SLU-PP-332
A synthetic exercise mimetic that activates estrogen-related receptors (ERRs) to replicate the molecular effects of aerobic exercise — increasing endurance, fat oxidation, and mitochondrial function in mice without physical activity. It has never been tested in a human trial, and WADA banned it by name from 2027.
What is SLU-PP-332?
SLU-PP-332 is a synthetic small-molecule agonist of the estrogen-related receptors (ERRα, ERRβ, ERRγ) developed by a St. Louis collaboration between the pharmacology group of Thomas Burris (then at the Center for Clinical Pharmacology, Washington University School of Medicine and St. Louis College of Pharmacy, now at the University of Florida) and the medicinal chemists of John K. Walker at Saint Louis University, whose institution gives the compound its 'SLU' prefix. It is not a peptide — it's a small molecule — but has gained significant attention in the performance and longevity community as an "exercise in a pill." In mice, SLU-PP-332 activates the same genetic program that aerobic exercise turns on: it increases fatigue-resistant type IIa muscle fibers, boosts mitochondrial function, increases energy expenditure, enhances fatty acid oxidation, and improves exercise endurance on treadmill tests. Beyond muscle, it has shown remarkable effects in heart failure (improved ejection fraction and survival, published in Circulation) and kidney aging. Two anti-doping laboratories published metabolite-detection methods for it in 2026, and WADA then named SLU-PP-332 and SLU-PP-915 on its 2027 Prohibited List under section S4.4, effective 1 January 2027.
What SLU-PP-332 Is Investigated For
SLU-PP-332 is investigated as an exercise mimetic — specifically for endurance enhancement, metabolic syndrome, heart failure, age-related kidney dysfunction, and sarcopenia — and the strongest evidence to date is for heart failure in mouse pressure-overload models, where Circulation published improved ejection fraction, reduced fibrosis, and increased survival driven primarily by ERRγ. Supporting mouse data spans multi-organ ERR-mediated benefits: increased type IIa oxidative muscle fibers and treadmill endurance (ACS Chemical Biology 2023), metabolic syndrome reversal, and reversal of age-related kidney mitochondrial dysfunction. The honest caveats dominate the picture: all efficacy data is preclinical in mice, no human clinical trials have been conducted, and there is no validated human dose, pharmacokinetic profile, or safety framework. The compound is also not a peptide but a small molecule, chronic pan-ERR activation across multiple organ systems has unknown long-term consequences, and anti-doping laboratories published SLU-PP-332 metabolite detection methods in 2026 signaling imminent WADA listing.
History & Discovery
SLU-PP-332 was developed in the laboratory of Thomas Burris at Saint Louis University as a synthetic pan-agonist of the estrogen-related receptors (ERRα, ERRβ, ERRγ) — orphan nuclear receptors that serve as master transcriptional regulators of mitochondrial biogenesis, oxidative phosphorylation, and fatty acid metabolism. The Burris lab had spent years characterizing ERR pharmacology and recognized that the receptor family represented an unusually direct molecular handle on the genetic program activated by aerobic exercise. The headline ACS Chemical Biology paper (2023) showed that SLU-PP-332 activates an ERRα-dependent acute aerobic exercise transcriptional response in mouse skeletal muscle and enhances treadmill endurance. Subsequent papers extended the profile across organ systems: metabolic syndrome (J Pharmacol Exp Ther 2024), heart failure with improved ejection fraction and reduced fibrosis (Circulation 2024), age-related kidney mitochondrial dysfunction (2023), and pilot work in age-related muscle atrophy (2025). The 'exercise mimetic' framing has driven significant attention from longevity, performance, and obesity communities, and a chemically distinct sister compound, SLU-PP-915, first reported in 2023, was shown to retain its effect when swallowed in a 2026 paper. Anti-doping researchers characterized the metabolites of both compounds in 2026, and WADA named them on its 2027 Prohibited List under section S4.4, effective 1 January 2027. Note that SLU-PP-332 is a small molecule, not a peptide — it is included on this site because it is widely discussed alongside performance and metabolic peptides in the optimization community.
