Peptide Schedule
SLU-PP-332Small moleculeNo amino acid sequence. Icon reflects category theme only.SLU-PP-332
Benefits
About SLU-PP-332
SLU-PP-332 is a synthetic small-molecule agonist of the estrogen-related receptors (ERRα, ERRβ, and ERRγ) developed at Saint Louis University and Washington University School of Medicine. It acts as an "exercise mimetic" — activating the same metabolic gene programs that aerobic exercise normally triggers, without requiring physical activity. In mouse studies, SLU-PP-332 increased energy expenditure, boosted fatty acid oxidation by 25%, and reduced body weight by 12% in diet-induced obese animals over 28 days. Treated mice ran 45% farther and 70% longer than untreated controls. Unlike GLP-1 agonists, SLU-PP-332 does not suppress appetite or reduce food intake. Instead, it works by binding the ligand-binding domain of ERRα and recruiting PGC-1α, driving transcription of genes governing mitochondrial biogenesis and oxidative phosphorylation. All published data come from animal models. No human clinical trials have been initiated, and no safety or efficacy data exist in people. This compound is strictly a research tool at present.
Who Should Consider SLU-PP-332
- Research subjects in preclinical metabolic studies
- Animal models of diet-induced obesity and metabolic syndrome
- Potential future application: individuals unable to exercise due to disability or chronic illness
- Potential future application: age-related muscle wasting (sarcopenia)
- Potential future application: metabolic syndrome and insulin resistance
How SLU-PP-332 Works
SLU-PP-332 is a pan-agonist of the estrogen-related receptors with highest potency at ERRα (EC50 = 98 nM), followed by ERRβ (EC50 = 230 nM) and ERRγ (EC50 = 430 nM). It binds to a hydrophobic trench adjacent to the ligand-binding domain, interacting with residues Leu345 and Phe377, and stabilizes the receptor in its active conformation. This promotes recruitment of the transcriptional coactivator PGC-1α, which amplifies the expression of genes governing mitochondrial biogenesis, fatty acid oxidation, and oxidative phosphorylation. Downstream, SLU-PP-332 induces expression of DDIT4 (an mTOR regulator) and activates an acute aerobic exercise transcriptional program in skeletal muscle — shifting fibers toward the oxidative Type IIa phenotype and increasing whole-body energy expenditure.
What to Expect
Decreased respiratory exchange ratio observed within 2 hours of first dose, indicating a shift toward fatty acid oxidation over carbohydrate metabolism.
Measurable increase in energy expenditure and early changes in gene expression related to mitochondrial biogenesis in skeletal muscle tissue.
Running endurance improved — mice ran 45% farther and 70% longer. Shift toward Type IIa oxidative muscle fibers becomes detectable.
12% body weight reduction in obese mice. Fat mass gain reduced by approximately 10-fold compared to untreated controls. Improved glucose tolerance and lower fasting insulin.
Dosing Protocol
| Level | Dose / Injection | Frequency |
|---|---|---|
| Beginner | 10mg | Daily |
| Moderate | 25mg | Daily |
| Aggressive | 50mg | Daily |
Note: Small-molecule ERR pan-agonist, not a peptide. Preclinical only — all data from mouse studies. Dosed at 50 mg/kg i.p. twice daily in published research. No established human dose exists. Oral bioavailability is under investigation.
How to Inject SLU-PP-332
No human administration protocol exists. In published mouse studies, SLU-PP-332 was administered intraperitoneally at 50 mg/kg twice daily. Oral and subcutaneous bioavailability in humans are unknown. Any investigational use should occur only under IRB-approved research protocols.
Cycling Protocol
No established cycling protocol for humans. Animal studies used continuous 28-day dosing. Extended use beyond study durations has not been evaluated.
Pharmacokinetics
Source: Estimated from murine PK data — plasma exposure 0.2 μM at 6 hours post-dose (30 mg/kg i.p.)
Loading the interactive decay curve.
Side Effects
No human safety data exist. In mouse studies, relatively minor changes in plasma cholesterol and liver enzyme levels were observed. Long-term toxicity, carcinogenicity, and reproductive safety have not been assessed in any species. All side effect information is extrapolated from animal models and should be interpreted with extreme caution.
Contraindications
- Pregnancy or breastfeeding — reproductive safety not assessed in any species
- No human safety data — contraindications are unknown
- Known hypersensitivity to SLU-PP-332 or related ERR agonists
- Liver disease — minor liver enzyme elevations observed in animal studies
- Hormone-sensitive conditions — ERR receptors interact with estrogen-related pathways
- Children and adolescents — no developmental safety data available
Drug Interactions
- Estrogen receptor modulators (SERMs, aromatase inhibitors) — potential pathway overlap with estrogen-related receptor signaling
- Diabetes medications (insulin, metformin, sulfonylureas) — may compound glucose-lowering effects based on animal data showing improved insulin sensitivity
- Lipid-lowering agents (statins, fibrates) — potential additive effects on fatty acid metabolism
- CYP450 substrates — metabolic interaction profile in humans is completely unknown
- Other exercise mimetics (AICAR, GW501516) — theoretical additive metabolic stress
Storage & Stability
Related Peptides
References
- A Synthetic ERR Agonist Alleviates Metabolic Syndrome (Billon et al., J Med Chem 2023)PubMed 37739806
- Synthetic ERRα/β/γ Agonist Induces an ERRα-Dependent Acute Aerobic Exercise Response and Enhances Exercise Capacity (Billon et al., Mol Metab 2024)PubMed 39521410
- The Cardiac Protective Effects of Novel Synthetic Pan-Estrogen Related Receptor Agonists SLU-PP-332 and SLU-PP-915 (Circulation 2021)Review