SLU-PP-332
Pan-ERR agonist
SLU-PP-332 (Pan-ERR agonist) is a metabolic & fat loss research compound. Synthetic pan-ERR (α/β/γ) agonist that switches on the endurance-exercise gene program via PGC-1α — mitochondrial biogenesis and fat oxidation, an 'exercise mimetic.'
SLU-PP-332 quick facts
| Reported research dose | 500mcg-1500mcg (Up To .5-4mg/kg) |
| Route | Subq |
| Frequency | 2-3x Daily AM/Mid/PM |
| Half-life | Very short (<1 hr) |
| Forms | Injectable, Oral |
| Evidence level | Mouse only — no human data |
Wildly promising on paper, but it's rodent-stage. Exciting, not proven — say that honestly.
How SLU-PP-332 works
Synthetic pan-ERR (α/β/γ) agonist that switches on the endurance-exercise gene program via PGC-1α — mitochondrial biogenesis and fat oxidation, an 'exercise mimetic.'
Proposed benefits
Endurance and fat oxidation as an 'exercise mimetic' (rodent-stage).
Where to get SLU-PP-332
SLU-PP-332 is sold in 3 forms. They are not interchangeable — the dose and the route differ, so pick the one this page describes unless you know why you want another.
SLU-PP-332 is a small molecule, not a peptide, and it doesn't dissolve in bacteriostatic water. Its supplier lists solubility only in DMSO (1–10 mg/ml) and ethanol (0.1–1 mg/ml).
The evidence for SLU-PP-332
Graded by what exists behind each claim.
Human clinical evidence
- No human trials: development stopped at preclinical, so the ceiling on any claim here is a rodent model — and these transfer poorly.
📊 Correlative data
- Recent arrival to the research market with a very thin practical record. Reported experience is dominated by the injectable route — it has poor oral bioavailability and a short half-life in the animal work, which most sellers do not mention.
- Beyond that the record is self-reported: community dosing logs are real information about tolerability and almost none about efficacy.
🧪 How the mechanism reads
- A pan-ERR agonist — estrogen-related receptors are orphan nuclear receptors that, despite the name, do not bind estrogen. ERRα is a master regulator of mitochondrial biogenesis, working with PGC-1α.
- Mouse work reported increased running endurance and fat loss without exercise and without reducing food intake — an energy-expenditure mechanism rather than an appetite one, which is what makes it interesting against the GLP-1 class.
- Driving mitochondrial biogenesis systemically is not free. More mitochondria means more electron transport and more reactive oxygen species, and the heart is among the most ERR-dense tissues in the body.
Why an empty tier is not a verdict → · What community dosing logs are worth →
How to read these tiers: they say how much human evidence exists, not how well something works — and ✗ flags harm, never a disappointing trial. How the evidence tiers work →
What SLU-PP-332 actually does
The estrogen-related receptors are not estrogen receptors, and the confusion in the name has cost this compound a lot of bad writing. ERR-alpha, ERR-beta and ERR-gamma were found by sequence similarity to the estrogen receptor. They do not bind estradiol. They are orphan nuclear receptors — no endogenous ligand has ever been identified — and they sit on DNA constitutively active. What regulates their output is not a hormone arriving but how much coactivator is available, and the coactivator is PGC-1alpha, the protein exercise itself induces.
That is why an ERR agonist is a plausible exercise mimetic and an estrogen-receptor drug is not. The ERR/PGC-1alpha axis controls the mitochondrial gene program: biogenesis, oxidative phosphorylation, fatty acid oxidation, the Krebs cycle. Training works in part by raising PGC-1alpha and letting it drive ERRs harder. A synthetic agonist proposes to drive the receptor directly, without the coactivator step and without the training.
