Research Peptides
A high-purity research compound studied in oestrogen-related receptor and mitochondrial metabolism research. Coming soon in 5mg and 10mg, with every batch independently tested and dispatched from the UK.
A high-purity research compound studied in oestrogen-related receptor and mitochondrial metabolism research. Coming soon in 5mg and 10mg, with every batch independently tested and dispatched from the UK.
SLU-PP-332 UK is Crown Peptides’ synthetic small-molecule oestrogen-related receptor agonist research compound, coming soon in 5mg and 10mg for laboratory research.
Supplied for laboratory research purposes only — not for human consumption or for medical, veterinary or diagnostic use.
SLU-PP-332 is a small synthetic molecule, not a peptide, with the chemical name 4-hydroxy-N′-(naphthalen-2-ylmethylene)benzohydrazide. It switches on the three oestrogen-related receptors, ERR-alpha, ERR-beta and ERR-gamma, a family of nuclear receptors that control the genes cells use to build mitochondria and burn fat for energy. Earlier synthetic agonists activated only ERR-beta and ERR-gamma; SLU-PP-332 activates all three, with its strongest effect on ERR-alpha. It sits alongside MOTS-c and NAD+ in the metabolic and mitochondrial research area.
The compound was developed by Thomas Burris, Cyrielle Billon, John Walker and colleagues, with the chemistry carried out at Saint Louis University, reflected in its SLU prefix. It was described in full in 2023 as a redesign of an older GlaxoSmithKline compound that activated only two of the three receptors. Because it works on gene transcription rather than on an enzyme, it gives researchers a different angle on the “exercise mimetic” idea from AMPK-based tools such as AICAR. Most of the published evidence so far comes from mice and cultured cells, and it has not been tested in clinical trials.
Also known as: SLU PP 332, SLUPP332, SLU-PP332, ERR pan-agonist 332, (E)-4-hydroxy-N′-(naphthalen-2-ylmethylene)benzohydrazide
SLU-PP-332 was first reported in 2023, in a study combining structure-based chemistry, muscle cell experiments and mouse studies, including mice lacking ERR-alpha in skeletal muscle. (Learn more) Since then the same research network has tested it in models of obesity, heart failure and kidney ageing, and it is studied alongside other mitochondrial research compounds such as SS-31 and 5-Amino-1MQ.
The ERRs were the first “orphan” nuclear receptors to be found: they resemble the oestrogen receptors but do not bind oestrogen, and no natural ligand has been identified for them. They are active on their own, and their activity is tuned by partner proteins, above all the PGC-1 coactivators. A 2008 review sets out how ERR-alpha and ERR-gamma act as the main route for PGC-1 activity, controlling large networks of genes for fat and glucose metabolism and for building and running mitochondria, and how mice lacking each receptor cope poorly with physiological stress. (Learn more)
The first small-molecule ERR agonists were reported by GlaxoSmithKline in 2005. They belonged to a chemical family called phenolic acyl hydrazones, and the lead compound, GSK4716, activated ERR-beta and ERR-gamma but not ERR-alpha. (Learn more) Using the crystal structure of ERR-gamma bound to GSK4716, the Saint Louis group modelled the compound in ERR-alpha and redesigned it, gaining about 50-fold in ERR-alpha potency. In cell reporter assays SLU-PP-332 had half-maximal concentrations of 98 nanomolar at ERR-alpha, 230 at ERR-beta and 430 at ERR-gamma, and it did not alter the activity of the oestrogen receptors or other nuclear receptors tested. (Learn more)
In the C2C12 mouse muscle cell line, SLU-PP-332 raised the ERR target gene PDK4 and increased mitochondrial respiration. In mice it increased mitochondrial content and mitochondrial DNA in muscle and shifted fibres towards the oxidative type IIa. Treated sedentary mice ran about 70% longer and 45% further on a treadmill test than controls. RNA sequencing of muscle found a gene pattern that overlapped significantly with the pattern seen after a single bout of aerobic exercise. When the experiment was repeated in mice lacking ERR-alpha in skeletal muscle, the treadmill difference disappeared, showing that ERR-alpha was required for that effect. (Learn more)
In a 2024 follow-up, the group gave SLU-PP-332 to diet-induced obese mice and to ob/ob mice, which lack the hormone leptin. They reported higher energy expenditure and fatty acid oxidation, less fat accumulation and improved insulin sensitivity in these models. (Learn more)
