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Research compound — not a dietary supplement
SLU-PP-332 is a research compound, not a regulated dietary supplement. It is sold for research or off-label use. The evidence below is largely preclinical (animal and in-vitro) or early-stage, so no evidence score is assigned. This page is provided for transparency and education — it is not a recommendation to use. Consult a qualified healthcare provider, and be aware that purity, dosing, and legal status vary by jurisdiction.
What the evidence says
Most SLU-PP-332 studies are mechanism or observational rather than RCTs that measure a clinical effect — keep findings provisional.
Most evidence is from mixed-quality studies published 2023–2025.
Based on 5 studies
Confidence
LowBy outcome
SLU-PP-332 has an evidence score of 3/10 — emerging evidence based on 5 indexed studies. A very new preclinical 'exercise mimetic' research chemical with NO human data of any kind — every result below is from mice or cultured cells. SLU-PP-332 is a synthetic agonist of the estrogen-related receptors (ERRα/β/γ), orphan nuclear receptors that drive the mitochondrial/oxidative gene program normally switched on by aerobic exercise. In mice it boosted running endurance and fat oxidation, alleviated diet-induced obesity, and improved heart-failure outcomes — a genuinely interesting mechanism. But it has never been tested in a single human, it isn't an approved drug or a lawful supplement, the original compound isn't even orally bioavailable (mouse studies inject it), and its long-term safety is completely unknown. This entry exists to inform, not to recommend. Representative study: PMID 36988910.
The commonly studied dose of SLU-PP-332 is No legitimate or recommended dose — SLU-PP-332 is an unapproved grey-market research chemical with no human dosing data and no quality control. We do NOT provide a dosing protocol. The only published dosing is in mice, and notably the original compound is not orally bioavailable — the mouse studies administer it by injection (intraperitoneal), so the orally sold powders do not even match how it was studied.. Individual needs vary — start at the lower end of the range and adjust based on how you respond.
AICAR (Acadesine)
Mostly mechanism / observationalA grey-market AMPK activator marketed as an 'exercise mimetic' on the strength of a single famous mouse study — Narkar 2008, where 4 weeks of AICAR boosted treadmill running endurance 44% in sedentary mice. That endurance signal has NEVER been shown in humans. The only human trials of AICAR (as the drug acadesine) were for a completely different purpose — protecting the heart during cardiac-bypass surgery — and the large, definitive RED-CABG randomized trial was NEGATIVE. AICAR has poor oral bioavailability (it's injected in studies), is WADA-banned as a doping agent, and is not an approved drug or a regulated supplement. There is no human exercise-performance evidence.
Last reviewed June 2026 · evidence from 5 studies · how we score
This information is for educational purposes only. It is not a substitute for professional medical advice. Always consult a qualified healthcare provider before starting, stopping, or changing any supplement or medication.
SLU-PP-332 — synthetic pan-ERR (estrogen-related receptor) agonist / 'exercise mimetic'
A very new preclinical 'exercise mimetic' research chemical with NO human data of any kind — every result below is from mice or cultured cells. SLU-PP-332 is a synthetic agonist of the estrogen-related receptors (ERRα/β/γ), orphan nuclear receptors that drive the mitochondrial/oxidative gene program normally switched on by aerobic exercise. In mice it boosted running endurance and fat oxidation, alleviated diet-induced obesity, and improved heart-failure outcomes — a genuinely interesting mechanism. But it has never been tested in a single human, it isn't an approved drug or a lawful supplement, the original compound isn't even orally bioavailable (mouse studies inject it), and its long-term safety is completely unknown. This entry exists to inform, not to recommend.
A very new and mechanistically interesting 'exercise mimetic' — a synthetic pan-ERR agonist that consistently boosted endurance, fat oxidation, and metabolic/cardiac outcomes across several mouse models — but with zero human data of any kind (no safety, no pharmacokinetics), an unproven translation to people, and a grey-market supply chain. Promising mechanism, but unproven and very early.
