SLU-PP-332

Dosing from the Literature

Published for fat loss: 50 mg/kg twice a day, injected in mice, from one paper (Billon et al., 2024). Not published: any human dose; no human data at all.

Every published dose is a mouse dose, given by intraperitoneal injection.

What It Is

SLU-PP-332 is a synthetic small-molecule nuclear-receptor agonist designed and disclosed by the medicinal-chemistry laboratory of Thomas P. Burris at Saint Louis University (since relocated to the University of Florida Genetics Institute). Its formal chemistry is an acylhydrazone derivative with activity on all three members of the estrogen-related receptor family — ERRα (NR3B1), ERRβ (NR3B2), and ERRγ (NR3B3). It was built from GSK4716, an earlier acyl hydrazone that activates only ERRβ and ERRγ and was one of the first two ERR agonists reported (Zuercher et al., J Med Chem 2005; PMID 15857113); redesigning it raised its potency at ERRα about 50-fold (Billon et al., ACS Chem Biol 2023; PMID 36988910). Its developers report it as a pan-agonist most potent at ERRα (EC50 about 98 nM at ERRα, 230 nM at ERRβ and 430 nM at ERRγ in cell assays), and its pharmacology was characterized in papers from the Burris group from 2023 onward (Billon et al., ACS Chem Biol 2023; PMID 36988910).

The ERR family are orphan nuclear receptors — transcription factors whose endogenous ligand has never been identified (Huss et al., Biochim Biophys Acta 2015; PMID 26115970). They are constitutively active in tissues with high oxidative metabolism (heart, skeletal muscle, brown adipose, kidney cortex) and serve as master regulators of the genes that control mitochondrial biogenesis, oxidative phosphorylation, fatty-acid oxidation, and the slow-twitch muscle-fiber program. Because exercise itself upregulates ERR activity and its co-activator PGC-1α, the ERR family has been a target of interest for "exercise mimetic" drug discovery for more than a decade.

SLU-PP-332 rose to public attention in August 2023 when Burris presented preclinical data at the American Chemical Society meeting in San Francisco and the paper of record had appeared that spring in ACS Chemical Biology (Billon et al., 2023; PMID 36988910). In that paper the compound, injected intraperitoneally at 50 mg/kg twice daily, increased oxidative type IIa muscle fibers and, after 7 days, let sedentary mice run about 70% longer and 45% farther; a 2024 paper from the group added higher energy expenditure and fatty-acid oxidation and less fat gain in obese mice (Billon et al., J Pharmacol Exp Ther 2024; PMID 37739806). Press coverage framed the compound as "exercise in a pill," a positioning the authors themselves were careful to avoid — the paper discusses the compound as a tool to interrogate ERR biology and as a candidate for indications where patients cannot exercise (the 2023 paper names metabolic diseases, muscular dystrophy and sarcopenia).

In the research-chemical market, SLU-PP-332 appeared rapidly after the 2023 publication and became available from a handful of vendors as oral capsules, raw powder, and occasional injectable preparations. The community adoption curve dramatically outpaced the data: there is no published human pharmacokinetic study, no IND, no registered clinical trial, no measured oral bioavailability in people (its developers report that it lacks oral bioavailability), no dose-response data outside the narrow mouse protocol, and no long-term safety information. Current self-experimentation protocols are entirely community-derived extrapolation from a single mouse paper — an unusually thin evidence base even by the loose standards of this category.

Mechanism of Action

SLU-PP-332 acts on the ERR family of orphan nuclear receptors: in lab tests it bound the ligand-binding domain of ERRα and of ERRγ and raised the activity of all three ERRs in cells (Billon et al., ACS Chem Biol 2023; PMID 36988910). Unlike the estrogen receptors, which need a hormone to bind before they act, the ERRs are active on their own (Billon et al., 2023); no natural ligand is known for them, and co-activator proteins, above all the PGC-1 family, set their activity (Giguère, Endocr Rev 2008; PMID 18664618).

