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SLU-PP-332

Estrogen-Related Receptor (ERR) Agonist for Metabolic and Mitochondrial

Function

SLU-PP-332 is a synthetic small-molecule compound developed as a potent pan-agonist of the estrogen-related receptors (ERRs) a family of orphan nuclear receptors that serve as master regulators of mitochondrial function, oxidative metabolism, and cellular energy production. Developed through a structure-based design approach at Saint Louis University and the University of Health Sciences and Pharmacy in St. Louis, SLU-PP-332 represents the first synthetic ERR agonist with sufficient potency at ERRα and appropriate pharmacokinetic properties for in vivo use. Research positions SLU-PP-332 as an exercise-mimetic metabolic agent, meaning it activates many of the same intracellular pathways triggered by endurance training without directly stimulating the nervous system. Unlike stimulants or hormones, SLU-PP-332 works at the gene- regulatory level, influencing how cells generate and use energy. The compound has demonstrated preclinical efficacy in enhancing exercise endurance, increasing fatty acid oxidation, reducing fat mass, improving insulin sensitivity, and ameliorating heart failure in animal models. It is important to note that SLU-PP-332 is not a peptide in the traditional sense it is a small- molecule synthetic compound with a defined chemical structure. All published evidence is preclinical, with no human clinical trials conducted as of this writing. A startup company, Pelagos Pharmaceuticals, has been co-founded by the compound’s developers to pursue further development and eventual clinical translation.

Compound Information

Property Detail Compound Name SLU-PP-332 Synonyms ERR pan-Agonist 332, SR9861 CAS Number 303760-60-3 Chemical Name (E)-4-Hydroxy-N’-(naphthalen-2-ylmethylene)benzohydrazide Molecular Formula C₁₈H₁₄N₂O₂ Molecular Weight 290.32 Da Classification Synthetic small-molecule pan-ERR agonist (exercise mimetic) Primary Target ERRα (EC₅₀ = 98 nM), ERRβ (EC₅₀ = 230 nM), ERRγ (EC₅₀ = 430 nM) Selectivity Selective over ERα, ERβ, and other closely related nuclear receptors

Physical Form White to beige powder

How It Works

SLU-PP-332 operates through a fundamentally different mechanism than stimulants, hormones, or traditional performance-enhancing compounds. Rather than forcing energy output or modulating neurotransmitters, it acts at the level of gene transcription to improve the cellular machinery responsible for energy production.

Estrogen-Related Receptors: The Master Metabolic Regulators

ERRα, ERRβ, and ERRγ are orphan nuclear receptors—transcription factors that belong to the nuclear hormone receptor superfamily but have no known natural hormone ligand. Despite their name, ERRs are not activated by estrogen and do not participate in estrogen signaling. They are, however, structurally related to estrogen receptors, which is how they received their designation. ERRs are highly expressed in energy-demanding tissues including skeletal muscle, heart, brown adipose tissue, brain, and kidneys. These receptors regulate the expression of hundreds of genes controlling mitochondrial biogenesis, fatty acid oxidation, oxidative phosphorylation, the tricarboxylic acid (TCA) cycle, and skeletal muscle metabolic flexibility. ERRα in particular governs exercise-induced stress adaptation and physiological adaptations that occur in response to endurance training. Genetic studies have shown that mice lacking ERRα or ERRγ develop reduced muscle oxidative function, diminished exercise endurance, and even lethal cardiomyopathy.

Pan-ERR Agonism and Receptor Activation

SLU-PP-332 binds to and activates all three ERR isoforms, with highest potency at ERRα (EC₅₀ = 98 nM), followed by ERRβ (EC₅₀ = 230 nM) and ERRγ (EC₅₀ = 430 nM). The compound stabilizes the active conformation of the receptors and promotes recruitment of coactivator proteins, particularly PGC-1α (peroxisome proliferator-activated receptor gamma coactivator 1- alpha), which is itself a master regulator of mitochondrial biogenesis. SLU-PP-332 displays selectivity over estrogen receptor alpha (ERα), estrogen receptor beta (ERβ), and several other closely related nuclear receptors, meaning it does not produce estrogenic effects.

