Skip to product information
a pharmaceutical vial labeled SLU-pp-332, 10 mg, Batch No.002, dated 26-08-2025. The vial is transparent with a gray rubber stopper, matte aluminum cap, and white label, set against a soft beige background.
1/2
SLU-pp-332 10mg vial

SLU-pp-332 10mg vial

€80,00 EUR
Taxes included.

NOT FOR HUMAN CONSUMPTION

SLU-PP-332 is a small-molecule pan–estrogen-related receptor (ERR) agonist/modulator reported by researchers at Saint Louis University as a pharmacologic “exercise mimetic.” By activating ERRα/β/γ (NR3B family)—transcription factors that partner with PGC-1α—SLU-PP-332 up-regulates programs for mitochondrial biogenesis, fatty-acid oxidation (FAO), and oxidative phosphorylation (OXPHOS). In diet-induced-obese mice, the compound has been described to increase whole-body energy expenditure, limit weight gain, and improve glucose tolerance without requiring additional exercise. It is not FDA/EMA-approved; available data are pre-clinical.

Additional Benefits of SLU-PP-332 Now Under Investigation

Benefit Key take-aways
1 Energy-expenditure & weight control In obese mice, SLU-PP-332 raises VO₂/EE and reduces adiposity largely independent of food intake, aligning with ERR-driven oxidative remodeling. <br/><em>bioRxiv preprint (SLU group); Cell Metabolism (ERR biology)</em>
2 Glycaemic control & insulin sensitivity Improves glucose tolerance and insulin tolerance with increased skeletal-muscle Akt signalling and reduced hepatic lipogenesis. <br/><em>bioRxiv preprint; Diabetes (mechanistic context)</em>
3 Endurance/fitness phenotype In treadmill assays, treated mice exhibit longer time-to-exhaustion and greater running distance, consistent with PGC-1α/ERR endurance programs. <br/><em>bioRxiv preprint; Journal of Physiology (PGC-1α/ERR context)</em>
4 Hepatic steatosis Down-regulates SREBP1c/FASN and up-regulates CPT1A/PPARα targets, reducing liver triglycerides in NAFLD models. <br/><em>bioRxiv preprint; Hepatology (ERR in hepatic lipid flux)</em>
5 Mitochondrial biogenesis Increases mtDNA copy number, OXPHOS complex expression, and PGC-1α target genes in muscle and brown/brite fat. <br/><em>bioRxiv preprint; Nature Reviews Molecular Cell Biology (mitochondrial control)</em>
6 WAT browning & BAT activation Induces UCP1, DIO2, and thermogenic genes with smaller adipocyte size, pointing to beige fat recruitment. <br/><em>bioRxiv preprint; Molecular Metabolism (ERR thermogenesis)</em>
7 Anti-inflammatory shift Reduces TNF-α/IL-6 and crown-like structures in adipose tissue, aligning with improved insulin signalling. <br/><em>bioRxiv preprint; Cardiovascular Diabetology (context)</em>
8 Exercise additivity Additive benefits when layered on voluntary running—higher oxidative gene expression and endurance than either alone. <br/><em>bioRxiv preprint; Exercise-genomics reviews</em>
9 Lipids & cardiometabolic profile Lowers plasma TG/TC and improves HDL:TG ratios in rodents; human relevance pending. <br/><em>bioRxiv preprint; Journal of Lipid Research (ERR lipid biology)</em>

2. Molecular Mechanism of Action

2.1 Target Pharmacodynamics

  • Primary targets: ERRα/β/γ nuclear receptors (constitutive transcription factors) that are co-activated by PGC-1α.

  • SLU-PP-332 action: Stabilizes/activates ERR transcriptional complexes, increasing transcription of FAO/OXPHOS/mitochondrial genes across oxidative tissues (skeletal muscle, heart, BAT, liver).

  • Physiologic analogy: Mimics transcriptional changes seen after endurance exercise or cold-induced thermogenesis.

2.2 Down-stream Biology

Pathway Functional outcome Context
PGC-1α–ERR transcriptional axis ↑ Mitochondrial biogenesis (NRF1/TFAM), ↑ OXPHOS, ↑ FAO Muscle, BAT, liver
PPAR/AMPK cross-talk ↑ CPT1A/ACADs, ↑ lipid oxidation; partial AMPK convergence Liver, muscle
Myofiber remodeling Shift toward oxidative type I/IIA fibers; ↑ capillary density genes Skeletal muscle
Thermogenic program ↑ UCP1/UCP3, ↑ DIO2, ↑ β-oxidation → ↑ EE BAT/brite WAT
Inflammation/ECM ↓ Pro-inflammatory cytokines, ↓ adipose fibrosis markers Adipose/liver

3. Pharmacokinetics

  • Route/form: Small-molecule administered to rodents; detailed human PK unknown.