The specific achievement of this molecule, in its own paper's words. Billon 2023 states the problem it was built to solve: “although ERR-beta/gamma agonists have been designed, there have been significant difficulties in designing compounds with ERR-alpha agonist activity”, and “there are limited synthetic agonists that can be used to target ERRs in vivo”. SLU-PP-332 is reported as a synthetic ERR pan agonist that targets all three isoforms but has the highest potency for ERR-alpha. ERR-alpha is the muscle-metabolism isoform and it was the hard one to drug; that is the compound's actual claim to novelty.
What it does to a muscle cell. Billon 2023 reports SLU-PP-332 increasing mitochondrial function and cellular respiration in a skeletal muscle cell line. Not gene expression alone — respiration, the functional output.
And what it did to a muscle. In mice it increased the type IIa oxidative skeletal muscle fibers and enhanced exercise endurance, and it induced an ERR-alpha-specific acute aerobic exercise genetic program, with the paper reporting that ERR-alpha activation was critical for enhancing exercise endurance Billon 2023. The fiber-type detail is the mechanistically satisfying part: type IIa is the fast oxidative fiber, the one endurance training expands at the expense of the purely glycolytic type IIx. The drug moved the muscle in the direction training moves it, and the paper showed the effect required the receptor rather than merely correlating with it.
The pan part is not a rounding error. ERR-gamma is heavily expressed in heart, and Xu 2023 reports pan-ERR agonists from this program ameliorating heart failure through enhanced cardiac fatty acid metabolism and mitochondrial function — in Circulation. That is an argument for the class and it is also the reason nobody should describe this compound as muscle-selective. It engages the cardiac receptor by design.
Cell, rodent, human — and where it stops
Step one, chemistry and cells. The pan-ERR series was built and screened against all three subtypes Hampton 2023; SLU-PP-332 emerged from it as the tool with the highest ERR-alpha potency Billon 2023, and it raised mitochondrial function and cellular respiration in a skeletal muscle cell line.
Step two, mice, exercise. Billon 2023: type IIa oxidative fibers up, running endurance up, an ERR-alpha-specific acute aerobic exercise gene program induced, and the endurance effect shown to depend on ERR-alpha activation. This is the study every vendor page paraphrases and almost none of them names.
Step three, mice, metabolic disease. Billon 2023 gave SLU-PP-332 to diet-induced obese mice and to ob/ob mice and reported that it mimics exercise-induced benefits on whole-body metabolism including increased energy expenditure and fatty acid oxidation, accompanied by decreased fat mass accumulation, and that it reduced obesity and improved insulin sensitivity in models of metabolic syndrome. Two different disease models, one compound, consistent direction.
Step four, mice, heart. Xu 2023 in Circulation: pan-ERR agonists improved heart failure outcomes by enhancing cardiac fatty acid metabolism and mitochondrial function. Three phenotypes — endurance, metabolic syndrome, heart failure — one receptor family, and every one of them in a mouse.
Step five, humans: there is no step five, and what came instead is telling. No phase 1. No human pharmacokinetics. No safety database. No dose. The most recent publication on this molecule is Moller 2026, an in vitro metabolism and analytical characterization study of SLU-PP-332 and SLU-PP-915 run for doping control — a laboratory working out which metabolites a urine test should target. The chemistry for catching people using this drug was published before any human had taken it in a trial.
Step six, and this is the part specific to this molecule rather than to the class: the follow-up compound exists because of a route problem. Billon 2025 is titled “An orally active estrogen receptor-related receptor agonist, SLU-PP-915, enhances aerobic exercise capacity”. A medicinal chemistry program does not announce oral activity as the headline of a successor compound unless the predecessor lacked it. SLU-PP-332 is the predecessor.
The obstacles, named one at a time. (1) Every efficacy read-out is running capacity or fat mass in a mouse, and mouse running capacity is not a validated surrogate for anything in a person. (2) The receptor is orphan and constitutively active, so there is no physiological exposure range to calibrate a human dose against — unlike every hormone-receptor drug, there is no ‘what does a hard training session do’ comparison to anchor to. (3) The program's own successor compound was developed for oral activity Billon 2025, which places the route this site's card lists — subcutaneous — outside both the published rodent work and the successor's design rationale. (4) The dose range on this card, 500 to 1,500 µg, described as up to 0.5–4 mg/kg, is not derived from any published human study, because none exists.