Induction of the Acute Aerobic Exercise Genetic Program

One of SLU-PP-332’s most distinctive features is its ability to induce an acute aerobic exercise genetic program in skeletal muscle via ERRα-dependent activation. This program centers on the upregulation of DDIT4 (DNA damage-inducible transcript 4), a key protein induced after short bouts of aerobic exercise that is responsible for triggering a cascade of physiological adaptations to exercise. This activation leads to increased expression of genes involved in mitochondrial biogenesis, oxidative phosphorylation, and fatty acid metabolism—effectively mimicking what happens in muscle tissue after endurance training.

Mitochondrial Biogenesis and Enhanced Respiration

SLU-PP-332 increases mitochondrial function and cellular respiration in skeletal muscle cell lines (C2C12 myotubes). This includes increased basal and maximal oxygen consumption rates, improved respiratory control ratios (the ratio of ATP-linked respiration to proton leak), enhanced oxidative phosphorylation coupling efficiency, and increased expression of the ERR target gene pyruvate dehydrogenase kinase 4 (Pdk4). The result is not merely more mitochondria, but mitochondria that operate with improved metabolic efficiency.

Muscle Fiber-Type Transition

When administered to mice, SLU-PP-332 increased the proportion of type IIa oxidative skeletal muscle fibers—the fatigue-resistant fibers associated with endurance capacity. This shift toward a more oxidative muscle phenotype is a hallmark adaptation of endurance training, further supporting SLU-PP-332’s classification as an exercise mimetic.

Cardiac Metabolic Regulation

In cardiac tissue, ERRα and ERRγ serve as central regulators of energy metabolism. The normal adult myocardium derives 60–90% of its ATP from fatty acid oxidation. SLU-PP-332 and the related compound SLU-PP-915 activate cardiac fatty acid oxidation programs, upregulating fatty acid transporters (CD36), beta-oxidation enzymes (acyl-CoA dehydrogenases), and carnitine shuttle components. In pressure overload heart failure models, this metabolic reprogramming restored fatty acid profiles toward healthy patterns and normalized TCA cycle intermediates. Genetic knockdown studies identified ERRγ as the primary mediator of these cardioprotective effects.

Benefits

SLU-PP-332’s mechanism of action produces a broad spectrum of preclinical metabolic benefits. Rather than forcing energy output, the compound improves the capacity of cells to produce and sustain energy.

Enhanced Mitochondrial Function

and brown fat

supply

Increased Fat Oxidation and Metabolic Flexibility

Exercise-Mimetic Effects

Cardiometabolic Support

Glucose Metabolism and Insulin Sensitivity

Anti-Obesity Effects

Emerging Applications

women (human primary cell culture study)

penetrant properties

and muscle-wasting conditions

What the Science Shows

SLU-PP-332 has been evaluated in a growing body of peer-reviewed preclinical research from leading academic institutions. The following summarizes the key published studies.

Billon et al. (2023) – Exercise Mimetic Discovery

Journal: ACS Chemical Biology, 18(4), 756–771

This foundational study reported the identification and characterization of SLU-PP-332 as a synthetic ERR pan-agonist with the highest potency for ERRα. In C2C12 skeletal muscle cells, SLU-PP-332 increased the expression of ERR target genes including Pdk4, enhanced mitochondrial respiration, and promoted mitochondrial biogenesis. When administered to C57BL/6J mice (30 mg/kg intraperitoneally), the compound demonstrated plasma exposure of 0.2 µM and muscle exposure of 0.6 µM at six hours post-injection. Mice treated with SLU-PP- 332 showed increased type IIa oxidative skeletal muscle fibers and significantly enhanced exercise endurance on treadmill testing. The study established that the exercise-enhancing effects were ERRα-dependent, as ERRα activation was critical for the observed improvements. The induction of an acute aerobic exercise genetic program was unique to ERR agonists and was not reported for other exercise-mimetic targets such as PPARδ or REV-ERB.

Billon et al. (2024) – Metabolic Syndrome Treatment

Journal: Journal of Pharmacology and Experimental Therapeutics, 388(2), 232–240 This study examined SLU-PP-332’s effects in mouse models of obesity and metabolic syndrome. Diet-induced obese (DIO) C57BL/6J mice and ob/ob mice were administered SLU-PP-332 at 50 mg/kg intraperitoneally, twice daily, for 28 days (DIO) or 12 days (ob/ob). The compound mimicked exercise-induced benefits on whole-body metabolism, including increased energy expenditure, enhanced fatty acid oxidation, and decreased fat mass accumulation without changes in food intake. In DIO mice, SLU-PP-332 reduced liver triglyceride content, decreased adipocyte size in white adipose tissue, and improved glucose tolerance. In ob/ob mice, the compound increased fatty acid metabolism and energy expenditure. Muscle glycogen content increased and in vivo muscle glucose uptake improved in treated animals. Blood lipid profiles and liver enzyme levels showed favorable changes. The study concluded that pharmacological activation of ERR may be an effective method to treat metabolic syndrome and obesity.