How It Works
SLU-PP-332 activates a family of receptors called ERRs (estrogen-related receptors) that serve as master switches for the genes your body turns on during aerobic exercise. When activated, these receptors increase mitochondrial activity (your cells' power plants), shift muscle fibers toward the fatigue-resistant type used for endurance, and ramp up fat burning — producing many of the metabolic benefits of a workout without the physical activity.
SLU-PP-332 is a synthetic pan-agonist of estrogen-related receptors alpha, beta, and gamma (ERRα/β/γ), with highest potency for ERRα: in the cell-based reporter assay that defined it, the half-maximal effective concentrations were 98 nM at ERRα, 230 nM at ERRβ, and 430 nM at ERRγ — a 4.4-fold preference for ERRα over ERRγ, which is a tilt rather than true selectivity. ERRs are orphan nuclear receptors that regulate mitochondrial biogenesis, oxidative phosphorylation, and fatty acid metabolism — the core metabolic adaptations of aerobic exercise. In skeletal muscle, SLU-PP-332 induces an ERRα-dependent acute aerobic exercise genetic program, increasing type IIa oxidative muscle fibers and enhancing treadmill endurance in mice. In human myoblasts grown from muscle biopsies — the only published experiment using human tissue — it upregulated PGC-1α, SIRT1, ERRα, and FNDC5 (the irisin precursor) while reducing lactate dehydrogenase release, ROS production, and senescence markers. In metabolic syndrome models, it increased energy expenditure and fatty acid oxidation, reduced fat mass, and improved insulin sensitivity. In heart failure (pressure overload model), it significantly improved ejection fraction, reduced fibrosis, and increased survival without changing cardiac hypertrophy — with ERRγ identified as the primary cardioprotective mediator. Ejection fraction in untreated mice fell to 33.8% by six weeks against 68.2% in sham-operated animals; SLU-PP-332 improved it from week four, while SLU-PP-915 acted from week two and also rescued stroke volume and cardiac output, which SLU-PP-332 did not. Multi-omics analysis confirmed activation of fatty acid metabolism and mitochondrial function gene networks. In aging kidney, it reversed mitochondrial dysfunction and inflammation.
Evidence Snapshot
Human Clinical Evidence
None. SLU-PP-332 has not entered human clinical trials. All evidence is from mouse models and cell culture. The next-generation orally active compound SLU-PP-915 may be closer to clinical development.
Animal / Preclinical
Strong and multi-organ. Exercise/muscle: increased type IIa oxidative fibers and enhanced treadmill endurance in mice, which after seven days of twice-daily dosing ran about 70% longer and 45% further than vehicle-treated animals (ACS Chemical Biology, 2023). Metabolic syndrome: reduced obesity, increased energy expenditure, improved insulin sensitivity in obese mice (J Pharmacol Exp Ther, 2024). Heart failure: improved ejection fraction, reduced fibrosis, increased survival in pressure overload model (Circulation, 2024). Kidney: reversed age-related mitochondrial dysfunction and inflammation (2023). Muscle atrophy: a 2025 pilot study that is not an animal study at all — it treated primary myoblasts grown from muscle biopsies of 20 women undergoing hip replacement, raising SIRT1, PGC-1α, ERRα, and FNDC5 and lowering markers of cytotoxicity, oxidative stress, and senescence. It is the closest thing to human data that exists, and it is cells in a dish, not a person.
Mechanistic Rationale
Strong. ERRs are well-established master regulators of mitochondrial biogenesis and oxidative metabolism. The connection between ERR activation and exercise adaptation is supported by extensive prior research on PGC-1α/ERR signaling. SLU-PP-332's effects are consistent with predicted ERR biology across multiple organ systems.
Research Gaps & Open Questions
What the current literature has not yet settled about SLU-PP-332:
- 01Human pharmacokinetics, oral bioavailability, dosing, and safety are entirely uncharacterized — no published Phase 1 trial exists for SLU-PP-332 or its successor SLU-PP-915.