SLU-PP-332 pharmacokinetics — how much of it actually gets in
The only published pharmacokinetic statement about SLU-PP-332 is one clause long, and it is worth reading exactly. Billon 2023: the compound “has sufficient pharmacokinetic properties to be used as an in vivo chemical tool”. That is the whole of it. No half-life, no oral bioavailability, no clearance, no volume of distribution, no Cmax, no AUC, in any species. ‘Sufficient to be a chemical tool’ is a much weaker claim than it sounds: it means the compound stays around long enough, at high enough concentration, to test a hypothesis in a mouse. It is not a claim about a therapeutic exposure and it is explicitly not a claim about a person.
The strongest inference available, and it comes from the successor compound's title. Billon 2025 presents SLU-PP-915 as an orally active ERR agonist that enhances aerobic exercise capacity. Oral activity is what that paper is selling. In a program run by the same group on the same receptor family, announcing oral activity for compound B is a statement about compound A. This site's card for 332 lists the half-life as very short, under one hour — consistent with that reading and, like the dose range, not traceable to a published measurement.
What degrades it, measured — in a tube, for the purpose of catching users. Moller 2026 characterized the in vitro metabolism of both SLU-PP-332 and SLU-PP-915 and defined the analytical targets a doping laboratory should screen for. In vitro metabolism of a small molecule means liver preparations: the cytochrome-P450 oxidation and conjugation screen that normally precedes a first-in-human dose. So the metabolic fate of this compound has been mapped in a tube in order to detect it in urine, and never in a person in order to dose one. That is an unusual order to do things in, and it is now true of both compounds in the series.
The arithmetic a reader can actually do. Take this card's own range at face value: 500–1,500 µg subcutaneously in an 80 kg adult is 6–19 µg/kg. The same card also quotes 0.5–4 mg/kg, which for the same person is 40–320 mg. Those two figures do not describe the same quantity at all — depending which ends you compare they sit between about twenty-five and six-hundred-fold apart — and both are printed as the dose. Neither is anchored to a published human study, and the gap between them is the clearest possible illustration of what happens when a rodent mg/kg number and a community microgram number end up on the same line.
And a species caution that runs against the naive conversion. Mice clear small lipophilic molecules substantially faster per kilogram than humans do, because clearance scales with surface area rather than mass. A straight mg/kg transfer from a mouse to a person therefore overshoots, sometimes by an order of magnitude. Without a measured human half-life there is no way to turn a mouse dose into a human one, and no published rodent-to-human scaling has been attempted for this molecule.
What would have to be true, and how you would know it was not
Four predictions with a marker, a direction and a window. The second is the one that would demonstrate the mechanism cheaply, and the fourth cuts against the compound.
1. Endurance performance should improve before body composition does. The rodent phenotype is type IIa oxidative fiber expansion and running endurance Billon 2023, and fiber-type and mitochondrial adaptations show up in performance well before they show up on a scale. Measure a fixed submaximal test — same route, same effort, VO2 or heart rate at a fixed pace, or time to exhaustion at a fixed load — at baseline and at 6 weeks, with training volume held constant. Improvement in body composition without improvement in endurance would be the wrong order for this mechanism and would point at something other than ERR.
2. Resting heart rate and submaximal heart rate should fall for the same work. Increased mitochondrial density and oxidative capacity lower the cardiac cost of a fixed workload. Log resting heart rate daily on waking and the heart rate at a fixed submaximal effort weekly. This is free, it is sensitive, and it is the closest home proxy that exists for the mitochondrial claim.
3. Fasting glucose and HbA1c should improve if anything is reaching the receptor. Billon 2023 reported improved insulin sensitivity and reduced obesity in two mouse models of metabolic syndrome. Draw Fasting Glucose, Fasting Insulin and Hemoglobin A1c (HbA1c) at baseline and 12 weeks. Extrapolation from mouse to human, labeled as such — but it is the one animal result with a routine human assay behind it.