SLU-PP-332 is a small-molecule synthetic agonist of the estrogen-related receptors (ERRα, ERRβ, ERRγ) — orphan nuclear receptors that, together with the coactivator PGC-1α, govern mitochondrial biogenesis, oxidative phosphorylation, fatty-acid oxidation, and the Krebs cycle in skeletal muscle and heart.
Because these are the same transcriptional programs that aerobic exercise activates, ERR agonists have been pursued as pharmacological 'exercise mimetics.' SLU-PP-332 was the first synthetic compound to achieve meaningful ERRα agonist activity (ERRβ/γ agonists existed before, but ERRα had been hard to drug), which is what makes it scientifically notable.
The foundational study (Billon et al., 2023, ACS Chemical Biology) showed that in mice SLU-PP-332 triggers an ERRα-dependent acute aerobic-exercise transcriptional response in muscle and enhances exercise capacity (running distance/time).
A 2024 follow-up (Billon et al., J Pharmacol Exp Ther) reported that it alleviates features of diet-induced obesity and metabolic syndrome in mice; a 2024 Circulation paper (Xu et al.) found that SLU-PP-332 and a sibling compound, SLU-PP-915, improved ejection fraction, reduced fibrosis, and increased survival in a mouse pressure-overload heart-failure model by enhancing cardiac fatty-acid metabolism and mitochondrial function; and a 2023 paper (Wang et al., Am J Pathol) showed pan-ERR agonism reversed mitochondrial dysfunction and inflammation in the aging mouse kidney.
A small 2025 pilot (Bonanni et al., Front Physiol) applied SLU-PP-332 to myoblasts cultured from muscle biopsies of physically inactive women — an ex-vivo cell experiment that probes the PGC-1α/ERRα axis in human-derived cells, but is emphatically not a human clinical trial.
Here is the honest, load-bearing caveat: ALL of this is preclinical. There has never been a published human trial of SLU-PP-332 — no phase-I safety study, no pharmacokinetic study in people, nothing. It is not approved by any regulator and is not a lawful dietary-supplement ingredient.
The original compound is not even orally bioavailable (the mouse work uses injection), which is precisely why chemists designed the distinct, orally active analog SLU-PP-915 — so any orally sold 'SLU-PP-332' product is doubly questionable.
The mechanism is promising and the mouse data are consistent, but ERRs sit at the center of cellular energy metabolism in heart, muscle, kidney, and brain, and the consequences of pharmacologically activating them long-term in humans are entirely uncharacterized.
The score is therefore very low: an intriguing exercise-mimetic mouse-and-cell story with zero human data, sandboxed out of all goal- and stack-based recommendations.
SLU-PP-332 is a synthetic agonist of the estrogen-related receptors — orphan nuclear receptors that regulate mitochondrial and oxidative-metabolism gene programs. It was the first synthetic compound with meaningful ERRα agonist activity. Demonstrated only in mouse and cell systems; never measured in humans.
ERR activation, with the coactivator PGC-1α, upregulates mitochondrial biogenesis, oxidative phosphorylation, fatty-acid oxidation, and Krebs-cycle genes — the same transcriptional response triggered by aerobic exercise. In mice SLU-PP-332 induced this 'exercise signature' in muscle. Established in rodent and cell models, with no human confirmation.
By switching on the oxidative gene program without exercise, SLU-PP-332 increased running endurance and fat/fatty-acid oxidation and improved metabolic and cardiac outcomes in mouse models. Whether any of this translates to humans is entirely unknown — there are no human data.
How SLU-PP-332 works — from molecular targets to health outcomes. Click an edge to see supporting research.This visualization is in beta — pathways are being refined and expanded.
Tap node to isolate • Pinch to zoom • Tap edge for research
No legitimate or recommended dose — SLU-PP-332 is an unapproved grey-market research chemical with no human dosing data and no quality control. We do NOT provide a dosing protocol. The only published dosing is in mice, and notably the original compound is not orally bioavailable — the mouse studies administer it by injection (intraperitoneal), so the orally sold powders do not even match how it was studied.
