SLU-PP-332
Synthetic Pan-ERR Agonist | Exercise Mimetic & Metabolic Modulator
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What is SLU-PP-332?
SLU-PP-332 is a lab-made small molecule, not a peptide, that switches on the same cellular energy pathways normally triggered by exercise, which is why researchers nickname it an 'exercise mimetic.' It's studied in animal models for effects on mitochondria (the cell's energy-producing structures) and metabolic research, with no human clinical trials conducted yet. Research-grade SLU-PP-332 sold here is intended strictly for laboratory study, not for use in people or animals.
Key terms:
SLU-PP-332 is a synthetic small molecule.
SLU-PP-332 is a lab-made small molecule developed at Saint Louis University. It switches on the estrogen-related receptors (ERRs), with the strongest effect at ERR-alpha. Researchers call it an 'exercise mimetic' because it activates metabolic pathways the body normally engages during exercise, with no physical activity. Reported effects: more mitochondrial biogenesis (cells building new energy factories), more fatty acid oxidation, higher energy expenditure. In animal models researchers reported 12% weight reduction in 28 days, a 70% increase in endurance, plus changes in insulin sensitivity, cardiac markers, and age-related mitochondrial function. These findings are preclinical, with reported favorable safety profiles across several animal models and no human clinical trials yet. University of Florida researchers are working to advance it toward human studies and an oral pill form.
Key research areas
- Exercise mimetic effects without physical activity
- Significant weight reduction (12% in 28 days in animal studies)
- 70% increased endurance capacity
- 25% enhanced fatty acid oxidation
- Improved insulin sensitivity
- Reduced hepatic steatosis
- Cardiac protection and reversal of age-related mitochondrial dysfunction
- Enhanced muscle oxidative capacity
Researched dosing
This table shows the animal-study dosing used in published SLU-PP-332 research; there is no established or approved human dose, and an oral formulation is still in development.
| Phase | Dose | Frequency | Route |
|---|---|---|---|
| Standard metabolic-model protocol | 50 mg/kg (animal dosing) | Twice daily | Intraperitoneal injection (IP) |
| Acute exercise-performance models | 50 mg/kg (animal dosing) | Single dose 1 hour pre-exercise | Intraperitoneal injection (IP) |
| Extended-course models | 50 mg/kg (animal dosing) | Twice daily for 4-8 weeks | Intraperitoneal injection (IP) |
| No established human-research dose | No approved human dose | Awaiting clinical trials | Oral formulation in development |
Commonly cycled 8 weeks on, 0+ weeks off.
How it works
At the cell level, SLU-PP-332 research looks at how the compound activates estrogen-related receptors that switch on genes for mitochondrial growth and energy use — the terms below describe those downstream signaling steps.
Binds to and activates estrogen-related receptors (ERRα, ERRβ, ERRγ) which regulate gene expression for energy metabolism. Upregulates PGC-1α (master regulator of mitochondrial biogenesis), activates AMPK pathway (cellular energy switch), increases mitochondrial density up to 1.8-fold, enhances oxidative phosphorylation and ATP production, promotes fatty acid oxidation, induces type IIa oxidative muscle fiber genes, and activates acute aerobic exercise genetic programs.
Molecular data
This figure — molecular weight — is the chemistry ID researchers use to confirm a SLU-PP-332 sample's identity; unlike most compounds in this encyclopedia, it's a small molecule rather than a chain of amino acids, so it doesn't have a peptide sequence.
- Weight
- 290.32 Da
- Length
- 0 amino acids
- Type
- Synthetic ERR agonist
Research applications
This section lists the research areas — metabolic, exercise-performance, cardiovascular, and kidney research among them — that scientists have studied for SLU-PP-332 in animal models; there have been no human clinical trials, and human safety and effects remain unknown.