- 02Whether mouse exercise-mimetic effects translate to clinically meaningful human endurance, body composition, or metabolic outcomes is unproven.
- 03Long-term safety of chronic pan-ERR activation in humans — ERRs regulate genes across cardiac, hepatic, renal, muscle, and metabolic tissues, and chronic agonism could have unintended effects.
- 04Relevance to clinical heart failure, where the mouse data are most striking, requires properly designed human trials of SLU-PP-915 or a successor.
- 05Whether SLU-PP-332 produces meaningful muscle hypertrophy or strength gains (as opposed to fiber-type shifts and endurance) is not supported by current data — it is more analogous to endurance training than resistance training. One caveat cuts against the tidy version of that story: the original mouse study reported a grip-strength increase after two weeks of dosing, a single measure in a single experiment that has never been followed up.
- 06Sex differences — every published mouse experiment used male animals. Given that the estrogen-related receptors are named for their structural kinship to the estrogen receptor, the complete absence of female data is a conspicuous hole.
- 07Cancer risk runs in the opposite direction from the therapeutic story and has never been resolved. The same laboratory built an ERR inverse agonist, SLU-PP-1072, on the finding that blocking ERRα/γ disrupts prostate cancer cell metabolism and triggers cell death. If switching these receptors off kills those cells, nobody has established what switching them on chronically does in a person with an undetected tumor.
- 08Combination with other longevity-targeted compounds (rapamycin, metformin, NAD+ precursors, GLP-1 agonists) is widely discussed but entirely unstudied.
Forms & Administration
SLU-PP-332 has been administered via intraperitoneal injection in mouse studies. A chemically distinct sister compound, SLU-PP-915, was first reported in 2023 and shown in 2026 to keep comparable efficacy when given by mouth in mice, adjusted for systemic exposure. Neither is available for human use. These are strictly research compounds not available through legitimate medical channels.
Dosing & Protocols
The ranges below reflect protocols commonly discussed in the literature and by clinicians — not a prescription. Actual dosing for any individual should be determined by a qualified healthcare provider who knows the patient.
Typical Range
There is no human dose because SLU-PP-332 has not entered human clinical trials. The published rodent work used intraperitoneal injection at two dose levels: 50 mg/kg twice daily (100 mg/kg/day) for the muscle and endurance experiments, and 25 mg/kg twice daily (50 mg/kg/day) for the six-week heart-failure study, with a single 30 mg/kg injection used to measure tissue exposure. Allometric scaling to humans is fraught and the oral bioavailability of SLU-PP-332 itself is poor, which is the design motivation for the orally active successor SLU-PP-915.
Frequency
Mouse protocols have used daily intraperitoneal dosing over study durations of days to weeks. Human dosing schedules are not established because no clinical trials have been conducted.
Timing Considerations
Time of day
No human regimen exists. The mouse protocols dosed twice daily at the start and end of the light phase, tying administration to the animals' light cycle rather than to training.
Relative to meals
Undefined. The rodent papers do not describe fasted dosing, and there is no human data.
Relative to exercise
Undefined. The mouse endurance experiments dosed on a fixed twice-daily schedule for days before treadmill testing, not around individual sessions.
Cycle Length
There is no concept of a validated human cycle. Chronic ERR activation across multiple organ systems carries unknown long-term implications, and the published mouse studies are too short to characterize chronic safety in any species.
Protocol Notes
SLU-PP-332 is a research compound, not a clinical drug. It is sold by research-chemical suppliers for laboratory use only, and use in humans is unauthorized in every jurisdiction. The 'exercise in a pill' framing has driven a grey-market following, but this framing oversells the data — SLU-PP-332 replicates a portion of the molecular response to exercise, not the full multisystem effect, and all efficacy data come from mouse models. The orally active successor SLU-PP-915 is also strictly a research compound with no human exposure data. Anyone using SLU-PP-332 should understand that they are taking an unstudied small molecule outside any regulated pharmacovigilance framework, that ERRs regulate genes across cardiac, hepatic, renal, muscle, and metabolic tissues, and that the chronic effects of pan-ERR agonism in humans are entirely uncharacterized.