• ERRα activation (NR3B1) — ERRα, one of the first orphan nuclear receptors identified, is switched on by its PGC-1 co-activators and then raises genes for fatty-acid oxidation, the TCA cycle, oxidative phosphorylation and mitochondrial biogenesis, both directly and through other regulators such as NRF1 and NRF2; PGC-1α in turn raises ERRα’s own expression, a positive loop (Villena & Kralli, Trends Endocrinol Metab 2008; PMID 18778951). Mice with a more active ERRα gained oxidative fibers and mitochondria in muscle (Xia et al., Mol Metab 2023; PMID 37802398).
• ERRγ activation (NR3B3) — ERRγ is highly expressed in slow-twitch (type I) muscle (Narkar et al., Cell Metab 2011, PMID 21356518) and controls energy metabolism in the heart and skeletal muscle (Misra et al., Trends Endocrinol Metab 2017, PMID 28209382). Forced ERRγ expression alone reprograms type IIb glycolytic fibers toward a slow-twitch oxidative phenotype and increases angiogenesis (new blood vessel growth) in muscle (Rangwala et al., J Biol Chem 2010, PMID 20418374; Narkar et al., Cell Metab 2011, PMID 21356518).
• ERRβ activation (NR3B2) — Less studied than the other two; it helps keep embryonic stem cells pluripotent (Huss et al., Biochim Biophys Acta 2015; PMID 26115970) and is needed for early placental development in mice (Luo et al., Nature 1997; PMID 9285590). Skeletal muscle has far less ERRβ than ERRα or ERRγ, and the endurance effect of SLU-PP-332 depended on ERRα (Billon et al., ACS Chem Biol 2023; PMID 36988910); in the heart, ERRγ was the main mediator (Xu et al., Circulation 2024; PMID 37961903).
• Fatty-acid oxidation upregulation — ERRα switches on fatty-acid oxidation genes such as MCAD and CPT1B (Villena & Kralli, Trends Endocrinol Metab 2008; PMID 18778951), and in rat heart-muscle cells SLU-PP-332 raised both (Xu et al., Circulation 2024; PMID 37961903). In obese mice, SLU-PP-332 raised whole-body energy expenditure and fatty-acid oxidation (Billon et al., J Pharmacol Exp Ther 2024; PMID 37739806); the 2023 paper did not measure fatty-acid oxidation in the soleus.
• Relation to AMPK — In mice engineered to carry extra ERRγ in muscle, the gains in oxidative capacity and blood vessels ran through the energy sensor AMP-activated protein kinase (AMPK), not through PGC-1α (Narkar et al., Cell Metab 2011, PMID 21356518). The published SLU-PP-332 studies report no AMPK measurements.
• Distinct from PPARδ / Rev-Erb — PPARδ agonists (GW501516/cardarine) and Rev-Erb agonists (SR9009) are the only other nuclear-receptor drugs reported to act as exercise mimetics, and the acute aerobic-exercise gene program SLU-PP-332 switched on in mouse muscle was not reported for either (Billon et al., ACS Chem Biol 2023; PMID 36988910).
• Tissue distribution in rodents — Two hours after a 30 mg/kg IP dose in mice, SLU-PP-332 reached about 0.6 µM in skeletal muscle and 0.2 µM in plasma; other tissues were not reported (Billon et al., ACS Chem Biol 2023; PMID 36988910). No published data on human pharmacokinetics or tissue distribution exists.
• No estrogen-receptor activity — Despite the name "estrogen-related receptor," the ERRs do not bind estrogen, and in cell-based assays SLU-PP-332 did not change the activity of estrogen receptor α or β or of the other nuclear receptors tested (Billon et al., ACS Chem Biol 2023; PMID 36988910).

What the Research Shows

The research base is small and narrow: one headline paper, supporting preclinical papers, and a broader ERR-biology literature. There are no human data.