Xu et al. (2024) – Heart Failure Treatment

Journal: Circulation, 149(3), 227–250

This landmark study from Baylor College of Medicine investigated the cardioprotective effects of two structurally distinct pan-ERR agonists SLU-PP-332 and SLU-PP-915 in a pressure overload-induced heart failure model. Eight-week-old mice underwent transaortic constriction (TAC) surgery and were administered ERR agonists by intraperitoneal injection for six weeks. Both compounds significantly improved ejection fraction, ameliorated cardiac fibrosis, and increased survival in heart failure mice—without affecting cardiac hypertrophy. RNA sequencing revealed that ERR agonists transcriptionally activated a broad spectrum of metabolic genes, particularly those involved in fatty acid metabolism and mitochondrial function. Metabolomics analysis showed substantial normalization of metabolic profiles in fatty acid/lipid and TCA cycle/oxidative phosphorylation metabolite pathways. Genetic knockdown experiments identified ERRγ (not ERRα) as the primary mediator of the cardioprotective effects. The authors noted that this study opens avenues to pursue ERR agonists with improved pharmacological properties for heart failure therapy.

Losby et al. (2024) – Autophagy Regulation

Journal: Molecular Pharmacology

This study demonstrated that ERR agonists, including SLU-PP-332, regulate autophagy through the transcription factor TFEB (transcription factor EB). This adds another dimension to the compound’s mechanism, as autophagy—the cellular self-cleaning process—is a critical mediator of exercise-induced health benefits and plays a role in protein quality control, mitochondrial turnover, and cellular stress resistance.

Frontiers in Physiology (2025) – Human Primary Cell Study

Journal: Frontiers in Physiology (Pilot Study) In a noteworthy pilot study, researchers set up primary myoblast cultures isolated from muscle tissue of physically inactive elderly women undergoing hip arthroplasty. Treatment with SLU- PP-332 significantly reduced LDH release (a marker of cell damage), decreased reactive oxygen species (ROS) production, reduced senescence-associated beta-galactosidase activity (a marker of cellular aging), and increased glutathione (GSH) levels. SLU-PP-332 also promoted upregulation of FNDC5 (the precursor of irisin, an exercise-induced myokine), activated Akt and Bcl-2 anti-apoptotic pathways, and positively influenced myotube formation and myosin heavy- chain expression during differentiation. This study represents the first evidence of SLU-PP-332’s effects in human primary cell cultures and confirms that ERR activation can reverse age-related alterations in human muscle cells from inactive individuals.

Wang et al. (2023) – Aging Kidney Protection

This study demonstrated that estrogen-related receptor agonism reversed mitochondrial dysfunction and inflammation in the aging kidney, showing anti-fibrotic and rejuvenating effects. These findings extend the potential therapeutic applications of ERR agonists beyond skeletal muscle and heart to renal health in aging.

Anti-Doping Considerations

Journal: Rapid Communications in Mass Spectrometry (2026)

Möller, Krug, and Thevis published in vitro metabolism and analytical characterization data for SLU-PP-332 and SLU-PP-915, explicitly noting the doping potential of these novel pan-ERR agonists. This signals that the World Anti-Doping Agency (WADA) is monitoring these compounds, and they are expected to be banned in competitive sports due to their clear exercise- mimetic and performance-enhancing properties.

Research Dosing Protocol

Important: No human dosing has been established through clinical trials. All dosing information below is derived from preclinical animal studies and is provided for educational and research reference purposes only. SLU-PP-332 is a research compound, not an approved therapeutic.