4. The prediction that cuts against it: the heart is a target organ, not a bystander. ERR-gamma is heavily expressed in myocardium and pan-ERR agonists change cardiac fatty acid metabolism and mitochondrial function Xu 2023. In a failing heart that was beneficial. Nobody has shown what happens in a healthy one. Reprogramming substrate preference in a normal myocardium is not obviously neutral, and there is no human data in either direction. The practical read-outs are resting heart rate, exercise tolerance, and any new palpitations or exertional breathlessness — and the honest statement is that no blood marker will catch this early, which is itself a reason for caution rather than for reassurance.
What nobody has tested yet
Nobody has measured the pharmacokinetics of SLU-PP-332 in any species, in public. The literature contains one clause — ‘sufficient pharmacokinetic properties to be used as an in vivo chemical tool’ Billon 2023 — and nothing else. A single-dose rodent study with plasma sampling, using the analytical method the doping laboratory has already validated Moller 2026, would produce the half-life and the oral fraction that every dose decision in this market currently guesses at.
Nobody has compared subcutaneous with oral or intraperitoneal dosing for this molecule. The market injects it; the successor compound was developed to be swallowed Billon 2025. Which route delivers more receptor occupancy per milligram of SLU-PP-332 specifically is unmeasured, and it is the difference between a working protocol and an expensive one.
Nobody has tested an ERR agonist alongside training in any species with a factorial design. The interesting question is not whether the drug substitutes for exercise — it is whether drug and training are additive, synergistic or redundant, since both converge on the same coactivator-receptor axis. If training already saturates PGC-1alpha-driven ERR-alpha activity, an agonist may add nothing to a trained person while doing a great deal for a sedentary one. That is a testable, four-arm mouse experiment and it has not been published for 332.
Nobody knows what chronic activation of a constitutively active orphan receptor does over years. Every other nuclear-receptor drug in medicine amplifies a signal the body already sends and can therefore be reasoned about against a physiological range. Here there is no ligand, no range, and no known feedback loop that switches the receptor off. The longest published exposure is a mouse study measured in weeks.
SLU-PP-332 — its own safety story, not its class's
There is no human safety data for this compound at all. No phase 1, no volunteer study, no case report, no pharmacovigilance. The published record is cell lines, mice, an in vitro metabolism study and a medicinal chemistry series. Everything below is mechanism-level reasoning and is labeled as such.
The cardiac receptor is the specific concern, and it is not speculative. ERR-gamma is heavily expressed in heart, and this compound is a pan agonist by design Billon 2023. The evidence that it engages the myocardium is positive evidence, published in Circulation: pan-ERR agonists changed cardiac fatty acid metabolism and mitochondrial function enough to improve heart failure Xu 2023. A drug potent enough to remodel a failing heart's substrate metabolism is potent enough to remodel a healthy one's, and nobody has looked at what that does.
The orphan-receptor problem, stated as a safety argument rather than a curiosity. With a hormone receptor there is a natural exposure envelope: a physiological range, a diurnal rhythm, a feedback loop. ERRs have none of those — they are constitutively active and regulated by coactivator supply. A synthetic agonist is therefore creating a signal that has no physiological precedent, and there is no known homeostatic mechanism that limits it. That is not a reason to assume harm; it is a reason no one can reason about the dose.
It will be a doping positive. Moller 2026 exists specifically to characterize SLU-PP-332 and SLU-PP-915 as “novel pan-ERR agonists with doping potential” and to define the metabolites a screening method should target. Any tested athlete should treat this as settled rather than as a future risk.
And the dose on this page cannot be relied on. The card carries two dose figures that, converted to the same units, sit between about twenty-five and six-hundred-fold apart, neither traceable to a human study. For a compound with no measured human half-life, no human safety data and a receptor with no physiological off-switch, that is the practical risk: the amount is a guess, the exposure is unmeasured, and there is no marker that reports either.
