SLU-PP-332 Research, Specifications & Scientific Information

Introduction

SLU-PP-332 exists because a receptor family had no chemistry.

The estrogen-related receptors — ERRα, ERRβ and ERRγ — are orphan nuclear receptors: transcription factors named for their sequence resemblance to the estrogen receptor, which do not bind estrogen and whose natural ligands, if any, remain unidentified. Genetic work had implicated them in the aerobic capacity of skeletal musculature. What the field lacked was a molecule that could switch them on, and ERRα in particular had resisted attempts to design an agonist for it ^[1].

SLU-PP-332 was reported in 2023 as a pan-agonist across all three subtypes, with the highest potency at ERRα and with pharmacokinetic properties adequate to serve as a chemical tool in mice ^[1]. It is three years old. It has no human data of any kind.

This page is a reference record of a young, entirely preclinical literature. It describes research. It contains no guidance of any kind on handling the material.

What Is SLU-PP-332?

A synthetic small molecule of molecular formula C18H14N2O2 and molecular weight 290.3 g/mol. Not a peptide, and listed in this library under peptide-adjacent research compounds.

Chemically it is an acylhydrazone: a 4-hydroxybenzoyl group joined through a hydrazide nitrogen to the carbon of naphthalene-2-carbaldehyde, with the resulting C=N double bond in the E configuration. Compounds of this class are made by condensing a hydrazide with an aldehyde, and the linkage they form is reversible under acidic aqueous conditions — a property worth knowing for any material handled in solution rather than as a solid.

The registers carry it under UNII 5YW57G7ADL, CAS registry number 303760-60-3 and PubChem compound identifier 5338394. It also appears in the literature as SR9861.

The compound's own authors describe it as a chemical tool: a molecule built to make experiments possible rather than a candidate medicine. That framing is accurate and this page keeps it.

It is not an approved medicine anywhere and has never been studied in a clinical trial.

SLU-PP-332 Specifications

SLU-PP-332 is a small synthetic molecule, not a peptide. PubChem carries it as compound identifier 5338394 with molecular formula C18H14N2O2 and a molecular weight of 290.3 g/mol, and the FDA/NCATS Global Substance Registration System carries the same structure under UNII 5YW57G7ADL with CAS registry number 303760-60-3 and the systematic name 4-hydroxybenzoic acid 2-(2-naphthalenylmethylene)hydrazide. Structurally it is an acylhydrazone: a 4-hydroxybenzoyl group joined through a hydrazide linkage to a naphthalene-2-carbaldehyde, with the C=N double bond in the E configuration. Acylhydrazones of this kind are formed by condensation of a hydrazide with an aldehyde and the linkage is reversible under acidic aqueous conditions, which is a chemical property worth knowing for a compound supplied as a solid and handled in solution. The compound also appears in the literature under the alternative code SR9861. No separate salt form is recorded.

Values that a public register does not carry are shown as not publicly characterised rather than estimated. Identifiers are reference values; the certificate of analysis supplied with a laboratory order is the record for a given lot.

How Does SLU-PP-332 Work?

By activating transcription factors, which means its proximate effect is a change in which genes are read.

The estrogen-related receptors are nuclear receptors of the NR3B subfamily. Like other nuclear receptors they bind DNA at specific response elements and regulate transcription; unlike the classical hormone receptors, no endogenous ligand has been established for them, which is what makes them orphans. They are known instead through genetics — what happens when they are removed or overexpressed — and that genetic evidence pointed at oxidative metabolism and at the aerobic capacity of skeletal musculature.

SLU-PP-332 agonises all three subtypes, with the greatest potency at ERRα ^[1]. The consequences reported downstream are transcriptional and metabolic: increased mitochondrial function and cellular respiration in a skeletal myocyte line, and in mice a shift in fibre composition and a transcriptional programme resembling the acute response to aerobic exercise.

The important qualifier is scope. Every statement in the preceding paragraph comes from cultured cells and from mice. No human study of this compound has been identified, so nothing is known about whether any of it happens in a person.

SLU-PP-332 Mechanism of Action

In vitro research

The 2023 characterisation established the compound's receptor profile and its cellular effects in one paper.

