Saint Louis University in the early 2000s. It is a pan-agonist of the oestrogen-related receptors ERR alpha, beta and gamma, most potent at ERR alpha. Its classification alongside peptides is a retail artefact, not a chemical one.
Does SLU-PP-332 affect oestrogen levels?
No. Despite the name "oestrogen-related receptors", these receptors have nothing to do with oestrogen. They do not bind oestrogen, and switching them on has no effect on oestrogen levels. The name comes only from the fact that the receptor proteins look structurally similar.
No. ERRs are orphan nuclear receptors named for structural homology to the oestrogen receptors. They do not bind oestradiol and agonism produces no change in circulating oestrogen. The naming has caused persistent confusion but carries no endocrine implication here.
Can it be reconstituted with bacteriostatic water?
No. SLU-PP-332 is insoluble in water and will not go into solution. What ends up in the syringe is water with particles floating in it, which is why people who mix it this way report inconsistent results. The research vehicle uses DMSO, PEG 300 and Tween 80.
No. The compound is hydrophobic: insoluble in water, sparingly soluble in DMSO (58 mg/mL), slightly soluble in ethanol (2 mg/mL). Bacteriostatic water yields a particulate suspension, not a solution, with the dose-delivery inconsistency that implies. Every published study used a DMSO-based vehicle; a common research formulation is 5% DMSO, 40% PEG 300, 5% Tween 80 and 50% sterile water, with DMSO as the actual solubilising agent, PEG 300 maintaining solubility and Tween 80 acting as surfactant.
What is the right dose?
Nobody knows. No human dose-finding study has ever been done. The mouse studies used doses that convert to roughly 140 to 560 mg per day for a 154 lb adult, while products on the market contain anywhere from 100 mcg to a few milligrams per capsule — a tiny fraction of that. Even with the right number on paper, the absorption problem remains.
Undetermined. No human dose-finding study exists. Published murine dosing ranged from 25 to 50 mg/kg daily by intraperitoneal injection. Standard allometric scaling (dividing by 12.3, per FDA conversion guidance) gives approximately 140 mg/day for a 154 lb adult from the 25 mg/kg regimen and approximately 560 mg/day from 50 mg/kg twice daily. Those estimates assume 100% bioavailability from intraperitoneal administration. Commercial products supply 100 mcg to a few milligrams per capsule, orders of magnitude below the research exposure.
Does oral SLU-PP-332 work?
The evidence is mixed at best. The compound does not dissolve in water, so how much gets absorbed from the gut is unpredictable and depends on bile, food and individual differences. No formal oral absorption study has been published. Claims of 40 to 50% oral bioavailability circulating online are made up — no study supports them. The researchers who developed it still inject it in every study and have written that the structure needs improving for oral delivery.
Unresolved and probably poor. The intestinal aqueous boundary layer is roughly 100 micrometres thick; a water-insoluble dry powder must dissolve and cross it, making absorption contingent on bile secretion, prandial fat, and inter-individual gut variation. No oral bioavailability study has been published, and the 40 to 50% figures circulating online have no supporting data. Co-administration with fats plausibly helps solubilise a lipophilic compound but is not demonstrated bioavailability. The developers continue to use parenteral dosing in every published study and have stated the need for structural optimisation for oral delivery.
Does SLU-PP-332 cause cancer?
No study has shown that it does. The concern is different: ERR alpha, the receptor it switches on, appears to be one that cancer cells use to grow. Blocking ERR alpha slows tumour growth in breast cancer, lung cancer and other types. Switching it on continuously has never been studied over the long term. Anyone with a history of cancer should avoid it. For healthy people the long-term risk is genuinely unknown, because no long-term study has been done.
No carcinogenicity has been demonstrated. The concern is mechanistic: ERR alpha dependence is documented across tumour types, ERR alpha knockdown roughly doubled tumour growth latency in xenograft models of oestrogen-receptor-negative breast cancer, and inhibition with the inverse agonist XCT-790 slows tumour growth in multiple models. Chronic agonism of a receptor that malignant cells exploit is an unquantified risk, particularly with occult early-stage disease. All published murine studies ran 28 days to 8 weeks and would not have detected neoplasia. Any history of malignancy is an absolute exclusion; for healthy users, long-term risk is unknown rather than reassuring.