SLU-PP-332 is not approved for human use by any regulatory authority and has not been tested in human clinical trials. There is no validated human dose, no established safety profile, and no monitoring framework for users of grey-market material.
Timeline of Effects
Onset
In mouse studies, acute transcriptional responses (gene expression changes consistent with the aerobic exercise program) emerged within hours of dosing. Functional changes (enhanced treadmill endurance, body composition shifts, metabolic improvements) emerged over days to weeks of repeated dosing. No human onset data exist.
Peak Effect
Mouse protocols have run for days to weeks; whether effects continue to accumulate, plateau, or attenuate with chronic dosing is largely uncharacterized. Cardiac improvements in heart failure models accumulated over the study duration. No information exists on peak human effect because no humans have been studied.
After Discontinuation
Mechanistically, ERR-mediated transcriptional effects would be expected to fade within days to weeks of stopping the compound as gene expression returns to baseline. The functional consequences (mitochondrial biogenesis, fiber-type shifts) might persist longer due to the slower turnover of structural adaptations. No formal washout data exist in any species.
Monitoring & Measurement
Bloodwork & Labs
- •Lipid panel — ERR-alpha agonism shifts fatty-acid oxidation in rodent work, so triglycerides and HDL are the most reactive markers to watch
- •Fasting glucose, fasting insulin (HOMA-IR), HbA1c
- •ALT and AST — hepatic metabolism is plausibly affected; useful to track
- •CBC — anchor
Functional & Performance Tests
- •Time to exhaustion on a fixed submaximal workload (treadmill, bike, or rower) — the endurance endpoint the rodent work produced
- •VO2 max via lab test or validated wearable algorithm
- •DEXA scan — body composition
- •Resting heart rate and HRR (wearable)
When to Test
Baseline, 6 weeks, 12 weeks.
Interpretation & Notes
SLU-PP-332 has no published human trials as of 2026 — the entire evidence base is rodent. That makes honest measurement more important than usual: you are testing whether a compound with no human safety data or dose-response curve is doing anything in your case, and the answer is often no. Submaximal time-to-exhaustion is a more sensitive endurance endpoint than VO2 max. Metabolic shifts at 12 weeks (lipids, HOMA-IR) are the secondary readout and are less prone to training-effect confounding. SLU-PP-332 will be in scope for WADA detection in the near term; athletes subject to testing should not use it. Routine labs available direct-to-consumer; VO2 max via university sports-science programs or performance clinics.
Common Questions
Can SLU-PP-332 actually replace exercise?
In mice, it activates many of the same molecular pathways as aerobic exercise — increased oxidative muscle fibers, enhanced mitochondrial function, improved endurance. But exercise has hundreds of effects beyond ERR activation (cardiovascular, neurological, hormonal, skeletal). SLU-PP-332 replicates part of the exercise response, not all of it. It's being studied more as a therapeutic for people who can't exercise (heart failure, severe obesity, immobility) than as a shortcut for healthy people.
How does SLU-PP-332 differ from other performance compounds?
Most performance compounds (steroids, SARMs, GH secretagogues) target muscle growth pathways. SLU-PP-332 targets metabolic fitness — the cellular machinery that uses oxygen, burns fat, and sustains endurance. It's more like endurance training than weight training in a pill. The closest comparison is the earlier exercise mimetic AICAR (AMPK activator).
Is SLU-PP-332 banned in sports?
Yes. WADA named SLU-PP-332 and SLU-PP-915 on its 2027 Prohibited List, in section S4.4 (Metabolic Modulators), effective 1 January 2027 — the entry reads 'SLU-PP-332, SLU-PP-915 and related substances.' Before that date it was already prohibited under the catch-all S0 category for unapproved substances. Testing is not hypothetical either: two 2026 laboratory papers mapped its metabolites specifically so doping-control labs could screen for it. The UCLA Olympic Analytical Laboratory identified 22 metabolites in human liver preparations and named eight as the most promising markers; a group at the German Sport University Cologne found nine.
