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SLU-PP-332

Also known as SR9861, ERR pan-agonist 332, 4-hydroxy-N'-(naphthalen-2-ylmethylene)benzohydrazide, exercise mimetic

Not a peptide but a small-molecule ERR agonist marketed as an 'exercise mimetic'; rodent data only.

preclinical Metabolic & weight research chemical

At a glance

Category
Metabolic & weight
Status
research chemical
Route
intraperitoneal injection in the mouse studies; sold for oral use
Half-life
No human pharmacokinetic data. The discovery paper reports that the compound has pharmacokinetic properties sufficient for use as an in vivo chemical tool in mice 1; that is the extent of what has been published.
Molecular weight
290.3 g/mol (C18H14N2O2); CAS 303760-60-3 8

SLU-PP-332 is not a peptide. It is a synthetic acylhydrazone that activates all three estrogen-related receptors, included here because it is sold by the same vendors as peptides and is searched for in the same breath. It has never entered a phase 1 trial: a ClinicalTrials.gov query in July 2026 returns zero registered studies 7. It is not approved as a medicine anywhere. It is nevertheless offered for sale online, usually as a capsule or an oral solution, under the marketing term 'exercise mimetic'. It originates from an academic medicinal-chemistry programme; the discovery paper carries a declared competing interest, with several authors holding stock in a company formed around ERR-based therapeutics 1.

Doping status: Not named on the 2026 Prohibited List and not covered by the S4.4 metabolic modulator entries, which name AMPK activators, PPAR-delta agonists and Rev-erb agonists but not ERR agonists; as a non-approved substance it falls under S0, prohibited at all times

Checked against the WADA 2026 Prohibited List. For a specific product and country, Global DRO is the lookup athletes are expected to use — the List names substances, not brand names.

This is a short entry. There is little or no published research on this compound, so there is correspondingly little to report. Empty dosing or reconstitution sections mean no credible figures exist — not that they were left out.

Mechanism of action

The estrogen-related receptors (ERR-alpha, -beta and -gamma) are orphan nuclear receptors that regulate mitochondrial biogenesis, oxidative fibre type and fatty acid oxidation in skeletal muscle and heart. Genetic work has linked them to exercise capacity, and ERR-alpha in particular has been difficult to activate pharmacologically. SLU-PP-332 was reported as a pan-agonist with the highest potency at ERR-alpha 1. In muscle cells it increased mitochondrial function and cellular respiration; in mice it increased type IIa oxidative fibres and induced a gene-expression programme resembling the acute response to aerobic exercise, and that programme depended on ERR-alpha 1.

The label 'exercise mimetic' describes a transcriptional resemblance, not an equivalence. What has been shown is that a drug can switch on some of the genes that exercise switches on, in a mouse. Exercise also loads bone and tendon, changes cardiac output, alters appetite and sleep, and acts on the brain, and none of that follows from activating a nuclear receptor. Treating the two as interchangeable is a marketing claim, not a finding.

What the research shows

Rodent and cell-culture data only, from a small number of groups, over roughly three years. No human being has knowingly received this compound under any published protocol, and no trial is registered 7. The animal work is real and has been published in reputable journals, but it is early-stage target validation, which is a different thing from evidence that a compound is safe or useful in people.

Research in humans

No published human studies. No phase 1 trial, no pharmacokinetics, no tolerability data, no maximum tolerated dose. A ClinicalTrials.gov search returns zero registered studies as of July 2026 7. The only human-derived work is in vitro: anti-doping laboratories have incubated the compound with human liver microsomes and liver S9 fraction to map its metabolites so that use in sport can be detected 56. That is human tissue in a test tube, not a human trial.

Animal and lab research

Billon and colleagues (2023) identified SLU-PP-332 as a synthetic pan-ERR agonist, showed increased mitochondrial function and respiration in a skeletal muscle cell line, and reported increased type IIa oxidative fibres and enhanced running endurance in mice, with the effect dependent on ERR-alpha 1. Follow-up work reported improvement of metabolic syndrome measures in mice 2, amelioration of heart failure through enhanced cardiac fatty acid metabolism 3, and reversal of mitochondrial dysfunction and inflammation in the ageing kidney 4. A structurally optimised successor, SLU-PP-915, has since been described as an orally active ERR agonist that enhances aerobic exercise capacity in animals.

Caveats. Every efficacy finding is in mice or cultured cells. The doses were given by injection in the original work, while the compound is sold to be swallowed, and no human oral bioavailability figure exists. There is no published chronic toxicology, carcinogenicity or reproductive toxicity study. ERRs are broadly expressed - heart, kidney, brown fat, brain - so a pan-agonist is not a muscle-targeted drug, and the consequences of activating all three subtypes systemically for months in a person are simply unknown. The discovery paper carries a declared financial interest 1. Finally, an important negative: no company has taken the compound into a phase 1 trial in the three years since the discovery paper, in a field with abundant funding, and that absence is itself information.

