What it is
SLU-PP-332 is not a peptide. It is a small man-made chemical. This site covers it because people often talk about it along with peptides.
It switches on a family of three proteins inside cells. They are called estrogen-related receptors, or ERRs. Despite the name, they do not respond to estrogen. They act like master switches for certain genes. These genes build mitochondria. Mitochondria are the parts of a cell that burn fat and sugar for energy. ERRs also play a key role in how muscle adapts to endurance exercise.
In mice, it made muscle act more like muscle trained for endurance. That is why its makers call it an “exercise mimetic” (something that copies some effects of exercise). So far it has only been studied in cells and in mice. It has never been tested in people. No medicine containing it is approved.
SLU-PP-332 is 4-hydroxy-N’-[(E)-naphthalen-2-ylmethylidene]benzohydrazide (C18H14N2O2, 290.3 g/mol), an acylhydrazone agonist of the estrogen-related receptors ERRα, ERRβ and ERRγ (NR3B1–3). The ERRs are constitutively active orphan nuclear receptors with no identified endogenous ligand; together with the coactivator PGC-1α they drive transcription of genes for mitochondrial biogenesis, oxidative phosphorylation, fatty acid oxidation and the Krebs cycle.
Billon et al. (2023) reported EC50 values of 98 nM at ERRα, 230 nM at ERRβ and 430 nM at ERRγ, making it a pan-agonist with the highest potency at ERRα. It increased mitochondrial respiration in C2C12 muscle cells and induced an acute aerobic-exercise gene programme in mouse muscle that depended on ERRα. In the heart-failure work, ERRγ was the main mediator of its transcriptional and protective effects.
Pharmacokinetics: two hours after 30 mg/kg intraperitoneally in mice, concentrations were about 0.6 µM in skeletal muscle and 0.2 µM in plasma. The developers later described it as lacking oral bioavailability. In pooled human liver S9 fractions it formed 22 metabolites, hydroxylated, reduced, glucuronidated or sulfated (Avliyakulov et al., 2026). No human data exist.
Who made it and when
SLU-PP-332 was designed by a team in St. Louis, Missouri. The team was led by Thomas Burris. He worked with Cyrielle Billon, John Walker and Bahaa Elgendy. The “SLU” in the name matches Saint Louis University, one of the places involved.
The team started from an older research chemical. That chemical switched on only two of the three ERRs. They changed its design until it also switched on the third one, ERR-alpha. In mice, the team found ERR-alpha was needed for the endurance effect.
The first full report came out in 2023. Mouse studies on obesity followed in 2024. Mouse studies on heart failure also came out in 2024. Some of the researchers own shares in, or helped start, small companies working on ERR drugs. But no company is known to have tested SLU-PP-332 itself in people.
Using structure-based design, the group optimised the ERRβ/γ-selective agonist scaffold GSK4716 for ERRα activity, gaining roughly 50-fold ERRα potency (Billon et al., ACS Chem Biol 2023; Saint Louis University, Washington University School of Medicine and St. Louis College of Pharmacy, Salk Institute and others). Follow-up papers covered diet-induced and genetic obesity (J Pharmacol Exp Ther 2024) and pressure-overload heart failure, together with a second pan-agonist, SLU-PP-915 (Xu, Billon et al., Circulation 2024). A 2026 paper described SLU-PP-915 as the orally active successor.
Disclosures: in the 2023 paper, Burris, Elgendy and Walker reported holding stock in Myonid Therapeutics, which works on ERR-based therapeutics. The Circulation paper discloses that co-author L. Zhang (Baylor) co-founded Pelagos Pharmaceuticals; a March 2024 American Chemical Society press release said Elgendy (Washington University School of Medicine) and colleagues hoped to test newer ERR agonists in animal models through Pelagos, a startup they had co-founded; and the 2026 SLU-PP-915 paper discloses that Burris holds stock in both Myonid and Pelagos, which it describes as developing ERR agonists, and that SLU-PP-915 is Saint Louis University intellectual property. No licence of SLU-PP-332 itself, no IND and no patent specific to it could be verified for this article.
What the data say
Mice were given injections twice a day for a week. They then ran about 70% longer and 45% farther on a treadmill before tiring. After about two weeks of injections, their muscle shifted toward fibres that use oxygen and resist tiring.
In obese mice, it raised the energy they used and the fat they burned. It cut fat gain and improved blood sugar control. In mice with a strained, failing heart, it helped the heart pump better. It also helped them live longer.
All of this comes from cells and mice. Much of it comes from one group of researchers working together. No person has been given it in a registered study. So nothing is known about its effects or safety in people. Anti-doping labs have already started tracking how the body breaks it down. This is so it can be detected in sport.
Exercise capacity: in 12-week-old male C57BL/6J mice (n=6 per group) given 50 mg/kg intraperitoneally twice daily, 7 days of treatment increased running time by about 70% and distance by about 45% versus vehicle; 15 days of treatment increased type IIa oxidative fibres. Enhanced endurance required ERRα (Billon et al., 2023).
Metabolic disease: in diet-induced obese and ob/ob mice, SLU-PP-332 increased energy expenditure and fatty acid oxidation, reduced fat mass accumulation and improved insulin sensitivity (Billon et al., 2024).
Heart failure: in a pressure-overload heart-failure model, SLU-PP-332 and SLU-PP-915 improved ejection fraction, reduced fibrosis and increased survival without changing hypertrophy; metabolomics showed normalisation of fatty acid and oxidative phosphorylation metabolites, and genetic studies identified ERRγ as the main mediator (Xu et al., 2024).
Human data: none. ClinicalTrials.gov lists no study of SLU-PP-332. No repeat-dose toxicology, genotoxicity or safety pharmacology studies have been published. Two 2026 studies, from a UCLA group (Avliyakulov et al.) and Möller et al. (Rapid Commun Mass Spectrom), characterised metabolites specifically for doping control.
Regulatory picture
There are separate points to know here.
Approval: No medicine containing SLU-PP-332 is approved by the FDA or any other regulator. No company is known to be developing it for people.
Compounding (when a pharmacy mixes its own version of a drug): It is not on any of the FDA’s compounding lists. It is not on the approved ingredients list. It is not in any of the three groups of nominated substances. So it has never been reviewed for that use.
Enforcement: No FDA warning letter naming SLU-PP-332 was found.
Sport: Anti-doping scientists say it could be used for doping. They have published work to help detect it. From 1 January 2027, the World Anti-Doping Agency’s banned list names SLU-PP-332 by name.
Being sold as a “research chemical” does not mean it has been checked for safety in people.
Approval: none. No IND-stage programme, NDA or foreign marketing authorisation could be identified, and no study is registered on ClinicalTrials.gov.
Compounding: SLU-PP-332 is not on the 503A bulks list in 21 CFR 216.23 and does not appear in Category 1, 2 or 3 of FDA’s list of substances nominated under section 503A (updated 2026-05-14), nor on FDA’s page of bulk drug substances that may present significant safety risks (updated 2026-04-22). It is not a component of any FDA-approved drug. Because it has not been evaluated under any of these pathways, this article records compounding status as unknown.
Enforcement: no FDA warning letter naming SLU-PP-332 was found in searches for this article.
Sport: Avliyakulov et al. (Drug Test Anal 2026) note that WADA prohibits exercise mimetics and metabolic modulators as a class. The 2027 Prohibited List (in force 2027-01-01) names SLU-PP-332 explicitly as an example under S4, according to USADA’s athlete advisory. Metabolite studies were published in 2026 to support detection in doping control.
