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Pan-ERR agonist · lyophilized vial
Also known as ERR pan-agonist 332
A synthetic pan-agonist of the estrogen-related receptors (ERR alpha, beta and gamma). Supplied as a lyophilized powder for research purposes only.
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Tested lot by lot at ≥99% purity. The Janoshik certificate for your lot is emailed with the order.
Everything Valtrax Research ships is bench material for in-vitro work. None of it is a drug, a supplement, a cosmetic, or a medical device, and none of it is intended for human or animal use, ingestion, or administration. Placing an order is your confirmation that you are a qualified researcher buying for lawful research, under every Canadian law and regulation that applies to you.
A hydrazide small molecule — no peptide backbone anywhere in it — that switches on all three estrogen-related receptors, ERRα, ERRβ, and ERRγ. These are orphan nuclear receptors: they sit at the head of oxidative metabolism and mitochondrial gene programs but have no known circulating ligand to switch them on, so a synthetic agonist is the only direct way in.
The program that gene set drives overlaps substantially with what endurance training turns on, which is where the "exercise mimetic" label in the literature comes from. This is the lyophilized vial presentation; the same compound is also stocked as a capsule.
The organizing question is whether switching the ERR axis on pharmacologically reproduces part of the training-adaptation state. Studies read the compound through mitochondrial biogenesis markers, fatty-acid oxidation, exercise capacity, and whole-animal energy expenditure, with skeletal muscle and adipose tissue as the primary systems.
The compound occupies the ERR ligand pocket and stabilizes the receptors in their active conformation. What follows downstream is transcription of the oxidative program: fatty-acid oxidation genes and the machinery of mitochondrial biogenesis. Because ERRα, β, and γ are all engaged, the reported effects are read as a pan-receptor response rather than an isoform-specific one.
Published work describes raised energy expenditure, a shift toward oxidative metabolism in skeletal muscle and adipose models, and acute exercise-like responses that depend on ERRα being present. Later chemistry has pushed the scaffold further, producing orally active analogues such as SLU-PP-915.
The molecule came out of a Saint Louis University medicinal-chemistry effort to find direct ERR agonists — a hard target precisely because these receptors are orphans. Simple phenol-amide scaffolds were built and screened until compounds emerged that could engage and activate the receptor.
From there the work moved into whole-animal metabolism: an acute, ERRα-dependent aerobic exercise response, then relief of metabolic-syndrome phenotypes. The compound has since become the reference tool for asking what pharmacological ERR activation actually does, and it now appears in anti-doping analytical literature as a detection target.
In vitro and animal studies
SLU-PP-332 is a synthetic agonist of the estrogen-related receptors (ERRα, ERRβ and ERRγ), a family of orphan nuclear receptors that regulate the transcriptional programme governing mitochondrial biogenesis and oxidative metabolism. It was developed in an academic medicinal chemistry programme, and the research framing from the outset has been the exercise mimetic question: whether activating the transcriptional response to endurance training can be uncoupled from the training itself.
The rodent work reports what that framing predicts. Published studies describe increased expression of genes associated with oxidative metabolism in skeletal muscle, increased mitochondrial function, improved running endurance in treated mice, and resistance to diet-induced obesity with increased energy expenditure. Effects on fatty acid oxidation and on markers of muscle fibre type shift have also been reported.
The mechanism is transcriptional, which has an important consequence for interpretation: effects accumulate over time as gene expression programmes change, rather than appearing acutely, and they depend on the receptor distribution of the tissue in question.
The receptor family targeted here is worth understanding because the name misleads. Estrogen-related receptors are so called for sequence homology with estrogen receptors, not because they bind estrogen — they do not, and they are constitutively active orphan receptors whose activity is governed largely by the availability of coactivators such as PGC-1α rather than by a circulating ligand.
That has a direct consequence for interpreting the compound. Because ERR activity normally rises through coactivator availability during exercise and metabolic stress, a synthetic agonist imposes activation independent of that physiological context. Whether transcriptional activation uncoupled from the signals that normally accompany it produces the same downstream programme is precisely the open question, and the rodent studies measured selected gene expression endpoints rather than the whole response.