  • Exposure: Pre-clinical reports indicate systemic exposure compatible with once-daily paradigms in mice; brain penetration unclear.

  • Half-life/clearance: Not publicly established; presumed hepatic/renal clearance typical of lipophilic transcription-modulators.

  • Drug–drug interactions: No clinical data; ERRs regulate metabolic enzymes, so indirect interactions are conceivable.

4. Pre-clinical and Translational Evidence

4.1 Obesity & Metabolic Syndrome

Diet-induced-obese mice treated with SLU-PP-332 display less weight gain, higher VO₂/EE, better glucose tolerance, and smaller adipocytes, with browning signatures in WAT.

4.2 NAFLD

Liver transcriptomics show suppressed lipogenesis and enhanced FAO, with lower hepatic triglycerides and improved transaminases in models prone to steatosis.

4.3 Exercise & Fitness

Skeletal muscle exhibits PGC-1α/ERR target induction, increased OXPHOS complexes, and improved treadmill endurance—recapitulating aspects of endurance training.

Evidence quality note: Data for SLU-PP-332 are pre-clinical (rodents/cells) and include institutional reports and preprints. Peer-reviewed, multicentre replication and human studies are not yet available.

5. Emerging Clinical Interests

Field Rationale Current status
Obesity/overweight ↑ EE without appetite suppression; oxidative remodelling Pre-clinical
NAFLD/NASH ↓ DNL, ↑ FAO; thermogenic support Pre-clinical
T2D/insulin resistance Improved insulin signalling & adipose inflammation Pre-clinical
Sarcopenic obesity/frailty Endurance/mitochondrial programs to augment function Concept/rodent
Cardiometabolic fitness Exercise-mimetic transcriptional shifts Concept/rodent

6. Safety and Tolerability

  • Human safety: Unknown (no clinical datasets).

  • On-target cautions: ERRα/γ are highly expressed in heart—chronic pan-ERR activation may alter cardiac energetics/arrhythmia susceptibility; careful CV monitoring would be required clinically.

  • Endocrine/GRN: ERRs cross-talk with estrogen/thyroid/PPAR programs; unintended transcriptional effects are possible.

  • Metabolic: Excessive EE could increase resting heart rate/temperature; weight loss without intake reductionraises nutrient deficiency risk if unmanaged.

  • Genotoxicity/oncogenicity: No GLP toxicology or carcinogenicity data have been disclosed.

Comparative safety matrix

Concern SLU-PP-332 (pan-ERR) AICAR (AMPK agonist) GW501516 (PPARδ agonist)
Mechanism Transcriptional “exercise” via ERRα/β/γ Energy stress sensor FAO/oxidative via PPARδ
Human data None Limited (investigational) None (rodent tumor signals at high dose)
CV impact Potential cardiac energetic effects Brady-like signals in some models ↑ endurance; tumor concerns in rodents
Regulatory status Pre-clinical Investigational Abandoned (safety)

7. Regulatory Landscape

  • Approvals: None.

  • Development stage: Discovery/lead-optimization to pre-clinical space; no registered human trials publicly reported as of 2025.

  • Access: Not available as a medicine; any grey-market product should be considered unregulated and unsafe.

8. Future Directions

  • Selectivity engineering: Bias toward ERRα/γ or tissue-targeted delivery (e.g., muscle- or liver-targeting) to improve benefit–risk.

  • Translational biomarkers: Indirect calorimetry (VO₂), acyl-carnitine profiles, mtDNA copy number, OXPHOS proteomics, and liver MRI-PDFF for early human PoC.

  • Combination strategies: Pair with diet/exercise, GLP-1/GIP agonists (metabolic) or SGLT2i to diversify cardiometabolic benefits.

  • Safety program: Cardiac electrophysiology, mitochondrial toxicity, off-target nuclear-receptor profiling, and chronic tox in two species.

  • Phenotype targeting: Visceral-predominant obesity, NAFLD with low fitness, and statin-intolerant dysmetabolism where oxidative re-programming is compelling.

Selected References

  • Saint Louis University research communications and preprints describing SLU-PP-332 as a pan-ERR exercise-mimetic (mouse studies).

  • Cell Metabolism; Nature Reviews Endocrinology — Reviews on ERR–PGC-1α control of oxidative metabolism and exercise adaptation.

  • Molecular Metabolism; Journal of Lipid Research — ERR regulation of thermogenesis and lipid flux in adipose and liver.

  • Journal of Physiology; Nature Reviews Molecular Cell Biology — PGC-1α in endurance adaptations and mitochondrial biogenesis.

  • Cardiovascular Research — Cardiac roles of ERRα/γ and implications for pharmacologic activation.