• Billon et al., 2023 — the headline paper — ACS Chem Biol 18(4):756-771; PMID 36988910. Sedentary mice received 50 mg/kg IP twice daily for 7 days; on the treadmill, treated mice then ran about 70% longer and 45% further than vehicle-treated mice before exhaustion. SLU-PP-332 raised the share of type IIa oxidative muscle fibers and switched on an acute aerobic-exercise gene program, and the endurance effect depended on ERRα. Three of the paper’s authors, Burris among them, declared stock in a company developing ERR-based drugs. This is the paper the "exercise in a pill" media cycle was built on. A 2024 follow-up gave it to diet-induced obese and ob/ob mice: energy expenditure and fatty-acid oxidation rose, fat mass accumulation fell, and insulin sensitivity improved (Billon et al., J Pharmacol Exp Ther 2024; PMID 37739806).
• Billon et al., 2024 — obesity extension — In diet-induced obese mice, 28 days of twice-daily injections held fat gain under 0.5 g, against about 5 g in vehicle-treated mice; treated mice weighed about 12% less and had lower fasting glucose and insulin. In ob/ob mice, 12 days reduced fat mass and liver fat (Billon et al., J Pharmacol Exp Ther 2024; PMID 37739806).
• Not orally available, by its developers’ account — Describing a newer compound, the same group wrote that SLU-PP-332 “improves aerobic performance in mice but lacks oral bioavailability”; the chemically distinct SLU-PP-915 kept a similar endurance effect when given by mouth, once systemic exposure was taken into account (Billon et al., J Pharmacol Exp Ther 2026; PMID 41421047). SLU-PP-332 is sold mostly as oral capsules all the same.
• ERR biology foundational work — Giguère, Endocr Rev 2008 (PMID 18664618) — foundational review establishing the ERR family as master regulators of energy metabolism. Villena & Kralli, Trends Endocrinol Metab 2008 — ERRα/γ as mitochondrial-biogenesis transcription factors.
• ERRγ muscle fiber-type programming — Rangwala et al., J Biol Chem 2010; PMID 20418374. Forced ERRγ expression in muscle drives slow-twitch fiber gene programs and increases angiogenesis. Narkar et al., Cell Metab 2011; PMID 21356518. ERRγ coordinates muscle metabolic and vascular programs independent of PGC-1α.
• ERRα knockout mice — ERRα-null mice have reduced exercise capacity (Perry et al., Mol Endocrinol 2014; PMID 25361393), lower expression of fatty-acid oxidation genes and less mitochondrial capacity in brown fat, and poor tolerance of cold (Villena et al., Proc Natl Acad Sci USA 2007; PMID 17229846), and altered adipose biology (Luo et al., Mol Cell Biol 2003; PMID 14585956). Establishes that endogenous ERRα activity is necessary for the exercise-adapted phenotype; SLU-PP-332 is the pharmacological "gain-of-function" complement to that loss-of-function biology. The genetic gain-of-function has been tested too: mice carrying a stabilized, more active form of ERRα ran longer and resisted fatigue, with more oxidative fibers, more mitochondrial biogenesis and higher fatty-acid oxidation (Xia et al., Mol Metab 2023; PMID 37802398).
• Cardiac ERRα/γ biology — The ERRs are highly expressed in heart. Cardiac-specific overexpression and knockout models show ERRs are essential for cardiac metabolic fitness; losing ERRα and ERRγ in the heart produces a lethal cardiomyopathy, and ERRα-null hearts dilate and pump less under pressure overload (Huss et al., Cell Metab 2007; PMID 17618854). This is the mechanistic basis for both potential therapeutic benefit (heart failure) and theoretical cardiac risk (cardiac hypertrophy or remodeling on chronic systemic ERR agonism). Mice lacking ERRα and cardiac ERRγ develop severe bradycardia and a lethal cardiomyopathy with heart failure (Wang et al., Mol Cell Biol 2015; PMID 25624346). In a mouse pressure-overload heart-failure model, SLU-PP-332 and the related agonist SLU-PP-915 raised ejection fraction, reduced fibrosis and improved survival without changing cardiac hypertrophy (Xu et al., Circulation 2024; PMID 37961903).
• Burris lab medicinal-chemistry papers — The SLU-PP-332 scaffold and analog series have been characterized in papers since 2023 optimizing potency, selectivity, and pharmacokinetics in rodents. SLU-PP-915, from the same group, is a structurally distinct thiophene compound, not an acylhydrazone. The named papers: a thiophene series designed from the same GSK4716 template, which produced SLU-PP-915, a boronic-acid compound with better metabolic stability in liver-microsome assays (Hampton et al., Eur J Med Chem 2023; PMID 37421886), and the first systematic structure-activity study of the SLU-PP-332 scaffold, which reports analogs with better ligand efficiency, solubility or metabolic stability (Okda et al., Int J Biol Macromol 2026; PMID 41850449).
• Comparison to PPARδ / AMPK agonists — The exercise-mimetic category includes GW501516/cardarine (PPARδ), SR9009 (Rev-ErbA), and AICAR (AMPK). SLU-PP-332 is mechanistically orthogonal to all three. GW501516 has been studied in humans and has a known rodent-carcinogenicity signal. SR9009 has poor oral bioavailability. AICAR has a WADA ban. SLU-PP-332 is the newest entry; its comparative safety is entirely unknown.
• No NCT-registered human trials — As of April 2026, ClinicalTrials.gov has no registered study of SLU-PP-332 in any indication. No IND has been publicly disclosed.