Preclinical Dosing Reference

Model Dose Route Duration/Notes C57BL/6J (lean) 30 mg/kg IP injection Single dose PK study; plasma 0.2 µM, muscle 0.6 µM at 6 hr C57BL/6J (lean) 50 mg/kg BID IP injection 28 days; exercise endurance enhancement DIO mice (obese) 50 mg/kg BID IP injection 28 days; metabolic syndrome treatment ob/ob mice 50 mg/kg BID IP injection 12 days (shortened due to IP tolerance); energy expenditure increase TAC heart failure 50 mg/kg BID IP injection 6 weeks; cardiac function improvement C2C12 cells 10 µM In vitro Mitochondrial respiration and gene expression studies

Oral Bioavailability Considerations

One of the most important practical considerations with SLU-PP-332 is oral bioavailability. Based on available preclinical data, oral bioavailability appears low to moderate, with first-pass hepatic metabolism likely reducing circulating levels significantly. Higher oral doses would be required to achieve meaningful systemic exposure compared to injection. This is not because the compound is weak—it is highly potent at the receptor level (EC₅₀ = 98 nM for ERRα) but because absorption efficiency limits how much reaches the target tissues after oral ingestion.

Why DMSO Injection Should Be Avoided

Some experimental users have attempted to inject SLU-PP-332 dissolved in DMSO. This approach is strongly discouraged for several reasons: DMSO is a powerful transdermal and systemic carrier capable of transporting contaminants directly into the bloodstream; injection

with DMSO bypasses natural metabolic safeguards; no safety data exists for injectable SLU-PP- 332 in humans; and the risk profile increases dramatically without improving the underlying biology. From a research-safety standpoint, oral administration at appropriately scaled doses is far more defensible than attempting injectable delivery with aggressive solvents.

Side Effects

SLU-PP-332 has demonstrated a favorable safety profile in published preclinical studies, though the evidence base is still relatively limited compared to compounds with longer research histories.

Preclinical Safety Data

composition shifted toward less fat, but overall weight was stable)

showed favorable changes or no adverse effects in treated mice

major safety signals

Tolerability Concerns

reduced tolerance of twice-daily intraperitoneal injections—likely related to the injection procedure itself rather than the compound

administration; oral tolerability in long-term studies has not been fully characterized

Theoretical Safety Considerations

target effects, including potential cardiac hypertrophy risk with chronic ERRγ overactivation. However, the heart failure study (Xu et al., 2024) showed improved cardiac function without worsening hypertrophy.

long-term oncological monitoring, though SLU-PP-332 actually downregulated cell-cycle genes in cardiac cells in vitro

pan-ERR agonists, though published data on SLU-PP-332 shows favorable liver enzyme profiles

humans

What SLU-PP-332 Is Not

SLU-PP-332 is not a stimulant, not a hormone, not a traditional fat-burner, and not a replacement for training or nutrition. It does not produce jitteriness, appetite suppression through CNS mechanisms, hormonal disruption, or the side-effect profiles associated with those compound classes. Its effects are gradual and adaptive, not acute.

Contraindications and Precautions

Because SLU-PP-332 has not undergone human clinical trials, formal contraindications have not been established. The following precautions are based on the compound’s mechanism of action and general pharmacological principles.

cannot be recommended during pregnancy or nursing.

breast cancer). While ERR agonism in skeletal muscle and heart appears beneficial, the effects of pan-ERR activation on existing tumors are not characterized and could theoretically promote tumor metabolism.

individuals with pre-existing cardiac conditions should exercise extreme caution, as the compound’s effects on human cardiac tissue are unknown.

liver function may have altered drug exposure and should not use this compound without medical supervision.

governing bodies due to its clear exercise-mimetic and performance-enhancing properties. Anti-doping detection methods are already under development.

agonists, REV-ERB ligands), diabetes medications (due to glucose-lowering effects), and lipid-lowering agents have not been characterized.

Comparison with Related Compounds

SLU-PP-332 belongs to a growing class of exercise-mimetic and metabolic-enhancing compounds. The following table contextualizes its position relative to other agents.

Compound Mechanism Strengths Limitations SLU-PP-332 Pan-ERR agonist Potent exercise mimicry, Low oral bioavailability, (ERRα/β/γ); exercise- fat oxidation, cardiac preclinical only, no human mimetic gene program protection, non-hormonal, data, WADA concern activation non-stimulant GW501516 PPARδ agonist; fatty Oral bioavailability, well- Withdrawn from acid oxidation and studied exercise mimetic, development due to cancer endurance enhancement potent endurance effects concerns in long-term animal studies; WADA-banned SR9009/SR9011 REV-ERB agonist; Increases energy Very low oral circadian metabolism expenditure, reduces fat, bioavailability, short half- regulation modulates circadian life, recent concerns about rhythm off-target effects AICAR AMPK activator; mimics Well-characterized AMPK Requires injection, limited energy depletion pathway, promotes glucose muscle-specific effects, signaling uptake and fat oxidation WADA-banned GSK4716 ERRβ/γ agonist (no Earlier-generation ERR No ERRα activity, limited ERRα activity) agonist; proof-of-concept potency (EC₅₀ 215–340 nM), tool not suitable for in vivo use 5-Amino-1MQ NNMT inhibitor; NAD+ Oral bioavailability, Different mechanism class, salvage pathway reduces fat cell size, limited human data, does not modulation supports metabolic health directly mimic exercise

