Mitochondrial Function & Respiration
In skeletal muscle cell lines, SLU-PP-332 increased mitochondrial function and cellular respiration. Research has examined induction of electron transport chain components and fatty-acid oxidation genes.
Overview
What is SLU-PP-332?
SLU-PP-332 is a synthetic small-molecule agonist of the estrogen-related receptors ERRα, ERRβ, and ERRγ, developed at Saint Louis University. Research has characterized it as an exercise mimetic: in mouse studies it activated an acute aerobic exercise gene program, increased mitochondrial function and cellular respiration in skeletal muscle cells, and shifted fiber-type composition toward oxidative Type IIa fibers. It is a small organic molecule rather than a peptide.
SLU-PP-332 (ERR Pan-Agonist 332) is supplied strictly as a reference material for in vitro and preclinical investigation. All characterization data described here is drawn from peer-reviewed literature and laboratory analysis; nothing herein constitutes a claim of clinical effect in humans.
Investigational Scope
Documented Research Areas
The following domains summarize directions explored across published studies and laboratory models. Each reflects observations reported in rodent models, in vitro systems, or the peer-reviewed record.
Acute Aerobic Exercise Program
Mouse studies documented an ERRα-dependent acute aerobic exercise transcriptional response, including induction of DDIT4, alongside measured increases in exercise endurance capacity.
Oxidative Fiber Specification
Research reported an increase in fast oxidative Type IIa fibers in treated mice, examined as a structural correlate of the compound's effects on endurance performance.
Obesity & Metabolic Syndrome Models
In diet-induced obese and leptin-deficient mouse models, treatment was associated with increased energy expenditure and fatty-acid oxidation, reduced fat-mass accumulation, and improved insulin sensitivity.
Proposed Mechanism
Mechanistic Pathway
Mechanistic steps below are hypothesized from in vitro assays and animal-model data reported in the literature. They describe biochemical interactions observed under controlled experimental conditions.
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1
Pan-ERR Receptor Agonism
SLU-PP-332 activates all three estrogen-related receptor isoforms with reported EC50 values of approximately 98 nM (ERRα), 230 nM (ERRβ) and 430 nM (ERRγ), with selectivity over ERα, ERβ and related nuclear receptors.
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2
ERRα / PGC-1 Transcriptional Program
ERRs partner with PGC-1 coactivators to drive transcription of mitochondrial biogenesis and oxidative metabolism genes, the axis through which the compound's metabolic effects have been attributed in published work.
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3
DDIT4 Induction
Induction of DDIT4 was identified as a marker of the acute exercise-response signature triggered by receptor activation, reported as ERRα-dependent in knockout comparisons.
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4
Fatty-Acid Oxidation Genes
Gene programs associated with fatty-acid oxidation and oxidative fiber specification were upregulated in treated muscle tissue, consistent with increased substrate utilization observed in metabolic assays.
Technical Data
Molecular Specifications
| Amino Acid Sequence | N/A — non-peptide small molecule |
|---|---|
| Molecular Weight | 290.3 g/mol |
| Molecular Formula | C₁₈H₁₄N₂O₂ |
| CAS Number | 303760-60-3 |
| Storage | −20°C long-term, protected from light and moisture |
References
Selected Literature
The following peer-reviewed references informed the research summaries on this page. Citations are provided for scientific context only.
- Billon C, et al. (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.
- Billon C, et al. (2024). A synthetic ERR agonist alleviates metabolic syndrome. Journal of Pharmacology and Experimental Therapeutics, 388(2), 232–240.
- Xu W, et al. (2024). Novel pan-ERR agonists ameliorate heart failure through enhancing cardiac fatty acid metabolism and mitochondrial function. Circulation, 149(3), 227–250.
- Wang XX, et al. (2023). Estrogen-related receptor agonism reverses mitochondrial dysfunction and inflammation in the aging kidney. American Journal of Pathology, 193(12), 1969–1987.
- Bonanni R, et al. (2025). Targeting ERRs to counteract age-related muscle atrophy associated with physical inactivity: a pilot study. Frontiers in Physiology, 16, 1616693.
Research Disclaimer
This product is intended strictly for laboratory research purposes only. It is not a drug, food, cosmetic, or dietary supplement and is not intended to diagnose, treat, cure, or prevent any disease. It is not for human or animal consumption. All information presented is derived from published scientific literature and is provided for educational reference only. By purchasing, the buyer affirms they are a qualified researcher or institution and assume full responsibility for the safe and lawful handling of this material.