All information below describes the compound's chemical identity, laboratory handling, and the published research literature. It describes molecular targets and results in laboratory and animal models only — not effects in humans — and is not evidence of any human benefit.
What Is SLU-PP-332?
SLU-PP-332 is a synthetic small-molecule agonist of the estrogen-related receptors (ERRα, ERRβ, and ERRγ), a subfamily of orphan nuclear receptors. It was first described by Billon, Elgendy, Burris and colleagues at Saint Louis University — the source of the "SLU" prefix in its name. Chemically it is a naphthalenyl benzamide (IUPAC name 4-hydroxy-N-[(Z)-naphthalen-2-ylmethylideneamino]benzamide), not a peptide, and it does not occur in nature; it is a designed chemical probe used as a reference agonist in receptor-pharmacology research. Its reported in vitro potency is highest at ERRα (EC50 ≈ 98 nM), with additional activity at the β and γ isoforms.
It is supplied as a reference compound for in vitro and animal research use only. The sections below summarize its chemical identity, laboratory handling, the molecular targets and model systems examined in the published literature, and the primary references — without describing outcomes, efficacy, or effects in humans.
Research Targets & Pathways
Published preclinical literature has examined SLU-PP-332 in relation to several molecular systems. These are pathway associations reported in laboratory and animal models; refer to the cited studies for methods and findings.
- ERRα (estrogen-related receptor alpha) — the primary molecular target characterized in reporter-gene assays (EC50 ≈ 98 nM).
- ERRβ and ERRγ — the additional isoforms bound within the same nuclear-receptor subfamily, giving the compound its pan-ERR classification.
- PGC-1α / ERR transcriptional axis — examined as the coactivator context in which ERR transcription factors operate.
- Mitochondrial-biogenesis gene networks — studied via oxidative-phosphorylation (OXPHOS) and electron-transport-chain transcript panels.
- Fatty-acid-oxidation gene networks — examined in oxidative-tissue transcriptional assays.
Model Systems Studied
SLU-PP-332 has been used as a test compound across a range of published preclinical model systems, primarily in mice and in vitro cell assays. Refer to the cited literature for study designs, endpoints, and findings.
- Cell-based reporter assays — ERRα/β/γ luciferase reporter-gene systems used to characterize receptor activation.
- Metabolic-syndrome rodent models — diet-induced obese mice, leptin-deficient (ob/ob) mice, and normal-chow C57BL/6 mice.
- Cardiac models — the transaortic-constriction (TAC) pressure-overload mouse model.
- Skeletal-muscle and exercise-capacity assays — treadmill endurance testing and muscle oxidative-gene expression panels in mice.
- In vitro metabolism — hepatic-microsome metabolite-profiling systems developed for anti-doping detection.
Note: the in vivo SLU-PP-332 literature is early and centered on a small number of research groups; independent replication remains limited.
Stability & Handling
SLU-PP-332 is a defined small molecule supplied as a lyophilized powder, and it is handled differently from peptides. The published literature and supplier handling notes describe dissolution in an organic solvent (DMSO) to form a concentrated stock, followed by stepwise dilution into aqueous buffer or culture media for in vitro work. As a small molecule it is not subject to the proteolytic degradation that constrains peptide handling; however, it has limited aqueous solubility and is light- and moisture-sensitive as a dry powder, so aqueous dilutions are prepared fresh from the DMSO stock immediately before use.
Molecular & Technical Profile
C18H14N2O2 | MW 290.32 g/mol | CAS 303760-60-3 | PubChem CID 5338394
Storage, Reconstitution & Working Concentrations
Storage, reconstitution, and working-concentration values are general laboratory guidance for in vitro and animal research; always confirm against the lot-specific Certificate of Analysis. Note: the published in vivo SLU-PP-332 data are early-stage and independent replication remains limited.
Current Research Status
As of the time of this writing, SLU-PP-332 has not been approved by the U.S. Food and Drug Administration (FDA) for any human use, and no estrogen-related receptor (ERR) agonist of this class has been approved as a human drug product. The available evidence base is preclinical, derived from rodent and in vitro models, where the compound is often described in the literature as an "exercise mimetic" chemical probe. Translation to human clinical contexts has not been established through controlled clinical trials. The material described here is a research-grade chemical for laboratory use only and is not an approved drug product. Ongoing research continues to characterize the compound's receptor-pharmacology and metabolic-gene profile and to define which experimental findings may have translational relevance.
Research FAQ
Is SLU-PP-332 approved for human use?
No. SLU-PP-332 has not been approved by the FDA for any human use, and no ERR agonist has been approved as a human drug. The evidence base is preclinical (rodent and in vitro models), and the compound is supplied for laboratory research use only — not for human consumption.
What is SLU-PP-332's molecular formula and class?
A synthetic small-molecule pan-ERR agonist (not a peptide) — molecular formula C18H14N2O2, MW 290.32 g/mol, CAS 303760-60-3, PubChem CID 5338394; IUPAC name 4-hydroxy-N-[(Z)-naphthalen-2-ylmethylideneamino]benzamide.
How is SLU-PP-332 stored and prepared?
Store the powder at −20°C, desiccated and protected from light. Dissolve in DMSO to form a concentrated stock, then dilute into aqueous buffer or culture media; keep final DMSO at or below 0.1% v/v in assays and avoid repeated freeze–thaw of the stock.
What targets has SLU-PP-332 been studied for?
Preclinical work has characterized it as a pan-agonist of ERRα, ERRβ and ERRγ (highest reported in vitro potency at ERRα, EC50 ≈ 98 nM), examined within mitochondrial-biogenesis and fatty-acid-oxidation gene networks across metabolic-syndrome and cardiac rodent models. Note the early-stage, limited-replication caveat noted above.
Selected References
- Billon C, Sitaula S, Banerjee S, Welch R, Elgendy B, 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, Schoepke E, Avdagic A, et al. (2024). A Synthetic ERR Agonist Alleviates Metabolic Syndrome. Journal of Pharmacology and Experimental Therapeutics, 388(2):232–240.
- Xu W, Billon C, Li H, et al. (2024). Novel Pan-ERR Agonists Ameliorate Heart Failure Through Enhancing Cardiac Fatty Acid Metabolism and Mitochondrial Function. Circulation, 149(3):227–250.
- Giguère V. (2008). Transcriptional control of energy homeostasis by the estrogen-related receptors. Endocrine Reviews, 29(6):677–696.
- Avliyakulov N, et al. (2026). Analysis and Identification of In Vitro Metabolites of Exercise Mimetic SLU-PP-332 ERRα/β/γ Agonist for Doping-Control Purposes. Drug Testing and Analysis.