SLU-PP-332’s distinguishing feature is its activation of the acute aerobic exercise genetic program via ERRα, which was not reported for PPARδ or REV-ERB agonists. Additionally, unlike GW501516, SLU-PP-332 has not shown carcinogenic signals in preclinical studies, though long-term oncological data is limited. The compound’s cardiac benefits represent a unique therapeutic advantage not shared by other exercise mimetics.

Success Tips

Based on preclinical evidence and the compound’s pharmacological profile, the following considerations may help optimize research outcomes with SLU-PP-332.

Set Appropriate Expectations

context.

output.

required.

Optimize the Metabolic Environment

PP-332 with endurance training may produce synergistic metabolic adaptations.

the mitochondrial biogenesis programs that SLU-PP-332 activates.

excessive refined carbohydrates) create a favorable metabolic environment for ERR agonist effects.

during rest.

Practical Research Considerations

purity) and certificates of analysis.

involving DMSO.

pharmacokinetic property, not a reflection of compound potency.

section).

comprehensive metabolic optimization strategy.

Storage and Handling

Powder Storage

Solution Preparation and Storage

may be required for full dissolution).

appropriate co-solvents.

→ Tween 80 → distilled water, ensuring clarity at each step.

windows per the certificate of analysis.

General Handling

may vary.

recommended handling procedures.

Legal Status

FDA and Regulatory Status

SLU-PP-332 is not an FDA-approved drug. It has not undergone human clinical trials and does not hold an approved New Drug Application (NDA) or Investigational New Drug (IND) designation in public records. The compound remains in the preclinical research stage. A startup company, Pelagos Pharmaceuticals, has been co-founded by the compound’s developers (based at Washington University and the University of Health Sciences and Pharmacy in St. Louis) to pursue further development, with the goal of eventual clinical translation. No clinical trial registrations for SLU-PP-332 appear on ClinicalTrials.gov as of this writing.

Research Chemical Classification

SLU-PP-332 is available from laboratory chemical suppliers (including Sigma-Aldrich, Cayman Chemical, Tocris, MedChemExpress, and Selleck Chemicals) as a research chemical for laboratory use only. Products are labeled “not for human consumption” and “for research use only.” It is not classified as a dietary supplement, food additive, or pharmaceutical product.

Anti-Doping Status

SLU-PP-332 is expected to be prohibited by the World Anti-Doping Agency (WADA) and sports governing bodies. Anti-doping researchers have already published in vitro metabolism and analytical detection methods for SLU-PP-332 and SLU-PP-915 (Möller, Krug & Thevis, 2026), explicitly noting the doping potential of these compounds. Competitive athletes should consider SLU-PP-332 a prohibited substance.

Product Source: For pharma-grade research compounds that are third party tested and have the highest purity: www.Biolongevitylabs.store Researchers can use the code “JFDISCOUNT” at checkout for 15% off. Get SLU-PP-332 here

