Explainers · November 10, 2026

SLU-PP-332 Has a Doping Test Before It Has a Human Study

Anti-doping chemists in Cologne mapped how human liver enzymes would break down an "exercise mimetic" that no registered trial has ever given to a person. That order of events is the explainer.

A heavy brass precision laboratory instrument on a dark bench beside a single slim cream folder lying closed and plainly empty.

Start with the thing most likely to be wrong in your head already: SLU-PP-332 is not a peptide. It is a small synthetic molecule, and it only appears in conversations about research peptides because it is discussed and circulated alongside them. Nothing about peptide chemistry, peptide stability or peptide handling transfers to it.

What it is, is an agonist of the estrogen-related receptors.

What an estrogen-related receptor is, and is not

ERRα, ERRβ and ERRγ are nuclear receptors — proteins that sit inside a cell, bind a small molecule, and then switch sets of genes on or off. They are described as "orphan" receptors because no natural hormone has been identified that binds them.

The name is a trap. "Estrogen-related" refers to a family resemblance in protein sequence, not to estrogen signalling. ERRs do not bind estrogen and are not part of the estrogen pathway. What they do govern, across the published work, is transcription of mitochondrial and metabolic genes. A compound that activates all three at once is called a pan-ERR agonist. SLU-PP-332 is one; so is a related compound, SLU-PP-915.

What "exercise mimetic" means in the papers

A systematic review published in Revista Médica de Chile in April 2026 gathered the animal and cell literature on pan-ERR agonists from 2020 to 2024. Its summary of what these compounds do, in those models:

  • They induce a gene-expression program resembling acute aerobic exercise, dependent on ERRα, including activation of the genes Ddit4 and Slc25a25.
  • They raise fatty-acid oxidation, shift muscle toward type IIa fibres, and extend endurance in rodents.
  • In obesity models, they reduced adiposity, raised basal energy expenditure and produced better glycaemic control, without evident toxicity in those studies.
  • In aging rodent kidneys, they restored mitochondrial function and lowered inflammation markers.

That is a real and coherent body of preclinical work. It is also, in the reviewers' own concluding sentence, incomplete: "Clinical trials are needed to confirm their efficacy and safety in humans." As of that review, none had been done.

The part worth noticing

In April 2026, Rapid Communications in Mass Spectrometry published a study from the Center for Preventive Doping Research at the German Sport University Cologne, with the European Monitoring Center for Emerging Doping Agents. Tristan Möller, Oliver Krug and Mario Thevis characterised SLU-PP-332 and SLU-PP-915 by liquid chromatography with high-resolution tandem mass spectrometry, then ran both compounds through human liver S9 fraction and human liver microsomes — isolated liver enzyme preparations — to find out what human liver chemistry would do to them.

They identified nine metabolites of SLU-PP-332: six phase I products and three phase II conjugates. SLU-PP-915 produced seven, all phase I. Three of the SLU-PP-915 metabolites were then synthesised outright and confirmed by nuclear magnetic resonance. The authors state the purpose plainly: the work "may help to uncover the illicit use of these novel compounds as potential performance-enhancing substances."

So before any person has received this compound in a registered study, a laboratory has worked out what the urine would look like.

The chemistry is still a work in progress

In March 2026, the International Journal of Biological Macromolecules published the first systematic structure–activity analysis of the SLU-PP-332 scaffold, from a group at Washington University in St. Louis with the University of Florida. They synthesised fourteen analogues and tested them against human ERRα, ERRγ and the downstream gene response.

Several analogues matched SLU-PP-332's transcriptional response, or matched it in particular contexts, while showing better ligand efficiency, solubility or metabolic stability. The paper's own description of SLU-PP-332 is the useful phrase: "a well-established exercise mimetic and widely used chemical probe." A chemical probe is a tool for asking questions about a receptor in a laboratory. It is not the same category of object as a drug candidate, and the paper is explicitly a roadmap for designing something better.

Nothing in the registry

A search of ClinicalTrials.gov on 9 November 2026 for SLU-PP-332 or SLU-PP-915 as an intervention returned no studies. Not recruiting, not completed, not terminated, not withdrawn. Zero records.

Why a detection method arrives first

This is not sinister, and understanding why is the point of the whole article.

Anti-doping laboratories work from the open literature. A compound with a published synthesis, a plausible performance-related mechanism and rodent endurance data is one they expect to encounter in samples whether or not a pharmaceutical company ever develops it. Building the assay before the compound shows up is exactly the job. The Cologne group has done this repeatedly for compounds that reached athletes long before they reached a phase 1.

What follows from that is the reading we would ask anyone to take away: a detection method is not evidence about a compound's effect or its safety in people. It is evidence that someone with a laboratory expects the compound to turn up.

What has not been studied

  • No registered clinical trial of SLU-PP-332 or SLU-PP-915 exists, so there is no human efficacy data and no human safety data of any kind.
  • No published human pharmacokinetics. The metabolite mapping was done in isolated liver enzyme preparations in a tube, not in a person.
  • "Without evident toxicity" in the systematic review describes the obesity-model studies it summarised, over their own durations. No long-term toxicology programme has been published alongside the metabolic findings.
  • Whether the rodent transcriptional program produces any measurable change in a human: untested.
  • Any combination with anything else: untested.

What to watch

Two things. First, a phase 1 appearing in a registry under either name — that would be the first human data of any kind. Second, whether the compound that gets there is SLU-PP-332 itself or one of the analogues from the 2026 structure–activity work, which would tell you the original molecule was always the probe and never the candidate.

Sources

  1. de Souza-Lima J, Astrosa-Martin BD, Galaz-Rodríguez CA, et al. Pharmacological Activation of ERRα/β/γ as an Exercise Mimetic: Potential Therapeutic Applications. Rev Med Chil (2026)
  2. 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 Commun Mass Spectrom (2026)
  3. Okda HE, Zhao P, Hayes M, et al. Chemical optimization of the exercise mimetic SLU-PP-332 enables insight into estrogen-related receptor signaling. Int J Biol Macromol (2026)
  4. ClinicalTrials.gov intervention search, 9 November 2026: no registered studies for SLU-PP-332 or SLU-PP-915

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