Origin

IMPORTANT: SLU-PP-332 is NOT a peptide, despite being commonly sold and discussed alongside peptide research compounds. It is a synthetic small-molecule drug — a designed pan-agonist of the three estrogen-related receptor subtypes (ERRα, ERRβ, ERRγ), orphan nuclear receptors unrelated to estrogen signaling itself. It was developed and first reported by academic pharmacology labs (Washington University in St. Louis / Saint Louis University / University of Florida groups) as a chemical tool to probe ERR biology.

Mechanism

ERRs are master transcriptional regulators of mitochondrial biogenesis, oxidative phosphorylation, and fatty acid oxidation, and are activated physiologically during aerobic exercise. SLU-PP-332 binds and activates all three ERR subtypes (with highest potency at ERRα), driving an ERRα-dependent gene program that mimics acute aerobic exercise — including induction of Ddit4 and Slc25a25, increased type IIa oxidative muscle fiber content, and enhanced cellular respiration — without the animal actually exercising.

Research summary

Evidence

All published evidence is preclinical: cell-based assays and mouse studies show SLU-PP-332 increases mitochondrial function and exercise endurance, reduces fat mass, and improves insulin sensitivity in diet-induced-obesity and metabolic syndrome mouse models. A 2026 structure-activity-relationship paper further characterizes its binding and identifies analogues (including the orally bioavailable follow-up compound SLU-PP-915) with improved pharmacokinetics. No human pharmacokinetic, safety, or efficacy data exist; a 2026 doping-control analytical paper characterizes its metabolites specifically because anti-doping labs are watching for illicit human use, which underscores that it is being taken by people despite zero human trials.

Evidence tier: Research chemical — see the methodology note for how this is assessed.

Citations

Synthetic ERRα/β/γ Agonist Induces an ERRα-Dependent Acute Aerobic Exercise Response and Enhances Exercise Capacity — Billon et al., 2023
A Synthetic ERR Agonist Alleviates Metabolic Syndrome — Billon et al., 2024
An orally active estrogen receptor-related receptor agonist, SLU-PP-915, enhances aerobic exercise capacity — Billon et al., 2025
Chemical optimization of the exercise mimetic SLU-PP-332 enables insight into estrogen-related receptor signaling — Okda et al., 2026
[Pharmacological Activation of ERRα/β/γ as an Exercise Mimetic: Potential Therapeutic Applications] — de Souza-Lima et al., 2026

Reported benefits

In mice only: increased treadmill endurance, increased oxidative (type IIa) muscle fiber proportion, and improved aerobic capacity
In mouse obesity/metabolic syndrome models: reduced fat mass, increased energy expenditure, improved insulin sensitivity
Proposed (unproven in humans) as a mitochondrial-biogenesis and 'exercise mimetic' strategy for sarcopenia, metabolic disease, and aging-related muscle decline

Dosing protocols reported in the literature & community

These are protocols reported by compounding pharmacies, published trials, or self-experimentation communities — not a prescription. Start low, especially for anything new.

Reported dosing protocols
Route	Reported protocol
not established for humans	All published dosing is intraperitoneal or oral administration in mice at research doses (mg/kg); no human dosing protocol exists, and self-administration in humans is unstudied off-label use of a research chemical with unknown human pharmacokinetics

Side effects

No human safety data exists at all — side effect profile in humans is unknown
Mouse studies report no evident toxicity at studied doses, but this does not establish human safety
Flagged by anti-doping researchers as a potential performance-enhancing substance of concern, implying real-world human use is already occurring ahead of any safety data

Safety notes

Community & reddit notes (anecdotal — not clinical evidence)

Discussed in fitness/longevity research-chemical circles as a next-generation 'exercise mimetic,' often mentioned in the same breath as peptide compounds even though it is chemically distinct; self-experimenters extrapolate mouse dosing to humans by body-weight scaling, a practice with no validated basis and no reported pharmacokinetic grounding.