Metabolic Health
Preclinical studies show 12% body weight reduction in 28 days without appetite suppression or increased activity. Fat mass gain <0.5g vs ~5g in controls. Decreases white adipocyte size and shifts metabolism toward lipid utilization. Significantly improved glucose tolerance in obese mice with lower fasting glucose and insulin levels. Enhanced insulin sensitivity comparable to first-line diabetes medications. Increases resting energy expenditure by 25% for fatty acid oxidation. Reduced hepatic steatosis, decreased hepatic triglycerides, and enhanced hepatic fatty acid oxidation with potential therapeutic applications for non-alcoholic fatty liver disease.
Exercise Performance
70% increase in running time and 45% increase in distance. Increased type IIa oxidative muscle fibers. Progressive grip strength improvements. Activates acute aerobic exercise genetic programs without requiring physical activity.
Cardiovascular
Cardiac improvements including improved ejection fraction and reduced fibrosis. Structural cardiac and muscle remodeling with continued treatment.
Longevity
Reversal of age-related mitochondrial dysfunction. Sustained longevity effects in preclinical aging studies. Reduction of cellular senescence markers maintained long-term.
Kidney Protection
Reversal of age-related kidney decline in 21-month-old mice. Reduced albuminuria, prevented podocyte loss, restored mitochondrial architecture. Decreased inflammatory cytokines and senescence markers.
Anti Inflammatory
Reduced inflammatory and senescence markers in aging tissues. Decreased cytokines associated with age-related inflammation.
Dosage reference
- Doses used in research
- No established research dose — animal studies only.
- Frequency in studies
- Not established for human research; animal studies dosed twice daily.
- Handling
- Reconstituted solution — research use only; not for administration
- Timeline reported in studies
- Human timeline unknown - animal studies show effects within hours to weeks
- Storage
- Research compound storage requirements vary
- Cycle length
- Not established — animal studies ran 4-8 weeks.
- Break between cycles
- Unknown — no human data available.
Interactions
This list shows which other metabolic-research peptides and compounds are studied alongside SLU-PP-332, and why some combinations call for monitoring.
Reconstitution & storage
This describes how researchers prepare a SLU-PP-332 solution in the lab — since it's a lipophilic small molecule rather than a peptide, it requires a solvent like DMSO instead of the water-based mixing used for most peptides.
- This is a lipophilic small molecule, not a peptide - it will NOT dissolve in water-based solutions
- Dissolve SLU-PP-332 in pure anhydrous DMSO first to create a stock solution (up to 50-125 mg/mL)
- For in vivo use, dilute DMSO stock with carriers: 10% DMSO + 10% Tween 80 + 80% PBS (from published studies)
- Alternative formulation: 10% DMSO + 40% PEG300 + 5% Tween 80 + 45% saline
- Oil-based alternative: 10% DMSO + 90% corn oil
- Ensure solution is completely clear before adding each solvent - use vortex, ultrasound, or gentle warming
- Final DMSO concentration should not exceed 10% for in vivo applications
- Store the reconstituted solution refrigerated (2–8°C), labeled with the date and concentration, for laboratory research use only.
Lyophilized: -20°C to -80°C, use within 1 month at -20°C; 6 months at -80°C
Reconstituted: 2-6°C, use within Avoid repeated freeze-thaw cycles; use DMSO stock solutions within recommended timeframe
Open the SLU-PP-332 reconstitution calculatorQuality indicators
These are the checks researchers use to confirm a SLU-PP-332 sample is pure and correctly identified — since it is not FDA-approved and has no established manufacturing standards, sourcing verification matters more than usual.
Insoluble in water - use DMSO - SLU-PP-332 is a lipophilic small molecule that will not dissolve in water. Use DMSO as the primary solvent (50-125 mg/mL), not bacteriostatic water.
Research Chemical Only - NOT FOR HUMAN USE - SLU-PP-332 is NOT FDA approved and has NOT been tested in human clinical trials. It is legally available only for legitimate research purposes through licensed suppliers.