Sources read for this page
- Billon C. Synthetic ERRalpha/beta/gamma Agonist Induces an ERRalpha-Dependent Acute Aerobic Exercise Response and Enhances Exercise Capacity.. ACS Chem Biol 2023 · PMID 36988910
- Billon C. A Synthetic ERR Agonist Alleviates Metabolic Syndrome.. J Pharmacol Exp Ther 2023 · PMID 37739806
- Xu W, Billon C, Li H, Wilderman A, Qi L, Graves A, Rideb JRDC, Zhao Y, Hayes M, Yu K, Losby M, Hampton CS, Adeyemi CM, Hong SJ, Nasiotis E, Fu C, Oh TG, Fan W, Downes M, Welch RD, Evans RM, Milosavljevic A, Walker JK, Jensen BC, Pei L, Burris T, Zhang L. Novel Pan-ERR Agonists Ameliorate Heart Failure Through Enhancing Cardiac Fatty Acid Metabolism and Mitochondrial Function.. Circulation 2023 · PMID 37961903
- Hampton CS, Sitaula S, Billon C, Haynes K, Avdagic A, Wanninayake U, Adeyemi CM, Chatterjee A, Griffett K, Banerjee S, Burris SL, Schoepke E, Boehm T, Bess A, de Vera IMS, Burris TP, Walker JK. Development and pharmacological evaluation of a new chemical series of potent pan-ERR agonists, identification of SLU-PP-915.. Eur J Med Chem 2023 · PMID 37421886
- Moller 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 · PMID 41588687
- Billon C, Appourchaux K, Cote I, Burris TP. An orally active estrogen receptor-related receptor agonist, SLU-PP-915, enhances aerobic exercise capacity.. J Pharmacol Exp Ther 2025 · PMID 41421047
SLU-PP-332 — safety, predicted from mechanism
Predicted from mechanism, not from a human safety trial. How that reasoning works →
What the mechanism predicts
Derived from the molecule, not a trial.
- These act on mitochondrial function, NAD+ availability, sirtuin signaling or cellular clearance. The honest prediction is that acute harm is unlikely and the interesting risks are theoretical and long-range — which is a different shape of risk, not an absence of one.
- Growth and clearance signals cut both ways. Anything that improves the efficiency of cell survival is also improving it for cells you would rather not keep. Anything that pushes clearance hard is doing so indiscriminately.
- The near-term, practical ones: NAD+ precursors and infusions commonly cause flushing and a strong sensation if pushed fast, and several compounds in this class are stimulating enough to disrupt sleep.
What has actually been reported
- Generally well tolerated at studied doses. NAD+ infusion discomfort is rate-dependent and resolves by slowing down.
- The human evidence is mostly short trials with surrogate endpoints — a marker moved, not a life changed. That is worth knowing before you build a decade-long habit on it.
How to reduce the risk
Same mechanism as the prediction.
- Slow the infusion rate. Almost all NAD+ discomfort is rate, not dose. There is no prize for finishing quickly.
- Dose earlier in the day. Several of these are subtly stimulating, and sleep is where most of the repair you are paying for happens.
- Pick an endpoint you can actually measure, and take the baseline before you start. This is the class most prone to spending years on something with no way of knowing whether it did anything.
- Fix the basics first. Sleep, training and bloodwork move the same markers further than anything on this list, and they are free. A longevity compound stacked on four hours of sleep is a rounding error.
What it does to your bloodwork
A fact about the assay.
- There is no NAD+ assay worth ordering clinically. Judge this class on downstream markers — inflammatory markers, lipids, fasting glucose, and whatever your baseline panel showed as out of range.
Don't run this if
- Active malignancy, for the survival-signaling reasoning above.
- Pregnancy — uncharacterized.
The honest unknown
- Whether any of it extends healthspan in humans. Every honest person in this field is running on mechanism and animal data, and this catalog should say so rather than imply otherwise.