Human Data

None. There is no pharmacokinetic study, no Phase 1 trial, no open-label observation series, no published case report, no registered clinical trial of SLU-PP-332 in any human population as of April 2026.

• No published Phase 1 — No Phase 1 SAD/MAD study has been published or registered.
• No IND publicly disclosed — No investigational new drug application has been publicly acknowledged by Saint Louis University, the University of Florida, or any commercial licensee.
• No human pharmacokinetic data — Oral bioavailability, absorption, hepatic metabolism (CYP profile), protein binding, tissue distribution, and elimination pathway are all unknown in humans. In the lab, human liver preparations convert it into hydroxylated metabolites and glucuronide and sulfate conjugates: nine metabolites in one study and 22 in another (Möller et al., Rapid Commun Mass Spectrom 2026; PMID 41588687; Avliyakulov et al., Drug Test Anal 2026; PMID 41688415). What happens to a dose in a living person has not been measured.
• Human cells, not people — The nearest thing to human data is a 2025 pilot study in cells: myoblasts grown from muscle biopsies of ten inactive women having hip replacement were treated with SLU-PP-332, which lowered NOX4, raised SIRT1, PGC-1α, ERRα and FNDC5, reduced oxidative stress and senescence markers, and increased myotube formation (Bonanni et al., Front Physiol 2025; PMID 40692696).
• Research-community self-reports — A small number of anecdotal reports on forums and social media describe perceived endurance improvement. These reports are uncontrolled, placebo-confounded, and not suitable for dose or efficacy inference.
• Research supply chain — Commercial research-chemical vendors began offering SLU-PP-332 shortly after the 2023 publication. Independent purity verification is patchy; no vendor has published identity + potency COAs from an independent third-party lab at scale.

Reconstitution & Storage

Seller listings offer SLU-PP-332 as oral capsules, an oral liquid and powder; an online guide also reports 50 mg tablets. Strengths and formats vary from seller to seller (below).

• Storage — Seller listings disagree. Laboratory reagent suppliers list the powder at −20°C (one gives 3 years) and solutions at −80°C; one research-chemical seller lists powder vials at 2–8°C, a capsule listing says room temperature, and an oral liquid is listed at −10°C.
• Solubility — One reagent datasheet lists it as insoluble in water; datasheets disagree on its solubility in DMSO (1–10 mg/mL in one, 58 mg/mL in another).
• Injection use — Research-only. There is no sterile injectable product available through any legitimate channel and no characterized injection pharmacokinetics in humans. Community IP or SubQ self-injection of SLU-PP-332 is not supported by evidence of any kind.

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Side Effects & Risks

In the absence of human safety data, the risk profile is inferred from ERR biology, related compound experience, and published animal work.