Products Marketed for Human Consumption - Any SLU-PP-332 marketed, sold, or labeled for human consumption is illegal and potentially dangerous. Suppliers should clearly label as 'For Research Use Only' with proper regulatory disclaimers.
Unknown Purity or Contamination - Without proper laboratory testing (HPLC, mass spectrometry), purity and identity cannot be verified. Contaminated or misidentified compounds pose serious health risks.
No Quality Control Standards Exist - Since SLU-PP-332 is not approved for human use, there are no GMP (Good Manufacturing Practice) standards or USP monographs. Quality varies widely between suppliers.
Legitimate Research Supplier - If obtained for legitimate research, should come from reputable chemical suppliers (Cayman Chemical, Sigma-Aldrich, etc.) with Certificate of Analysis, proper labeling, batch numbers, and purity data (typically >98%).
What to expect
This timeline reflects what the animal-study literature reports at each research stage — research context for comparing studies, not a personal-results promise; human timelines are completely unknown.
Metabolic shift toward fat oxidation (decreased respiratory exchange ratio within 2 hours). Gene expression changes detectable at 3-6 hours. Measurable plasma (0.2 μM) and muscle (0.6 μM) concentrations at 6 hours. Enhanced exercise performance in acute dosing studies (1 hour post-dose).
Increased resting energy expenditure becomes measurable. Enhanced fatty acid oxidation (25% increase). Initial metabolic adaptations and mitochondrial remodeling begins. Improved grip strength becomes observable by day 6.
Significant weight reduction (up to 12% by day 28 in animal studies). Fat mass reduction dramatically different from controls (<0.5g vs ~5g gain). Improved glucose tolerance and insulin sensitivity. Enhanced exercise endurance (45-70% improvements in running performance). Muscle fiber type changes toward oxidative phenotype. Reduced hepatic steatosis becomes evident.
Cardiac improvements evident (improved ejection fraction, reduced fibrosis). Structural cardiac and muscle remodeling continues. Reversal of age-related kidney dysfunction (if applicable). Restoration of mitochondrial architecture in multiple tissues. Reduced inflammatory and senescence markers in aging tissues.
Safety notes
This section covers regulatory status and handling cautions for SLU-PP-332 — it has not been tested in humans, so this is reference context for laboratory researchers, not medical guidance.
- NOT FDA APPROVED - FOR RESEARCH USE ONLY
- Human safety profile is COMPLETELY UNKNOWN - extrapolation from animals is unreliable
- Legal status varies by jurisdiction - may be restricted or illegal in many areas
- NEVER use experimental compounds without medical supervision and regulatory approval
- Potential effects on insulin sensitivity - may interact with diabetes medications
- NOT FDA approved - research compound only
- No human clinical trials conducted as of current date
- Available only for legitimate research purposes through licensed suppliers
Regulatory status
- Not approved by the FDA for any indication.
- Supplied and described for laboratory research use only — not for human or veterinary use.
Community data
Community Insights
Based on data the community reported. Not clinical proof.
References
12% body weight reduction, 25% increase in fatty acid oxidation, improved glucose tolerance, and reduced hepatic steatosis. Fat mass gain was <0.5g vs ~5g in controls. No adverse pancreatic effects observed. (A Synthetic ERR Agonist Alleviates Metabolic Syndrome, 2024)
Reversal of age-related kidney decline in 21-month-old mice: reduced albuminuria, prevented podocyte loss, restored mitochondrial architecture, decreased inflammatory cytokines and senescence markers. (Estrogen-Related Receptor Agonism Reverses Mitochondrial Dysfunction in Aging Kidney, 2023)
70% increase in running time, 45% increase in distance, increased type IIa oxidative muscle fibers, and progressive grip strength improvements. ERRα confirmed as critical isoform via knockout studies. (Synthetic ERRα/β/γ Agonist Induces Acute Aerobic Exercise Response, 2023)