What is SLU-PP-915 and how is it different from SLU-PP-332?
SLU-PP-915 is a chemically distinct second pan-ERR agonist from the same St. Louis collaboration. It is not new — it was first described in a 2023 medicinal-chemistry paper and tested alongside SLU-PP-332 in the 2024 Circulation heart-failure study. What was published in 2026 is the demonstration that it still works when swallowed. The main pharmacological difference is oral bioavailability — SLU-PP-332 itself is poorly orally available, which is why the published mouse studies use intraperitoneal injection. SLU-PP-915 was designed to be orally active while retaining pan-ERR agonism, and it is the more plausible clinical-development candidate. Neither compound has entered human clinical trials, and both are strictly research compounds with no human exposure data. The 2026 anti-doping detection papers cover both molecules.
Has SLU-PP-332 ever been given to a human?
Not in any published or registered study. A September 2026 search of ClinicalTrials.gov found no trial of SLU-PP-332 or SLU-PP-915. The only published work involving human material is a 2025 pilot study that took muscle biopsies from 20 women undergoing hip replacement surgery, grew myoblasts from the tissue, and exposed those cells to the compound for 48 hours in a dish. Cells in a dish cannot tell you about absorption, dose, drug interactions, or what happens to a whole body over months. Everything else — the endurance numbers, the fat loss, the heart-failure survival benefit — comes from mice.
Is any company actually developing SLU-PP-332 as a drug?
Two small companies are working on ERR agonists, and the scientists behind the compound have stakes in both. Thomas Burris, who led the original work, discloses that he is a stockholder in Myonid Therapeutics and Pelagos Pharmaceuticals, both active in developing ERR agonists, and the geneticist who ran the heart-failure study, Lilei Zhang, is a cofounder of and consultant for Pelagos. The intellectual property behind the sister compound sits with Saint Louis University. None of this has reached a human trial: as of September 2026 there is no registered study of either compound. Commercial interest is real, but it is at the stage of company formation and patents, not medicine.
Is SLU-PP-332 safe for healthy people to use as a performance enhancer?
There is no honest evidence base to answer that question. All efficacy and safety data come from mouse studies, no human trials have been conducted, and the compound is sold by research-chemical suppliers outside any regulated pharmacovigilance framework. ERRs regulate gene expression across cardiac, hepatic, renal, muscle, and metabolic tissues, and the long-term consequences of chronic pan-ERR agonism in humans are entirely uncharacterized. The compound is being developed primarily as a therapeutic for patients who cannot exercise (heart failure, severe obesity, immobility) — that is the context in which a future regulated form might eventually be tested, not as a casual performance shortcut for healthy individuals.
Who SLU-PP-332 Is NOT For
- •Pregnancy and breastfeeding — no human safety data; ERRs regulate developmental gene expression and pan-ERR agonism during fetal or infant development carries unquantified risk.
- •Pediatric use — entirely unstudied; no plausible justification for use in a developing population.
- •Known cardiovascular disease — although mouse heart failure data show benefit, the same pharmacology in humans without supervision and with no monitoring framework is inappropriate. The cardiac data in mice are encouraging for the development of regulated therapeutics, not a justification for self-administration.
- •Active or recent-history cancer — ERRs (particularly ERRα) have documented roles in tumor metabolism and progression in several cancer contexts; chronic pan-ERR agonism in patients with malignancy carries theoretical risk that has not been studied.
- •Significant hepatic or renal impairment — first-pass metabolism, drug clearance, and the consequences of pan-ERR activation in compromised tissues are uncharacterized.
- •Athletes subject to anti-doping testing — SLU-PP-332 is named on the WADA 2027 Prohibited List under S4.4, and anti-doping laboratories published validated metabolite markers for it in 2026, so it is both banned and screenable.