Frequently Asked Questions

What exactly is SLU-PP-332? SLU-PP-332 is a synthetic small-molecule compound (not a peptide in the traditional sense) that activates estrogen-related receptors (ERRs)—a family of orphan nuclear receptors that regulate mitochondrial function, fatty acid oxidation, and energy metabolism. It mimics the cellular and metabolic effects of endurance exercise at the gene-regulatory level. Is SLU-PP-332 a hormone or does it affect estrogen? No. Despite the name “estrogen-related receptor,” ERRs are not activated by estrogen and do not participate in estrogen signaling. SLU-PP-332 is selective for ERRs over estrogen receptors (ERα and ERβ) and does not produce estrogenic effects. The naming reflects structural similarity to estrogen receptors, not functional overlap. Can SLU-PP-332 replace exercise? In preclinical models, SLU-PP-332 reproduces many of the metabolic and gene-expression changes associated with endurance exercise, but it does not replicate all benefits of physical activity. Exercise provides mechanical loading (important for bone and connective tissue health), cardiovascular conditioning, neurological benefits, and psychological well-being that a compound cannot fully replace. SLU-PP-332 is best understood as a research tool for studying exercise-mimetic signaling, not as a substitute for physical activity. Has SLU-PP-332 been tested in humans? No published human clinical trials exist as of this writing. All data is preclinical (animal models and cell culture). One pilot study used SLU-PP-332 on human primary myoblast cultures isolated from elderly women, showing promising results, but this is not the same as a human clinical trial. The developers have co-founded Pelagos Pharmaceuticals to pursue clinical development. Why is the oral dose higher than what might be expected for such a potent compound? SLU-PP-332 is highly potent at the receptor level (EC₅₀ = 98 nM for ERRα), but its oral bioavailability is low to moderate due to first-pass hepatic metabolism. This means a larger oral dose is needed to achieve sufficient systemic and tissue exposure. All published animal studies used intraperitoneal injection to bypass this limitation. Higher oral dosing is a pharmacokinetic consideration, not a sign of compound weakness. Will SLU-PP-332 be banned in sports? Almost certainly. Anti-doping researchers have already published detection methods for SLU- PP-332, and its clear exercise-mimetic, endurance-enhancing, and fat-oxidation properties place

it squarely in the category of performance-enhancing substances. WADA monitoring is expected, and formal prohibition is likely. How does SLU-PP-332 compare to GW501516 (Cardarine)? Both are exercise mimetics that enhance fatty acid oxidation and endurance, but they act through different targets (ERR vs. PPARδ). GW501516 was withdrawn from pharmaceutical development due to cancer concerns in long-term rodent studies. SLU-PP-332 has not shown carcinogenic signals, though long-term oncological data is limited. SLU-PP-332 additionally offers cardiac benefits that GW501516 does not provide. Both are WADA-prohibited.

Is SLU-PP-332 safe?

Preclinical data shows a favorable safety profile with no cytotoxicity, no adverse changes in blood chemistry, and no effects on food intake or activity levels. However, long-term safety in humans is entirely unknown. The compound has not been tested in human clinical trials, and any use outside of a research context carries unquantifiable risks.

References

1. Billon, C., Sitaula, S., Banerjee, S., Welch, R., Elgendy, B., Walker, J. K., & Burris, T. P. (2023). Synthetic ERRα/β/γ agonist induces an ERRα-dependent acute aerobic exercise response and enhances exercise capacity. ACS Chemical Biology, 18(4), 756–771. 2. Billon, C., Schoepke, E., Avdagic, A., Chatterjee, A., Butler, A. A., Elgendy, B., Walker, J. K., & Burris, T. P. (2024). A synthetic ERR agonist alleviates metabolic syndrome. Journal of Pharmacology and Experimental Therapeutics, 388(2), 232–240. 3. Xu, W., Billon, C., Li, H., Wilderman, A., Qi, L., Graves, A., et al. (2024). Novel pan-ERR agonists ameliorate heart failure through enhancing cardiac fatty acid metabolism and mitochondrial function. Circulation, 149(3), 227–250. 4. Losby, M., et al. (2024). The estrogen receptor-related orphan receptors regulate autophagy through TFEB. Molecular Pharmacology. 5. Wang, X., et al. (2023). Estrogen-related receptor agonism reverses mitochondrial dysfunction and inflammation in the aging kidney. The American Journal of Pathology. 6. Silvestri, M., Fantini, C., Duranti, G., Grazioli, E., et al. (2025). Targeting ERRs to counteract age-related muscle atrophy associated with physical inactivity: a pilot study. Frontiers in Physiology. 7. Möller, T., Krug, O., & Thevis, M. (2026). In vitro metabolism and analytical characterization of SLU-PP-332 and SLU-PP-915: novel pan-ERR agonists with doping potential. Rapid Communications in Mass Spectrometry, 40(8). 8. Nasri, H. (2024). New hopes on “SLU-PP-332” as an effective agent for weight loss with indirect kidney protection efficacy; a nephrology point of view. Journal of Renal Endocrinology, 10(1), e25143. 9. Rangwala, S. M., et al. (2010). Estrogen-related receptor alpha is essential for the expression of antioxidant protection genes and mitochondrial function. Biochemical and Biophysical Research Communications. 10. Fan, W., He, N., Lin, C. S., et al. (2018). ERRγ promotes angiogenesis, mitochondrial biogenesis, and oxidative remodeling in PGC1α/β-deficient muscle. Cell Reports.

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