Can be taken without food
| Form | Type |
|---|---|
| 💊None — unapproved grey-market research chemical | Recommended |
There is no legitimate pharmaceutical form. SLU-PP-332 is a chemical-probe ERR agonist used in mouse and cell research; it is not a medicine or a dietary supplement. A distinct, orally active analog (SLU-PP-915) exists only as a research tool.
Minimum: 1 weeks
Optimal: 1 weeks
Cycling: Not required
Note: No approved or validated timing — the compound has never been tested in humans. This library does not endorse or schedule its use.
Dose-response data unavailable. The current published research for SLU-PP-332 does not provide sufficient dose-specific outcome data to generate reliable dose-response curves.
Refer to the Dosage & Timing section above for recommended dose ranges based on available evidence.
There has never been a published human trial of SLU-PP-332 — no safety study, no pharmacokinetics, nothing. Every effect listed here is from mice or cultured cells and may not translate to people.
In mice, SLU-PP-332 induced an ERRα-dependent aerobic-exercise transcriptional response and increased running distance and time-to-exhaustion. A genuine preclinical signal — not demonstrated in humans.
In diet-induced-obese mice, SLU-PP-332 enhanced fatty-acid/fat oxidation and alleviated features of obesity and metabolic syndrome. Mouse-only finding.
In a mouse pressure-overload heart-failure model, SLU-PP-332 (and the sibling SLU-PP-915) improved ejection fraction, reduced fibrosis, and increased survival by enhancing cardiac fatty-acid metabolism and mitochondrial function. Mouse-only finding.
ERRs sit at the center of energy metabolism in heart, muscle, kidney, and brain. Effects of pharmacologically activating them long-term in humans are unstudied, and the safety profile in people is completely unknown because no human has ever been studied.
Avoid — there are no human trials, no approved use, and no quality-controlled product. The mouse evidence does not justify human self-experimentation.
Avoid — effects on cardiac and metabolic gene programs are demonstrated only in animals and are unstudied and unpredictable in people.
Avoid entirely — completely unstudied.
There are no human drug-interaction data of any kind. SLU-PP-332 broadly activates mitochondrial/oxidative-metabolism gene programs across heart, muscle, and kidney, so interactions cannot be predicted.
ERR agonism remodels cardiac and metabolic gene expression in animals. Combining it with heart-failure, antidiabetic, or other metabolic drugs has never been studied in humans; interactions are theoretically plausible and unpredictable.
Tip: No human has ever been studied — the side-effect profile in people is genuinely unknown. This is itself the warning.
Tip: ERRs regulate energy metabolism in heart, muscle, kidney, and brain; long-term human consequences of activating them are uncharacterized.
Tip: Grey-market material has no identity/purity/sterility guarantees; contaminants are possible.
Timing is flexible for SLU-PP-332 — consistent daily use matters more than the time of day. There is no validated human dosing schedule because the compound has never been tested in humans.
SLU-PP-332 should be used with caution — talk to a healthcare provider before taking it. The most commonly reported side effects are unknown human side-effect profile, unknown effects of long-term ERR / mitochondrial-program activation, harm from an unregulated, impure product. Use caution if any of these apply to you: Not an approved medicine and not a regulated dietary supplement — unapproved grey-market research chemical; do not self-source; No human safety data exists — every safety conclusion would be an extrapolation from mice; Pregnancy and breastfeeding (entirely unstudied).
Cardarine (GW501516)
Mostly mechanism / observationalAn abandoned PPARδ agonist 'exercise mimetic' that was NEVER approved — development was halted when long-term animal studies found tumors across multiple organs. There are NO human efficacy trials; the headline endurance result is from mice on a treadmill (Narkar 2008). The only human data is a tiny 2-week lipid/HDL study. It is banned by the World Anti-Doping Agency as a gene-doping agent and is sold only as an unregulated grey-market research chemical. The cancer signal — not the endurance hype — is the real story.