Drug & Supplement Interactions
Documented drug-interaction data for SLU-PP-332 in humans are nonexistent because no human clinical trials have been performed. Theoretical interactions follow from the pharmacology. Co-administration with metformin, AMPK activators, or other compounds affecting mitochondrial energy metabolism could produce additive or interfering effects on the same downstream pathways. Co-administration with other exercise-mimetic concepts (AMPK activators like AICAR, SIRT1 activators, mitochondrial cofactors) is widely discussed in optimization circles but entirely unstudied. The cardiac effects observed in mouse heart failure models raise theoretical interactions with conventional heart failure pharmacotherapy (ACE inhibitors, beta-blockers, SGLT2 inhibitors, ARNIs), where additive cardiac remodeling effects could occur but have not been characterized. Effects on drug-metabolizing enzymes (CYPs) and transporters have not been systematically studied. Anyone using SLU-PP-332 alongside chronic medications is doing so without any human pharmacokinetic data and should disclose use to their prescribing clinician.
Safety Profile
Common Side Effects
Cautions
- • Not approved for human use — strictly a research compound
- • No human clinical trials have been conducted
- • Prohibited in sport — named on the WADA 2027 Prohibited List (S4.4 metabolic modulators), in force 1 January 2027, and already covered by S0 before then
- • Gray market sources have unknown purity and composition
- • Long-term effects of chronic ERR activation are unknown
What We Don't Know
All data is from mouse models. Whether ERR agonism translates to meaningful exercise-like benefits in humans is unproven. Chronic pan-ERR activation could have unintended effects given that ERRs regulate genes across multiple organ systems. The next-generation compound SLU-PP-915 (orally active) may be more clinically relevant but also lacks human data.
Legal Status
United States
SLU-PP-332 is not FDA-approved for any use and appears in no registered clinical trial — a September 2026 search of ClinicalTrials.gov for SLU-PP-332, SLU-PP-915, and the two companies working on ERR agonists returned no studies. Whether a sponsor has filed an Investigational New Drug application is not publicly knowable, since those filings stay confidential until a trial is registered. It is sold by research-chemical suppliers for laboratory research use only. Human use is unauthorized. The successor SLU-PP-915 is in the same regulatory position.
International
No regulatory authority in any jurisdiction has approved SLU-PP-332. Its availability is uniformly limited to research-chemical channels and is not authorized for human use anywhere.
Sports & Competition
SLU-PP-332 is banned by name in sport from 2027. WADA added it to the 2027 Prohibited List under section S4.4 (Metabolic Modulators), published in September 2026 and in force from 1 January 2027, where the entry reads 'SLU-PP-332, SLU-PP-915 and related substances.' Until then it is already caught by the catch-all S0 category, which covers substances with no regulatory approval anywhere. The move matters: S0 substances are Specified Substances, while S4.4 substances are non-Specified, a category carrying a tougher starting sanction. It is prohibited both in and out of competition, and the 'related substances' wording extends to chemical analogues. WADA's S0 category (substances not approved by any government regulatory health authority for human therapeutic use) currently covers it, and the explicit listing under either S0, S2, or a stand-alone exercise-mimetic category is a near-term regulatory step. Athletes subject to WADA, USADA, or equivalent codes should treat SLU-PP-332 as prohibited in and out of competition.
Regulatory status changes over time. Verify current local rules with a qualified professional.
Myths & Misconceptions
Myth
SLU-PP-332 is a peptide.
Reality
SLU-PP-332 is a small-molecule synthetic ERR agonist, not a peptide. It is included on this site because it is widely discussed alongside performance and metabolic peptides in the longevity and optimization community, but the molecule, mechanism, and class are entirely distinct from peptide hormone analogs.
Myth
SLU-PP-332 replicates the full benefits of exercise.