Receptor profile. An agonist at ERRα, ERRβ and ERRγ, with the highest potency at ERRα. That last part is the achievement the authors emphasise, because ERRβ and ERRγ agonists already existed while ERRα agonist activity had proved difficult to design ^[1].

Cellular effects. In a skeletal muscle cell line, the compound increased mitochondrial function and cellular respiration ^[1].

Adequacy as a tool. The compound was reported to have sufficient pharmacokinetic properties to be used as an in vivo chemical tool — the minimum requirement for a molecule intended to answer questions in animals rather than in wells ^[1].

Subsequent chemistry from the same lineage has optimised the scaffold, both to improve properties and to use the resulting series as a probe of receptor signalling ^[7]. A successor compound, SLU-PP-915, was reported in 2026 as orally active ^[5] — a description that implies a limitation of the parent, since a property worth announcing in a successor is one the predecessor lacked.

Separately, the compound's in vitro metabolism has been characterised analytically, in work directed at detecting it and its successor in antidoping testing ^[6]. That paper is cited here because it is a fact about the compound's circulation outside research settings, and because it is part of the published record.

What Is SLU-PP-332 Being Researched For?

Four lines, all preclinical, all recent.

• Aerobic capacity of skeletal musculature. The founding line, and the one the compound was built for ^[1].
• Metabolic syndrome and obesity models. Effects in diet-induced obese and ob/ob mice ^[3].
• Cardiac failure models. Pan-ERR agonists examined for effects on cardiac fatty acid metabolism and mitochondrial function ^[4].
• The ageing kidney. Estrogen-related receptor agonism against mitochondrial dysfunction and inflammation ^[2].

There is no human research on this compound: no clinical trial, no registered study, no published human pharmacokinetics. That absence is the central fact about its evidence base and this page does not soften it.

One further point of context. The senior authors of the founding paper declare stock in a company focused on therapeutics based on these receptors, and the principal mouse studies come from a small set of collaborating groups. Declared interests are not a reason to discount a result — they are declared precisely so a reader can weigh it — but on a three-year-old literature with no independent human data, the concentration of authorship is part of the evidential picture.

Preclinical Research on SLU-PP-332

Animal research

Skeletal musculature and endurance. When administered to mice, the compound increased type IIa oxidative skeletal muscle fibres and enhanced exercise endurance. It induced an ERRα-specific acute aerobic exercise genetic programme, and — this is the part that makes the study informative rather than merely suggestive — ERRα activation was shown to be critical for the endurance enhancement ^[1].

Why that control matters. A compound that produces a phenotype might be doing so through its intended target or through something else entirely. Demonstrating that removing the target abolishes the phenotype ties the two together. Few of the preclinical-only compounds in this library have an equivalent experiment behind them, and it is the strongest single feature of this one's evidence base.

Metabolic syndrome models. In diet-induced obese and in ob/ob mice, administration was reported to increase whole-body energy expenditure and fatty acid oxidation, accompanied by decreased fat mass accumulation, with reduced obesity and improved insulin sensitivity in the metabolic syndrome models ^[3].

Cardiac and renal models. Pan-ERR agonists were reported to ameliorate heart failure in model systems through enhanced cardiac fatty acid metabolism and mitochondrial function ^[4], and estrogen-related receptor agonism was examined against mitochondrial dysfunction and inflammation in the ageing kidney ^[2].

Findings described in this section were observed in animals, and nothing in them establishes anything about humans. Diet-induced obesity in mice in particular has a long record of producing results that do not survive translation.

Current Research Status

Status as of September 22, 2026. This block is rendered from maintained fields, not from prose, so it cannot go stale in one place and stay current in another.

SLU-PP-332 vs Related Compounds

The comparisons below are mechanistic and evidential. No comparison of effect is made on this page.

AICAR :: The other compound in this library whose literature uses similar language about metabolic adaptation. The contrast in evidence is the point: AICAR has a completed, adequately powered phase 3 trial that returned a clear null, while SLU-PP-332 has no human data at all. Neither of those is the same as evidence of benefit.