A 2024 study tested SLU-PP-332 and a second, structurally different pan-ERR agonist, SLU-PP-915, in mice with heart failure caused by pressure overload. Both improved ejection fraction, reduced fibrosis and increased survival without changing heart enlargement, and they switched on genes for fatty acid metabolism and mitochondrial function. Genetic experiments showed that in the heart it was ERR-gamma, rather than ERR-alpha, that mainly carried the effect. (Learn more)
ERR levels fall in ageing human and mouse kidneys but were preserved in mice kept on lifelong caloric restriction. When 21-month-old mice were given SLU-PP-332 for eight weeks, the age-related rise in urine albumin, loss of podocytes, mitochondrial dysfunction and inflammatory signals through the cGAS-STING and STAT3 pathways were reversed, leading the authors to describe ERRs as caloric restriction mimetics in this model. (Learn more)
A 2025 pilot study took muscle biopsies from women having hip replacement surgery and grew myoblasts from the less active participants. In these cultured cells SLU-PP-332 raised SIRT1, PGC-1-alpha, ERR-alpha and FNDC5, lowered the oxidative enzyme NOX4, reduced markers of oxidative stress and senescence, and encouraged myotube formation. (Learn more)
Taken together, SLU-PP-332 is a well-defined chemical tool for studying ERR biology: a published structure with receptor-by-receptor potency data, genetic evidence of which receptor carries each effect, and a growing set of studies in muscle, metabolic, cardiac and kidney models. Nearly all of that work is in rodents and cultured cells, and much of it comes from a single research network.
Compound-level reference data. Batch-specific results appear on the Certificate of Analysis.
Work out concentration with the peptide calculatorCrown Peptides SLU-PP-332 will be supplied with batch-specific quality documentation appropriate to the material. Because SLU-PP-332 is an acyl hydrazone, a structure that can split back into its two building blocks, 4-hydroxybenzohydrazide and 2-naphthaldehyde, purity matters as much as identity: HPLC shows whether any of those breakdown products are present, while mass spectrometry confirms the intact molecule at about 290 daltons. The Certificate of Analysis should be used as the definitive source for identity, assay, purity and relevant impurity information.
Researchers working with SLU-PP-332 may also be interested in MOTS-c, 5-Amino-1MQ, NAD+, SS-31, AOD-9604 and L-Carnitine — other compounds studied in mitochondrial, energy metabolism and metabolic research.
SLU-PP-332 is a synthetic small molecule that activates all three oestrogen-related receptors, ERR-alpha, ERR-beta and ERR-gamma, with its highest potency at ERR-alpha. It was described in 2023 by researchers working with Saint Louis University and is used in laboratory research on mitochondrial function, muscle fibre type and energy metabolism in cells and rodent models.
They are three nuclear receptors, proteins that sit on DNA and switch sets of genes on or off. They were named for their resemblance to the oestrogen receptors, but they do not bind oestrogen. ERR-alpha and ERR-gamma are especially abundant in tissues with high energy demands, such as heart, skeletal muscle and kidney, where they control genes for mitochondria and fat burning.
No. Despite the similar names, the oestrogen-related receptors are a separate family. In the 2023 study, SLU-PP-332 did not change the activity of oestrogen receptor alpha or beta, or of the other nuclear receptors tested, in cell-based assays. Its activity was confined to the three ERRs.
The ERRs are switched on by default: they are active without any ligand, and partner proteins such as PGC-1-alpha turn their activity up further. An agonist like SLU-PP-332 binds a pocket in the receptor and increases that activity beyond its normal level. Designing such compounds for ERR-alpha proved especially difficult, which is why SLU-PP-332 attracted attention.
It grew out of GSK4716, a compound reported by GlaxoSmithKline in 2005 that activated ERR-beta and ERR-gamma but not ERR-alpha. The Saint Louis group used the crystal structure of GSK4716 bound to ERR-gamma to redesign it, gaining about 50-fold in ERR-alpha potency. Both share the same acyl hydrazone core linking a phenol to an aromatic ring.