Will it replace exercise?
No. Exercise switches on hundreds of different processes — AMPK, mTOR, BDNF, IGF-1, myokines, signals to bone density, immune function and many more. SLU-PP-332 switches on one. It copies one piece of a much larger system. Anyone expecting it to replace training will be disappointed.
No. Exercise engages hundreds of pathways in parallel, including AMPK, mTOR, BDNF, IGF-1, myokine release, osteogenic signalling and immune modulation. SLU-PP-332 engages the ERR axis alone, reproducing a single branch of the endurance adaptation programme. The "exercise in a pill" framing overstates the scope of a pan-ERR agonist.
Will it show up on a drug test?
Yes. WADA bans it under the S0 category for unapproved substances and also as a metabolic modulator and exercise mimetic. In 2026 the UCLA Olympic Analytical Laboratory identified 22 separate breakdown products of SLU-PP-332 specifically so that testers can detect it. Tested athletes in any sport will be flagged.
Yes. It is WADA-prohibited under S0 (unapproved substances) and under the metabolic modulator and exercise mimetic categories. Avliyakulov, Sobolevsky and Ahrens (2026) characterised 22 distinct in vitro metabolites using human liver microsomes expressly to establish a detection foundation for doping control. Detection infrastructure now exists.
References
- Billon C, Sitaula S, Banerjee S, et al. Synthetic ERR alpha/beta/gamma Agonist Induces an ERR alpha-Dependent Acute Aerobic Exercise Response and Enhances Exercise Capacity. ACS Chemical Biology. 2023;18(4):756-771.
- Billon C, Schoepke E, Avdagic A, et al. A Synthetic ERR Agonist Alleviates Metabolic Syndrome. Journal of Pharmacology and Experimental Therapeutics. 2024;388(2):232-240.
- Wang XX, Myakala K, Libby AE, et al. Estrogen-Related Receptor Agonism Reverses Mitochondrial Dysfunction and Inflammation in the Aging Kidney. American Journal of Pathology. 2023;193(12):1969-1987.
- Xu W, Billon C, Li H, et al. Novel Pan-ERR Agonists Ameliorate Heart Failure Through Enhancing Cardiac Fatty Acid Metabolism and Mitochondrial Function. Circulation. 2024;149(3):227-250.
- Bonanni R, Falvino A, Matticari A, et al. Targeting ERRs to counteract age-related muscle atrophy associated with physical inactivity: a pilot study. Frontiers in Physiology. 2025;16:1616693.
- Avliyakulov NK, Sobolevsky T, Ahrens E. Analysis and Identification of In Vitro Metabolites of Exercise Mimetic SLU-PP-332 ERR alpha/beta/gamma Agonist for Doping-Control Purposes. Drug Testing and Analysis. 2026;18(3):439-450.
- Stein RA, Chang CY, Kazmin DA, et al. Estrogen-related receptor alpha is critical for the growth of estrogen receptor-negative breast cancer. Cancer Research. 2008;68(21):8805-8812.
- Muduli K, Prusty M, Pradhan J, et al. Estrogen-Related Receptor Alpha (ERR alpha) Promotes Cancer Stem Cell-Like Characteristics in Breast Cancer. Stem Cell Reviews and Reports. 2023;19(8):2807-2819.
- Stein RA, Gaillard S, McDonnell DP. Estrogen-related receptor alpha induces the expression of vascular endothelial growth factor in breast cancer cells. Journal of Steroid Biochemistry and Molecular Biology. 2009;114(3-5):131-138.
- Huang JW, Guan BZ, Yin LH, et al. Effects of estrogen-related receptor alpha (ERR alpha) on proliferation and metastasis of human lung cancer A549 cells. Journal of Huazhong University of Science and Technology Medical Sciences. 2014;34(6):875-881.
This entry has been reviewed and expanded with additional reference material. Units are recomputed from the stated protocol.