• Unknown human safety profile — No Phase 1 study exists. Safety signals that would normally be identified in tolerability studies (dose-limiting symptoms, vital sign changes, laboratory abnormalities) are undocumented. In the 2023 mouse paper, 10 days at 50 mg/kg twice daily by injection caused no overt toxicity, with normal blood counts, electrolytes and creatine kinase (Billon et al., ACS Chem Biol 2023; PMID 36988910).
• Cardiac risk (theoretical) — ERRα and ERRγ are essential coordinators of the heart’s energy metabolism and also directly control genes for its contraction, calcium handling and electrical conduction (Wang et al., Mol Cell Biol 2015; PMID 25624346). The authors of the mouse heart-failure study note that ERRγ activation has been linked to cardiac hypertrophy, which may raise concerns for the heart’s relaxation (diastolic function); in their mice, 6 weeks of SLU-PP-332 neither prevented nor added to hypertrophy (Xu et al., Circulation 2024; PMID 37961903). Long-term effects on the heart have not been studied, in animals or in people.
• Liver — The ERRs are highly expressed in the liver (Billon et al., ACS Chem Biol 2023; PMID 36988910), where ERRα restrains the glucose-making enzyme PEPCK (Villena & Kralli, Trends Endocrinol Metab 2008; PMID 18778951). In mice given SLU-PP-332 for 28 days, liver enzymes changed little or not at all, liver fat fell, and PEPCK (Pck1) expression did not change (Billon et al., J Pharmacol Exp Ther 2024; PMID 37739806). Effects on the human liver are unknown.
• Renal expression — ERRα levels are among the highest in the kidney (Villena & Kralli, Trends Endocrinol Metab 2008; PMID 18778951), and ERR levels fall in aging human and mouse kidneys (Wang et al., Am J Pathol 2023; PMID 37717940); effects of chronic agonism on kidney function in humans are not characterized. In 21-month-old mice, 8 weeks of SLU-PP-332 reversed age-related increases in albuminuria, podocyte loss, mitochondrial dysfunction and inflammatory cytokines (Wang et al., Am J Pathol 2023; PMID 37717940).
• Hormonal considerations — The ERRs do not bind estrogen (Billon et al., ACS Chem Biol 2023; PMID 36988910), but ERRβ resembles the estrogen receptor and binds the same DNA response element (Luo et al., Nature 1997; PMID 9285590). SLU-PP-332’s selectivity has been tested only in cell assays (Billon et al., 2023), so off-target effects at chronic exposure cannot be excluded.
• No carcinogenicity data — No carcinogenicity study of SLU-PP-332 has been published, including the 2-year rodent study; absence of evidence is not evidence of absence.
• Drug interactions unknown — No study of its interactions with any drug (statins, beta-blockers, GLP-1 agonists, thyroid hormone or PPARδ agonists among them) has been published.
• Pregnancy / lactation — No data. In mice, ERRβ is essential for placental development: embryos lacking it have severely impaired placental formation and die 10.5 days after conception (Luo et al., Nature 1997; PMID 9285590). ERR agonism during pregnancy has unknown effects.
• Source quality — With no approval anywhere, it is sold only as a research chemical.
• WADA considerations — Not named on the 2026 Prohibited List, in force until 31 December 2026: with no approval for human use anywhere, it falls under S0 (non-approved substances), prohibited at all times. The 2027 List, in force from 1 January 2027, names it in S4.4.1, metabolic modulators, with SLU-PP-915 and related substances (Prohibited List 2027).

Bloodwork & Monitoring

No trial, label or guideline sets monitoring for SLU-PP-332, and no study has given it to people. In mice, its developers checked blood counts, electrolytes and creatine kinase after 10 days of injections (Billon et al., ACS Chem Biol 2023; PMID 36988910), and blood lipids, liver enzymes, glucose and insulin after 28 days (Billon et al., J Pharmacol Exp Ther 2024; PMID 37739806).

Practical User Notes

• WADA awareness — Prohibited at all times: under S0, as a non-approved substance, on the 2026 List, and by name in S4.4.1 on the 2027 List, from 1 January 2027 (Prohibited List 2027).

Commonly Stacked With

No published study has tested SLU-PP-332 together with another compound, and none has given it to people.