Reality
SLU-PP-332 activates a portion of the molecular response to aerobic exercise — ERR-mediated mitochondrial biogenesis, fatty acid oxidation, and oxidative fiber-type shifts. Exercise also produces cardiovascular adaptations, neurological effects, hormonal cascades, skeletal loading, and dozens of other downstream consequences that ERR activation does not replicate. SLU-PP-332 is being studied primarily as a therapeutic for people who cannot exercise (heart failure, severe obesity, immobility), not as a substitute for exercise in healthy individuals.
Myth
Because the published data come from a respected academic lab and reputable journals, SLU-PP-332 is safe for human use.
Reality
The published data are preclinical and exclusively in mouse models. The quality and rigor of the preclinical work is high, but it tells us about ERR pharmacology and about effects in mice — not about safety, dosing, or efficacy in humans. No human clinical trials have been performed. The compound is sold by research-chemical suppliers for laboratory use only and is not authorized for human use in any jurisdiction.
Myth
SLU-PP-332 is a niche research chemical that regulators have not noticed.
Reality
Regulators noticed. Anti-doping laboratories in Cologne and at UCLA both published metabolite maps of the compound in 2026 specifically so it could be screened for, and WADA then wrote it into the 2027 Prohibited List by name, adding 'and related substances' so that close analogues are covered too. That is an unusually quick path from first publication in 2023 to named prohibition — a sign that authorities treat the misuse risk as real rather than theoretical.
Myth
SLU-PP-332 is undetectable in anti-doping testing because it is so new.
Reality
Two 2026 papers — one from the UCLA Olympic Analytical Laboratory, one from the German Sport University Cologne — mapped the metabolites of SLU-PP-332 (and, in the Cologne paper, SLU-PP-915) precisely so that doping-control labs could screen for them, identifying 22 and nine metabolites respectively. WADA then added both compounds by name to the 2027 Prohibited List. The detection work came first and the ban followed it. Athletes who use SLU-PP-332 expecting to evade detection are likely to be wrong on a short time horizon.
Published Research
12 studiesChemical optimization of the exercise mimetic SLU-PP-332 enables insight into estrogen-related receptor signaling.
Analysis and Identification of In Vitro Metabolites of Exercise Mimetic SLU-PP-332 ERRα/β/γ Agonist for Doping-Control Purposes.
In Vitro Metabolism and Analytical Characterization of SLU-PP-332 and SLU-PP-915: Novel Pan-ERR Agonists With Doping Potential.
An orally active estrogen receptor-related receptor agonist, SLU-PP-915, enhances aerobic exercise capacity.
Targeting ERRs to counteract age-related muscle atrophy associated with physical inactivity: a pilot study.
Novel Pan-ERR Agonists Ameliorate Heart Failure Through Enhancing Cardiac Fatty Acid Metabolism and Mitochondrial Function.
A Synthetic ERR Agonist Alleviates Metabolic Syndrome.
Estrogen-Related Receptor Agonism Reverses Mitochondrial Dysfunction and Inflammation in the Aging Kidney.
Development and pharmacological evaluation of a new chemical series of potent pan-ERR agonists, identification of SLU-PP-915.
Synthetic ERRα/β/γ Agonist Induces an ERRα-Dependent Acute Aerobic Exercise Response and Enhances Exercise Capacity.
The foundational 2023 ACS Chemical Biology paper from the Burris lab. Established SLU-PP-332 as a pan-ERR agonist that reproduces the aerobic-exercise transcriptional program in mouse muscle and enhances treadmill endurance — the 'exercise mimetic' origin paper.
A Selective ERRα/γ Inverse Agonist, SLU-PP-1072, Inhibits the Warburg Effect and Induces Apoptosis in Prostate Cancer Cells.
WADA 2027 Prohibited List (S4.4 Metabolic Modulators; in force 1 January 2027)
Quick Facts
- Class
- Exercise Mimetic
- Tier
- D
- Evidence
- Preliminary
- Safety
- Limited Data
- Updated
- Sep 2026
- Citations
- 12PubMed
Also known as
Tags
Evidence Score
Clinical Trials
View Clinical TrialsLinks to ClinicalTrials.gov for reference. Listing does not imply endorsement.