Target class

SLU-PP-332 acts on nuclear receptors — transcription factors that regulate gene expression directly. AICAR acts on a kinase, indirectly, through a metabolite. 5-Amino-1MQ inhibits a methyltransferase. Three different mechanisms converging on overlapping metabolic questions.

SLU-PP-915

A successor compound from the same series, reported as orally active ^[5]. It is a separate substance and its findings are evidence about it.

Evidence position

Three years of literature, no human studies, concentrated authorship with declared commercial interests, and one strong genetic control experiment. That is an accurate summary and it is neither a recommendation nor a dismissal.

Chemical & Molecular Characteristics

The register record is straightforward. UNII 5YW57G7ADL, CAS registry number 303760-60-3, PubChem compound identifier 5338394, molecular formula C18H14N2O2, molecular weight 290.3 g/mol. The register's systematic name, 4-hydroxybenzoic acid 2-(2-naphthalenylmethylene)hydrazide, describes the same structure as PubChem's.

The geometry is part of the identity. The C=N bond of the hydrazone is specified as E. Acylhydrazones can in principle exist as E and Z isomers, so a structure quoted without stereochemistry is incomplete for this class of compound.

The linkage is condensation chemistry. An acylhydrazone is formed from a hydrazide and an aldehyde with loss of water, and the reaction is reversible under acidic aqueous conditions. That is a property of the bond type rather than an observation about any particular preparation, and it is the reason the analytical documentation for a given lot is the record of what that lot contains.

Two codes, one molecule. SLU-PP-332 and SR9861 refer to the same compound. No salt form is separately registered.

The sequence fields are blank because there is no sequence. This is a 290-dalton synthetic organic molecule containing no amino acids. It is grouped with the peptides in this library by the research questions asked of it, not by any structural relationship.

Frequently Asked Questions

Scientific References

1. Billon C, Sitaula S, Banerjee S, et al.. Synthetic ERRα/β/γ Agonist Induces an ERRα-Dependent Acute Aerobic Exercise Response and Enhances Exercise Capacity ACS chemical biology; 2023. PMID 36988910 doi:10.1021/acschembio.2c00720
2. Wang XX, Myakala K, Libby AE, et al.. Estrogen-Related Receptor Agonism Reverses Mitochondrial Dysfunction and Inflammation in the Aging Kidney The American journal of pathology; 2023. PMID 37717940 doi:10.1016/j.ajpath.2023.07.008
3. Billon C, Schoepke E, Avdagic A, et al.. A Synthetic ERR Agonist Alleviates Metabolic Syndrome The Journal of pharmacology and experimental therapeutics; 2024. PMID 37739806 doi:10.1124/jpet.123.001733
4. Xu W, Billon C, Li H, et al.. Novel Pan-ERR Agonists Ameliorate Heart Failure Through Enhancing Cardiac Fatty Acid Metabolism and Mitochondrial Function Circulation; 2024. PMID 37961903 doi:10.1161/CIRCULATIONAHA.123.066542
5. Billon C, Appourchaux K, Côté I, et al.. An orally active estrogen receptor-related receptor agonist, SLU-PP-915, enhances aerobic exercise capacity The Journal of pharmacology and experimental therapeutics; 2026. PMID 41421047 doi:10.1016/j.jpet.2025.103787
6. 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 communications in mass spectrometry : RCM; 2026. PMID 41588687 doi:10.1002/rcm.70039
7. Okda HE, Zhao P, Hayes M, et al.. Chemical optimization of the exercise mimetic SLU-PP-332 enables insight into estrogen-related receptor signaling International journal of biological macromolecules; 2026. PMID 41850449 doi:10.1016/j.ijbiomac.2026.151450

Every identifier above is resolved against PubMed, Crossref or ClinicalTrials.gov at build time, and the title returned by the register is compared with the title stored here. A page does not publish if a reference fails to resolve.

Research-Use Information

For in vitro research use only. This material is a laboratory reagent. It is not a drug, food, dietary supplement, or cosmetic and is not for human or veterinary use, including ingestion, injection, or any other administration. No information on this page describes or implies any effect in humans or animals. Sold only to researchers under our Terms of Sale.