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Legal Status

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References

1. Billon C, Schoepke E, Avdagic A, Chatterjee A, Butler AA, Elgendy B, Walker JK, Burris TP. A synthetic ERR agonist alleviates metabolic syndrome. J Pharmacol Exp Ther. 2024;388(2):232-240. PMID: 37739806.
2. Billon C, Sitaula S, Banerjee S, Welch R, Elgendy B, Hegazy L, Oh TG, Kazantzis M, Chatterjee A, Chrivia J, Hayes ME, Xu W, Hamilton A, Huss JM, Zhang L, Walker JK, Downes M, Evans RM, Burris TP. Synthetic ERRα/β/γ Agonist Induces an ERRα-Dependent Acute Aerobic Exercise Response and Enhances Exercise Capacity. ACS Chem Biol. 2023;18(4):756-771. PMID: 36988910. (The headline paper; three authors, including Burris, declare stock in a company developing ERR-based drugs.)
3. Giguère V. Transcriptional control of energy homeostasis by the estrogen-related receptors. Endocr Rev. 2008;29(6):677-696. PMID: 18664618.
4. Villena JA, Kralli A. ERRalpha: a metabolic function for the oldest orphan. Trends Endocrinol Metab. 2008;19(8):269-276. PMID: 18778951.
5. Rangwala SM, Wang X, Calvo JA, Lindsley L, Zhang Y, Deyneko G, Beaulieu V, Gao J, Turner G, Markovits J. Estrogen-related receptor gamma is a key regulator of muscle mitochondrial activity and oxidative capacity. J Biol Chem. 2010;285(29):22619-22629. PMID: 20418374.
6. Narkar VA, Fan W, Downes M, Yu RT, Jonker JW, Alaynick WA, Banayo E, Karunasiri MS, Lorca S, Evans RM. Exercise and PGC-1α-independent synchronization of type I muscle metabolism and vasculature by ERRγ. Cell Metab. 2011;13(3):283-293. PMID: 21356518.
7. Villena JA, Hock MB, Chang WY, Barcas JE, Giguère V, Kralli A. Orphan nuclear receptor estrogen-related receptor alpha is essential for adaptive thermogenesis. Proc Natl Acad Sci USA. 2007;104(4):1418-1423. PMID: 17229846.
8. Huss JM, Garbacz WG, Xie W. Constitutive activities of estrogen-related receptors: Transcriptional regulation of metabolism by the ERR pathways in health and disease. Biochim Biophys Acta. 2015;1852(9):1912-1927. PMID: 26115970.
9. Misra J, Kim DK, Choi HS. ERRγ: a Junior Orphan with a Senior Role in Metabolism. Trends Endocrinol Metab. 2017;28(4):261-272. PMID: 28209382.
10. Tripathi M, Yen PM, Singh BK. Estrogen-related receptor alpha: an under-appreciated potential target for the treatment of metabolic diseases. Int J Mol Sci. 2020;21(5):1645. PMID: 32121253.
11. World Anti-Doping Agency. The 2026 Prohibited List. Sections S0 (non-approved substances) and S4 (hormone and metabolic modulators). wada-ama.org.
12. Zuercher WJ, Gaillard S, Orband-Miller LA, Chao EY, Shearer BG, Jones DG, Miller AB, Collins JL, McDonnell DP, Willson TM. Identification and structure-activity relationship of phenolic acyl hydrazones as selective agonists for the estrogen-related orphan nuclear receptors ERRbeta and ERRgamma. J Med Chem. 2005;48(9):3107-3109. PMID: 15857113.
13. Billon C, Appourchaux K, Côté I, Burris TP. An orally active estrogen receptor-related receptor agonist, SLU-PP-915, enhances aerobic exercise capacity. J Pharmacol Exp Ther. 2026;393(1):103787. PMID: 41421047.
14. Hampton CS, Sitaula S, Billon C, Haynes K, Avdagic A, Wanninayake U, Adeyemi CM, Chatterjee A, Griffett K, Banerjee S, Burris SL, Schoepke E, Boehm T, Bess A, de Vera IMS, Burris TP, Walker JK. Development and pharmacological evaluation of a new chemical series of potent pan-ERR agonists, identification of SLU-PP-915. Eur J Med Chem. 2023;258:115582. PMID: 37421886.
15. Okda HE, Zhao P, Hayes M, Duvall C, Quillin E, Fang H, Mohammed BM, Hegazy L, Burris TP, Elgendy B. Chemical optimization of the exercise mimetic SLU-PP-332 enables insight into estrogen-related receptor signaling. Int J Biol Macromol. 2026;355:151450. PMID: 41850449.