Human data, where it exists
No human trials of SLU-PP-332 have been published. There is no human pharmacokinetic data, no safety dataset and no efficacy evidence in people for endurance, body composition or metabolic endpoints.
The compound is at an early academic stage. Its published record consists of medicinal chemistry characterisation and rodent pharmacology, largely from the laboratory that developed it and collaborators. Independent replication outside that group is limited simply because the compound is recent.
ERR biology itself is reasonably well studied as an academic target, and that background lends the rodent findings mechanistic plausibility. It does not substitute for human data, which does not exist in any form.
Common assertions, and what the record supports
SLU-PP-332 is marketed as exercise in a vial. The rodent data does show improved running endurance and metabolic changes resembling those induced by training, so the framing has a real basis. What it omits is that the comparison was made in mice, over short study durations, with the transcriptional endpoints chosen by the investigators.
Exercise produces mechanical loading, cardiovascular adaptation, neurological adaptation and endocrine changes that a transcriptional agonist does not reproduce. Even taking the rodent results at face value, the compound reproduces one arm of a multi-system adaptation.
A further claim treats early-stage academic compounds as equivalent in standing to trialled drugs because both appear in published papers. A phase 2 trial and a mouse endurance study are not the same category of evidence, and the distinction is the entire question for a compound at this stage.
Against the compounds it is most often confused with
Against 5-Amino-1MQ, the two are the closest pair on the metabolic shelf: both small molecules, both targeting cellular energy handling rather than appetite, both rodent-stage with no human data. They differ in target and in mechanism class — nuclear receptor agonism driving a transcriptional programme versus enzyme inhibition sparing NAD+ and SAM pools.
Against the incretin agonists, there is no overlap. Semaglutide and retatrutide act on cell-surface receptors to change appetite and insulin dynamics, and both have substantial human trial data. SLU-PP-332 acts inside the nucleus and has none.
Against MOTS-c on the longevity shelf, the resemblance is conceptual: both are described in their respective literatures as exercise mimetics, MOTS-c through AMPK activation as a mitochondrial-derived peptide, SLU-PP-332 through ERR-driven transcription. Different molecule classes, overlapping research question.
Adverse findings, toxicology gaps, material hazards
The dominant risk is the complete absence of human data. No adverse effect profile, no interaction data, no exposure range has been established in people.
The ERR receptors are not muscle-specific. ERRα in particular is expressed across many tissues and has been studied in oncology, where its activity has been associated with adverse outcomes in some tumour types. Systemically activating a nuclear receptor family with broad tissue distribution and roles in cell proliferation is a substantively different proposition from a targeted local effect, and the long-term consequences have not been characterised in any species.
Chronic toxicology at the exposures discussed has not been published. Cardiac tissue is metabolically active and ERR-responsive, and cardiac effects of sustained ERR agonism have not been adequately described.
Bench practice for this compound
SLU-PP-332 is a small molecule, not a lyophilized peptide, and the reconstitution practice written for peptides does not apply directly. Solubility and solvent compatibility should be confirmed against the lot documentation before preparing stock solutions.
Store as directed on this page, protected from light and moisture, with the container kept closed. Prepared solutions should be treated as having a shorter working life than the solid material.
This summary describes published research. It is not a protocol, not a recommendation, and not a statement that this compound is safe or effective for any use. Not for human or animal use.
Lin, H. et al. (2018). Design, synthesis, and evaluation of simple phenol amides as ERRγ agonists.
PubMedBillon, C. et al. (2023). Synthetic ERRα/β/γ Agonist Induces an ERRα-Dependent Acute Aerobic Exercise Response and Enhances Exercise Capacity.
PubMedBillon, C. et al. (2024). A Synthetic ERR Agonist Alleviates Metabolic Syndrome.
PubMedIndependent Janoshik verification of identity, purity, and net content accompanies every order as a per-lot certificate.
Janoshik Analytical, a laboratory Valtrax does not own, runs the testing — identity by mass spectrometry, purity by RP-HPLC at ≥99%, on the lot you receive.
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