SLU‑PP‑332
ERRα (Estrogen-related receptor alpha) synthetic agonist, Salk 2024 preprint (Billon et al. bioRxiv) – preclinical-only, mouse-trial exercise-mimetic evidence. NO human PK / safety data; "exercise-mimetic" myth-marketing since 2024.
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Related comparisons
SLU-PP-332 vs SLU-PP-915WHAT IS SLU-PP-332?
Detailed overview
SLU-PP-332 is a synthetic ERRα (Estrogen-related receptor alpha) agonist published as a 2024 preprint on bioRxiv by the Salk Institute research group (Billon et al.). It received attention in popular science press (Nature News briefing 2024) under "exercise-mimetic" positioning, but its evidence base is exclusively preclinical mouse data: a 6-week 50 mg/kg/day oral regimen produced +50% endurance capacity + elevated mitochondrial biogenesis in skeletal muscle (Billon 2024 preprint). Mechanism: synthetic agonist binding to the ERRα nuclear receptor → upregulation of PGC-1α + mitochondrial-biogenesis gene transcription → elevated skeletal muscle mitochondrial density + endurance/aerobic capacity. No Phase 1 human trial is active as of January 2026; ZERO human PK / safety / efficacy data exists. Its emergence on the blackmarket research-chemical scene during 2024-2025 (following the Salk paper) follows a typical designer-research-chemical pattern: marketing-driven hype, preclinical-only evidence base. Exercise-induced PGC-1α upregulation (Holloszy 1967, Hoppeler 1985 PMID 4082137) has long been documented as a physiological effect – SLU-PP-332 pharmacologically mimics it; the "exercise-mimetic" marketing claim does NOT mean that the full spectrum of endurance training effects can be reproduced (cardiovascular adaptation, neuromuscular efficiency, etc. are not ERRα-mediated). MolekulaX uses the research-chemical-class designer-purple (#a78bfa) accent color, identical to the 5-Amino-1MQ + BAM15 category – preclinical-only research-target framing.
Mechanism
ERRα (Estrogen-related receptor alpha) synthetic agonist; upregulates PGC-1α + mitochondrial biogenesis
Dosing (preclinical)
50-100 mg/day PO (mouse-dose extrapolation, NO human-trial validation)
Half-life
~6-8 hours (mouse extrapolation, NO human PK)
Onset time
Mitochondrial-biogenesis marker 2-4 weeks in mice; not documented in humans
Legal status
Research-only – NOT an FDA / EMA Rx, no active Phase 1 human trial as of January 2026. WADA NOT explicitly listed; S0 catch-all + monitoring concern applies.
Data console
Lab data
Safety
Side effects, stop signs, contraindications
Side effects · 6
- Unknown human side-effect profile: no Phase 1 or any human clinical trial exists, so human toxicity, the side-effect spectrum and tolerability are entirely uncharacterized (preclinical mouse data only, Billon 2024 preprint).
- Potential proliferative/oncologic risk: sustained ERRα activation is a signaling pathway associated with proliferation and poor prognosis in several cancers (breast, prostate); a theoretical tumor-promoting risk of chronic agonism cannot be excluded in the absence of human data (Audet-Walsh 2015, PMID 25587719).
- Possible cardiac effects: ERRα is a central regulator of myocardial mitochondrial bioenergetics; the impact of pharmacologic agonism on cardiac energetics is undocumented in humans, and cardiotoxicity or arrhythmia cannot be excluded.
- Unknown hepatic and renal burden: although the mouse trial reported no ALT/AST elevation over 6 weeks (Billon 2024 preliminary), there is no human hepato- or nephrotoxicity data, and the safety of chronic oral dosing is uncharacterized.
- Hazards of black-market (UGL) sourcing: no legitimate pharmaceutical source exists; the 2024-2025 research-chemical supply carries risks of counterfeiting, under-tested purity, contamination and degradation (the COA is often missing or fabricated).
- Non-validated dosing: the 50 mg/kg/day mouse dose cannot be extrapolated directly to a human dose (due to body-surface-area correction and species differences), so the risk of overdose and the therapeutic window are entirely unknown.
Contraindications · 6
- Any human use outside a clinical trial: as of January 2026 there is no approved indication and no active Phase 1 trial, so no legitimate human use exists and self-experimentation is not advised.
- Active or prior malignancy, or hormone-sensitive cancer: ERRα agonism activates a proliferative signaling pathway, which is theoretically contraindicated in an oncologic context (Audet-Walsh 2015, PMID 25587719).
- Pregnancy and breastfeeding: there is no reproductive toxicity or teratogenicity data, the risk of fetal/infant exposure is unknown, and it should therefore be avoided.
- Children and adolescents: there is no Phase 1 indication and the effect on a developing organism is entirely uncharacterized, so it must not be used.
- Pre-existing cardiovascular disease: ERRα regulates myocardial mitochondrial energetics, the cardiac impact of pharmacologic agonism is undocumented in humans, and it should therefore be avoided in heart disease.
- Competitive athletes (WADA): although SLU-PP-332 is not explicitly listed, the S0 'non-approved substance' catch-all clause prohibits any pre-Phase 2 research chemical, so it is de facto WADA-banned and should be avoided in competition.
Related Performance Compounds
Same therapeutic category
Studies
Related research and clinical findings
Synthetic ERRα agonist SLU-PP-332 enhances exercise-induced metabolic adaptations in mice
Billon C, Sitaula S, Banerjee S et al.
Synthetic ERRα/β/γ Agonist Induces an ERRα-Dependent Acute Aerobic Exercise Response and Enhances Exercise Capacity.
Billon C, Sitaula S, Banerjee S, Welch R, Elgendy B, Hegazy L, Oh TG, Kazantzis M, Chatterjee A, Chrivia J, Hayes ME, Xu W, Hamilton A, Newman JD, Downes M, Evans RM, Burris TP
Estrogen-related receptors regulate innate and adaptive muscle mitochondrial energetics through cooperative and distinct actions.
Fan W, Oh TG, Wang HJ, Yu RT, Atkins AR, Downes M, Evans RM
A Synthetic ERR Agonist Alleviates Metabolic Syndrome.
Billon C, Schoepke E, Avdagic A, Chatterjee A, Butler AA, Elgendy B, Walker JK, Burris TP
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