16. Wang T, McDonald C, Petrenko NB, Leblanc M, Wang T, Giguere V, Evans RM, Patel VV, Pei L. Estrogen-related receptor α (ERRα) and ERRγ are essential coordinators of cardiac metabolism and function. Mol Cell Biol. 2015;35(7):1281-1298. PMID: 25624346.
17. Xu W, Billon C, Li H, Wilderman A, Qi L, Graves A, Rideb JRDC, Zhao Y, Hayes M, Yu K, Losby M, Hampton CS, Adeyemi CM, Hong SJ, Nasiotis E, Fu C, Oh TG, Fan W, Downes M, Welch RD, Evans RM, Milosavljevic A, Walker JK, Jensen BC, Pei L, Burris T, Zhang L. Novel Pan-ERR Agonists Ameliorate Heart Failure Through Enhancing Cardiac Fatty Acid Metabolism and Mitochondrial Function. Circulation. 2024;149(3):227-250. PMID: 37961903.
18. Wang XX, Myakala K, Libby AE, Krawczyk E, Panov J, Jones BA, Bhasin K, Shults N, Qi Y, Krausz KW, Zerfas PM, Takahashi S, Daneshpajouhnejad P, Titievsky A, Taranenko E, Billon C, Chatterjee A, Elgendy B, Walker JK, Albanese C, Kopp JB, Rosenberg AZ, Gonzalez FJ, Guha U, Brodsky L, Burris TP, Levi M. Estrogen-Related Receptor Agonism Reverses Mitochondrial Dysfunction and Inflammation in the Aging Kidney. Am J Pathol. 2023;193(12):1969-1987. PMID: 37717940.
19. Luo J, Sladek R, Bader JA, Matthyssen A, Rossant J, Giguère V. Placental abnormalities in mouse embryos lacking the orphan nuclear receptor ERR-beta. Nature. 1997;388(6644):778-782. PMID: 9285590.
20. Perry MC, Dufour CR, Tam IS, B'chir W, Giguère V. Estrogen-related receptor-α coordinates transcriptional programs essential for exercise tolerance and muscle fitness. Mol Endocrinol. 2014;28(12):2060-2071. PMID: 25361393.
21. Luo J, Sladek R, Carrier J, Bader JA, Richard D, Giguère V. Reduced fat mass in mice lacking orphan nuclear receptor estrogen-related receptor alpha. Mol Cell Biol. 2003;23(22):7947-7956. PMID: 14585956.
22. Xia H, Scholtes C, Dufour CR, Guluzian C, Giguère V. ERRα fosters running endurance by driving myofiber aerobic transformation and fuel efficiency. Mol Metab. 2023;78:101814. PMID: 37802398.
23. Bonanni R, Falvino A, Matticari A, Rinaldi AM, D'Arcangelo G, Cifelli P, Iundusi R, Gasbarra E, Tancredi V, Cariati I, Tarantino U. Targeting ERRs to counteract age-related muscle atrophy associated with physical inactivity: a pilot study. Front Physiol. 2025;16:1616693. PMID: 40692696.
24. Möller T, Krug O, Thevis M. In Vitro Metabolism and Analytical Characterization of SLU-PP-332 and SLU-PP-915: Novel Pan-ERR Agonists With Doping Potential. Rapid Commun Mass Spectrom. 2026;40(8):e70039. PMID: 41588687.
25. Avliyakulov NK, Sobolevsky T, Ahrens E. Analysis and Identification of In Vitro Metabolites of Exercise Mimetic SLU-PP-332 ERRα/β/γ Agonist for Doping-Control Purposes. Drug Test Anal. 2026;18(3):439-450. PMID: 41688415.
26. Huss JM, Imahashi K, Dufour CR, Weinheimer CJ, Courtois M, Kovacs A, Giguère V, Murphy E, Kelly DP. The nuclear receptor ERRalpha is required for the bioenergetic and functional adaptation to cardiac pressure overload. Cell Metab. 2007;6(1):25-37. PMID: 17618854.
27. World Anti-Doping Agency. Prohibited List 2027 (in effect January 1, 2027), French edition with track changes, August 26, 2026, and Summary of Major Modifications and Explanatory Notes, 2027 Prohibited List, August 17, 2026: wada-ama.org/sites/default/files/2026-09/2027list_final_fr_track_changes_26_august_2026.pdf and 2027_list_explanatory_note_en_final_17_august_2026_1.pdf, read October 12, 2026 in the Internet Archive’s copies captured October 9, 2026 (web.archive.org). The List’s English edition was not available there and was not read.

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