What it is used for

  • Preclinical chemical tool for probing ERR biology in muscle, heart and kidney 134
  • Reference material in anti-doping research, where its metabolites have been characterised specifically so that its use in sport can be detected 56
  • Sold online as an 'exercise mimetic' or 'endurance' compound, with no validated indication, no established human dose and no human safety data 7

Dosing

  • There is no human dose. No phase 1 study has been run, no tolerability data exist and no ClinicalTrials.gov record exists to take a starting dose from 7.
  • The mouse work used injected doses 1. Converting a mouse intraperitoneal dose to a human oral dose without human pharmacokinetics is guesswork, and any milligram figure circulating online is an invention rather than a derivation.
  • Any dose figure attached to a product for sale should be read as a label, not as a studied quantity - PeptideX has found no published source for the numbers that circulate.
  • An incoherent oral self-dosing practice does exist, and the protocol section below records it as exactly that rather than as a tidy schedule. SLU-PP-332 is sold as capsules and oral solutions marketed as an 'exercise mimetic', and the circulating figures disagree by orders of magnitude: vendor capsules are commonly 250 mcg and the low-dose pattern runs a few hundred micrograms to roughly 1.5 mg daily, while other discussions and vendor write-ups quote several milligrams up to tens of milligrams, and the products themselves are labelled inconsistently, so users cannot reliably tell which is meant. Every one of these numbers traces to vendor labelling or aggregator tables rather than to a study, there is no human oral bioavailability figure, and the mouse work dosed by injection 1. The microgram-versus-milligram spread is itself the finding, and the protocol below preserves it rather than resolving it into a single number.

These figures describe what the literature and published protocols report. They are not advice and not a dosing instruction.

Protocols

Oral 'exercise mimetic' self-dosing (user-reported, figures incoherent)

user protocol — not validated

Source: Vendor capsule labelling, oral-solution products and dosing-aggregator tables

This is not a validated schedule. It is a pattern that circulates among users and sellers, reproduced because it is what people actually follow — not because it has been tested. No trial established these doses, this interval or this duration, and nobody is checking what is in the vial. Treat every number below as an assertion, not a finding.

Low-dose patternroughly 250-500 mcg by mouth once daily, anchored to the 250 mcg capsules vendors commonly sell; sometimes titrated toward 1-1.5 mg
High-dose patternseveral milligrams up to tens of milligrams daily, quoted in some vendor write-ups and aggregator tables
Reported cyclerun continuously for a few weeks, with no consistent off-period

There is no coherent protocol here, and the two patterns above are recorded to show that rather than to endorse either. They differ by roughly a hundredfold, and users in the same discussions cannot tell whether micrograms or milligrams are meant, because the products are labelled inconsistently and every figure traces to a vendor page or a dosing-aggregator table rather than to a study. No human oral bioavailability figure exists, so it is not even known how much of a swallowed dose is absorbed, and the original mouse work dosed by intraperitoneal injection rather than by mouth 1. No phase 1 trial has ever been run 7. The 'exercise mimetic' label describes a resemblance between some genes the compound switches on and some that exercise switches on in mice - not a demonstrated effect in a person.

Schedules are reproduced as their source states them. Units, IU and milligrams explains why the figures are not interchangeable between products.

Reconstitution

Sold as capsules or oral solutions; nothing to reconstitute. Material sold as a research chemical has no pharmaceutical quality control, and neither identity nor purity can be assumed.

Safety

Side effects

  • Unknown in humans - no person has been monitored on this compound in any published study
  • No adverse-effect profile has been established even in animals beyond the short treatment periods used in the efficacy studies
  • ERRs are expressed in the heart, kidney and brain as well as skeletal muscle, so a pan-agonist acts systemically; effects in those tissues have been reported as beneficial in specific mouse disease models 34 but have never been assessed for harm in a healthy human
  • The absence of reported side effects reflects the absence of humans in the literature, not safety

Do not use if

  • Everyone, in the practical sense: no indication has an established risk-benefit balance in a human being 7
  • Pregnancy and breastfeeding - no reproductive toxicity data have been published
  • Children and adolescents - no data
  • Any competitive athlete subject to anti-doping rules; detection methods for the compound and its metabolites have been published specifically to catch it 56

Interactions

Not studied in humans. In vitro metabolism work with human liver microsomes and S9 fraction identified six phase I metabolites and three phase II conjugates 5, which implies hepatic metabolism and therefore the potential for interactions with drugs that induce or inhibit the same enzymes - but no interaction study of any kind has been performed.

Sources