The synthetic ERR agonist popularly dubbed “exercise in a pill” based on preclinical mouse studies. Important caveat: the Burris-lab successor SLU-PP-915 paper (PMID 41421047) explicitly states SLU-PP-332 itself lacks oral bioavailability — community oral dosing is not pharmacologically supported by the originating literature.
SLU-PP-332 is a synthetic pan-agonist of the estrogen-related receptors (ERRα, ERRβ, ERRγ) — a family of orphan nuclear receptors that govern mitochondrial biogenesis, fatty acid oxidation, and oxidative metabolism. It was identified at Saint Louis University as part of a program to find drug-like ERR agonists.
It’s earned the nickname "exercise mimetic" because animal studies show it produces many of the same adaptations as endurance training — without any actual training. In mice, it extended running endurance by ~50% and produced measurable fat loss at unchanged food intake.
Not FDA approved. Preclinical research only (no completed human trials as of 2026). Not WADA prohibited — but check before competition, as metabolic agonists are on WADA’s monitoring list. Available as research chemical only.
Directly activates all three ERR isoforms. These receptors are downstream effectors of PGC-1α (the "master regulator" of mitochondrial biogenesis) — when ERR is active, the cell reads it as "we need more mitochondria."
Increases mitochondrial density and oxidative capacity in skeletal muscle. The same adaptation that endurance training produces — without the training.
Upregulates genes involved in beta-oxidation, causing cells to preferentially burn fat for fuel. Main mechanism for observed fat loss at unchanged intake.
Promotes type I (slow-twitch, oxidative) muscle fiber characteristics — which is why endurance gains are larger than strength gains in animal studies.
SLU-PP-332 is preclinical only — no human trials completed. The animal data is striking enough to drive significant community interest, but translate with appropriate skepticism.
| Benefit | Evidence |
|---|---|
| Endurance | ~50% longer treadmill running time in obese sedentary mice |
| Fat loss | Significant fat reduction at unchanged food intake in diet-induced obesity models |
| Metabolic rate | Increased oxygen consumption and energy expenditure |
| Mitochondrial density | Measurable increase in muscle mitochondrial content |
| Glucose tolerance | Improved insulin sensitivity in animal models |
| Stacks with MOTS-C | Complementary pathway — MOTS-C activates AMPK, SLU-PP-332 activates ERR; theoretical synergy |
Human dosing is not clinically established. Community doses are extrapolated from animal studies — treat results with appropriate caution.
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Start Tracking FreeHuman dosing is not clinically established. Start low (5 mg/day) and assess tolerance before increasing.
Important pharmacology caveat: The Burris lab’s 2026 paper introducing SLU-PP-915 (PMID 41421047), an orally bioavailable successor analog, explicitly states that SLU-PP-332 itself lacks oral bioavailability. The community oral-capsule protocol is therefore not supported by the originating preclinical literature; it predates and contradicts the lab’s own characterization. SubQ injectable forms exist but the only published bioavailability data is the 915 paper, which is about a different molecule. If the oral protocol is the intended use case, SLU-PP-915 is the more pharmacologically defensible compound.
Usually supplied as oral capsules or powder — no reconstitution required for oral. If supplied as injectable powder, reconstitute with 2 mL BAC water for ~2.5 mg/mL (for a 5 mg vial) and draw 0.4 mL = 40 units per 1 mg dose.
Pre-filled with a typical SLU-PP-332 setup. Edit any field — the draw updates live.
Insulin syringe — 100 units = 1 mL
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Human safety data is limited. Animal studies show a favorable profile, but translating to human side effects requires caution.
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Start Tracking FreeThat nickname comes from preclinical mouse studies where SLU-PP-332 extended treadmill running time by roughly 50% and drove fat loss at unchanged food intake. It is a striking animal result, not a validated human effect. No human trials have been completed, so calling it "exercise in a pill" is marketing shorthand, not data.
SLU-PP-332 is a synthetic pan-agonist of the estrogen-related receptors ERR-alpha, ERR-beta, and ERR-gamma. Those orphan nuclear receptors sit downstream of PGC-1-alpha and drive mitochondrial biogenesis, fatty acid oxidation, and a slow-twitch fiber shift. In mice this looks like the adaptations endurance training produces, without the training.
No completed human trials as of 2026. Everything published is preclinical (mice and cell work). Community dosing is extrapolated from animal studies, and the originating Burris lab paper on the successor compound SLU-PP-915 (PMID 41421047) explicitly states SLU-PP-332 itself lacks oral bioavailability, so the popular oral capsule protocol is not pharmacologically supported by the lab that discovered it.
Not FDA approved at any dose for any indication. It is available only as a research chemical. SLU-PP-332 is not currently on the WADA prohibited list, but metabolic agonists in this class are on WADA monitoring and likely to be flagged. Athletes should verify current WADA status before competition rather than trusting community claims.
Community protocols run 5 to 10 mg per day orally, once daily, in 4 to 8 week cycles with 4 week breaks. Those numbers are extrapolated from rodent studies, not from human dose-finding work, and the oral route itself is contradicted by the originating literature. If oral delivery is the goal, the successor SLU-PP-915 is the more pharmacologically defensible compound.
Human safety data is essentially absent. Early adopters anecdotally report mild first-week fatigue, increased exercise sweating, GI discomfort from oral dosing, and transient sleep disturbance. Assume the long-term profile is unknown: run short cycles and monitor CBC, CMP, and lipids every 4 to 8 weeks if using.
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