Not medical advice. If you take prescription medication or have a diagnosed condition, check this with a pharmacist or doctor.
SLU-PP-332 — interference & stacking
Predicted from mechanism, not from an interaction study. How mechanism-predicted claims are made →
What SLU-PP-332 moves on your bloodwork
Expected direction, not a measured one.
- hs-CRP (High-Sensitivity C-Reactive Protein) — ↓ expected to fall
Where these work, systemic inflammation is the plausible readout.
What to do: hs-CRP is cheap and moves. Baseline and 12 weeks. - HbA1c (Hemoglobin A1c) — ↓ expected to fall
Improved mitochondrial and metabolic function should show here if the effect is real at all.
What to do: The honest use of these markers is as a falsification test: if nothing moves in 12 weeks, the compound is not doing much for you. - Comprehensive Metabolic Panel (CMP) — ◆ worth watching
Liver and kidney function — the standard baseline for anything run long term.
What to do: Twice a year is enough on a stable protocol.
This class is where honest expectation-setting matters most: the markers above are how you find out whether anything happened, and for most of these compounds that question is genuinely open.
- How to work up to it, and when not to
- When to take it, and why that window
- Cycle length
- Time off between cycles
- Fasted or fed, and when in the day
- Needle gauge and injection site
- How the forms differ in dose
- Coach Cam's personal notes
- Which compounds push the same lever, and why the dose adds up faster than people count
- What blunts it — the stacks that waste your money
- What compounds the risk, so a side effect arrives sooner than any one of them suggests
- Coach Cam's read on running it alongside the rest of your protocol
Everything above is free and stays free. Skool is where it becomes a plan — SLU-PP-332 in an order, with the rest of what you're running.
Unlock in Skool — $10/mo →Bloodwork to run alongside SLU-PP-332
Baseline first, then again at 8–12 weeks.
| Marker | What it’s watching for |
|---|---|
| HbA1c (Hemoglobin A1c) | Where you started, so you can prove the change was real |
| Fasting Insulin | Moves years before HbA1c does — the earliest signal you get |
| Lipid Panel (Cholesterol, HDL, LDL, Triglycerides) | Rapid fat loss shifts triglycerides fast, in both directions |
| Comprehensive Metabolic Panel (CMP) | Liver, kidney and electrolytes while intake is restricted |
The Metabolic Health & Prediabetes panel covers these in one order — 8 markers, $81.45 with the discount applied.
Check results you already have → · All 103 markers A–Z
SLU-PP-332 — frequently asked questions
What is SLU-PP-332?
SLU-PP-332 (Pan-ERR agonist) is a metabolic & fat loss research compound. Synthetic pan-ERR (α/β/γ) agonist that switches on the endurance-exercise gene program via PGC-1α — mitochondrial biogenesis and fat oxidation, an 'exercise mimetic.'
Is the full SLU-PP-332 protocol on this page?
The reported research dose is on this page, along with how SLU-PP-332 works and the evidence behind it. The protocol — how to work up to it, frequency, cycle length, time off, what not to stack it with and Coach Cam's notes — is inside Skool.
What is the half-life of SLU-PP-332?
SLU-PP-332 has an approximate half-life of Very short (<1 hr), which is part of what determines how often it's dosed.
What forms does SLU-PP-332 come in?
SLU-PP-332 is available as: Injectable, Oral.
What's the evidence behind SLU-PP-332?
Current evidence level: Mouse only — no human data. SLU-PP-332 is offered for research purposes only and is not an approved medicine.
SLU-PP-332 inside a finished plan
One arm of 2 Protocol Blueprints, free to read in full.
What SLU-PP-332 is used for
SLU-PP-332 appears under 2 goals in the goal router.
Related Metabolic & Fat Loss compounds
Where this goes next
SLU-PP-332 is the mitochondrial arm of this plan. The page above is the free breakdown of one compound; the plan it belongs to — the dosing, the order to correct things in, the week-by-week schedule and what to retest — is a lesson inside Skool.