In full-length receptor assays its half-maximal concentrations were 98 nanomolar at ERR-alpha, 230 at ERR-beta and 430 at ERR-gamma, so it is about 2.3 times more potent at ERR-alpha than ERR-beta and 4.4 times more than ERR-gamma. It is therefore described as a pan-ERR agonist with a preference for ERR-alpha, rather than a selective one.
Older exercise mimetic work, such as studies of AICAR, targets AMPK, an enzyme that senses the cell’s energy level and acts within minutes by adding phosphate groups to other proteins. SLU-PP-332 instead acts on transcription factors, changing which genes are switched on, so its effects are studied through gene expression, mitochondrial content and fibre type over days to weeks.
In treated mice, muscle contained more mitochondria and mitochondrial DNA and more oxidative type IIa fibres. Sedentary mice ran about 70% longer and 45% further on a treadmill test than controls, and muscle gene expression overlapped with the pattern seen after a single bout of aerobic exercise, which is why the authors called it an exercise mimetic.
The researchers used mice in which ERR-alpha had been removed from skeletal muscle only. In normal littermates, SLU-PP-332 increased treadmill endurance and switched on genes such as Ddit4, Per1 and Alas2. In the knockout mice neither change occurred, which showed that ERR-alpha in muscle was needed for those particular effects.
Published mouse studies cover diet-induced and genetic obesity, where it raised energy expenditure and lowered fat mass; pressure-overload heart failure, where ERR-gamma was the main receptor involved; and the ageing kidney, where eight weeks in 21-month-old mice reversed several age-related changes. All of these are rodent findings from the same research network.
Yes, in culture. A 2025 pilot study grew muscle precursor cells from biopsies taken from less active women during hip surgery and treated them with SLU-PP-332, which raised PGC-1-alpha, ERR-alpha and SIRT1 and encouraged myotube formation. There are no published clinical trials of SLU-PP-332 in people.
SLU-PP-332 is not a controlled drug under the Misuse of Drugs Act 1971, including the Class C group covering anabolic steroids and growth hormones, and it is not a licensed medicine in the UK. It is sold in the UK as a research compound for laboratory use only, which is how Crown Peptides supplies it. This is general information, not legal advice.
SLU-PP-332 is coming soon to Crown Peptides in 5mg and 10mg vials, available singly or in packs of 3, 5 or 10 with a saving on every vial. Orders ship from the UK, and every batch is independently tested, with its Certificate of Analysis published on this page once stock arrives.
SLU-PP-332 weighs about 290 daltons, so a 5mg vial is roughly 17 micromoles and a 10mg vial roughly 34. Published cell work used it at 10 micromolar, so 5mg makes about 1.7 litres of medium at that concentration and 10mg about 3.4 litres. Its potency at ERR-alpha is around 98 nanomolar, so reporter assays use far less.
Keep the unreconstituted powder at -20°C ± 5°C, dry and away from light. The acyl hydrazone link at the centre of the molecule can slowly break down in water, so it is best kept dry, and published studies dissolved it in DMSO. Prepared solutions should follow storage conditions validated for your study design, and each batch’s Certificate of Analysis documents the material as dispatched.
Every batch is published openly — identity, purity and batch number, with no account needed.
Supplied for laboratory research purposes only — not for human consumption or for medical, veterinary or diagnostic use.
Each batch undergoes internal analytical verification using chromatographic and spectrometric methods prior to lyophilisation.
• HPLC Analysis
• Mass Spectrometry Confirmation
• Batch Traceability
By purchasing this product you confirm that you are a qualified researcher and that this compound will be used exclusively for laboratory research purposes.
This product is not intended for diagnostic or therapeutic use.
Any human or medical use is strictly prohibited.
Store in a cool, dry, secure and sterile environment away from any unauthorised persons or children.
Disclaimer: All products are sold strictly for laboratory research purposes only. Not for human or veterinary use, consumption, therapeutic, or diagnostic application. None of our products are medicines, and none are presented as such. By purchasing, you confirm you are a qualified professional and legally permitted to handle these materials in compliance with all applicable laws and regulations. Misuse, resale for unauthorised purposes, or unlawful application is strictly prohibited. Crown Peptides UK disclaims all liability for improper use, handling, or regulatory non-compliance.