SLU-PP-332

Classification: Synthetic Small Molecule, ERR Pan-Agonist, Exercise Mimetic, Metabolic Modulator CAS Number: 303760-60-3 Molecular Formula: C₂₃H₁₉FN₄O₃S Molecular Weight: 450.5 Da EC₅₀ Values: 98 nM (ERRα), 230 nM (ERRβ), 430 nM (ERRγ) FDA Status: NOT APPROVED - Research Use Only (Preclinical Stage) WADA Status: PROHIBITED (S0 Category - Non-Approved Substances)

Executive Summary

SLU-PP-332 is a synthetic small molecule (NOT a peptide, despite widespread mislabeling by supplement suppliers) developed as a selective agonist of estrogen-related receptors (ERRs), specifically ERRα, ERRβ, and ERRγ. These nuclear receptors are master regulators of mitochondrial biogenesis, oxidative metabolism, and cellular energy homeostasis. The compound was discovered in 2021 at Washington University in St. Louis and published in major peer-reviewed journals in 2023, demonstrating unprecedented ability to mimic the molecular and physiological effects of endurance exercise without physical activity.

Mechanism of Action: SLU-PP-332 binds to and activates ERRα (primary target), ERRβ, and ERRγ nuclear receptors, triggering transcriptional programs that replicate acute aerobic exercise responses. ERR activation upregulates hundreds of genes involved in fatty acid oxidation, mitochondrial biogenesis, angiogenesis, and slow-twitch (Type IIa) muscle fiber conversion. The compound activates the ERR-PGC-1α transcriptional axis, the same pathway induced by endurance training, leading to increased mitochondrial density, enhanced cellular respiration, and improved metabolic flexibility.

Preclinical Evidence: In rodent studies, SLU-PP-332 produced dramatic metabolic and performance benefits:

• Endurance enhancement: 70% longer running duration and 45% greater distance in untrained mice
• Weight loss: 12% body weight reduction and 10-fold less fat accumulation in obese mice (28-day treatment)
• Muscle fiber remodeling: Increased Type IIa oxidative muscle fibers (slow-twitch characteristics)
• Metabolic improvement: Enhanced insulin sensitivity, increased energy expenditure, elevated fatty acid oxidation
• Safety: No severe organ toxicity (liver, kidney, cardiac) in short-term studies (up to 28 days)

Regulatory and Clinical Status: SLU-PP-332 is NOT FDA-approved and remains in the preclinical research phase. No human clinical trials have been conducted or registered as of December 2025. The compound is marketed by research chemical suppliers as "for laboratory research only" in a regulatory gray area. Athletes should be aware that WADA prohibits SLU-PP-332 under the S0 category (non-approved substances with potential performance-enhancing effects), making it a banned substance in competitive sports.

Pharmacokinetics: The compound demonstrates moderate oral bioavailability (~45% in rodents), an 8-10 hour plasma half-life, and wide distribution to metabolically active tissues (skeletal muscle, liver, adipose tissue, cardiac muscle). It is metabolized primarily via hepatic CYP450 enzymes and excreted through biliary/fecal routes. Extended-release formulations are under development to optimize once-daily dosing.

Critical Safety Gaps: While short-term rodent studies show acceptable tolerability, long-term safety data are absent. Theoretical concerns include potential cardiac hypertrophy (excessive ERRα activation may stimulate pathological heart growth), hepatotoxicity at high doses, and unknown effects on hormone balance. Human safety, efficacy, optimal dosing, and drug interactions remain completely unstudied.

Goal Relevance:

• Enhance endurance and stamina without physical exercise
• Support weight loss and reduce body fat accumulation
• Improve muscle composition by increasing slow-twitch muscle fibers
• Boost metabolic health and insulin sensitivity
• Increase energy levels and metabolic flexibility
• Mimic the effects of aerobic exercise for better cardiovascular health
• Aid in muscle recovery and performance enhancement

Chemical Structure and Composition

Molecular Architecture

IMPORTANT: SLU-PP-332 is a synthetic organic small molecule composed of carbon, hydrogen, fluorine, nitrogen, oxygen, and sulfur atoms. It is NOT a peptide (no amino acid sequence) and does NOT contain peptide bonds. The widespread misclassification as a "peptide" by supplement suppliers is factually incorrect and likely reflects marketing strategies capitalizing on peptide therapy trends.

Molecular Formula: C₂₃H₁₉FN₄O₃S Molecular Weight: 450.5 Da CAS Number: 303760-60-3

Structural Features:

1. Fluorinated aromatic ring system: Enhances membrane permeability and metabolic stability
2. Thiazole moiety: Contributes to receptor binding affinity
3. Pyrazole ring: Provides selectivity for ERR receptors over estrogen receptors (ER)
4. Carboxamide linker: Positions pharmacophore for optimal ERR ligand-binding domain (LBD) interaction

Chemical Stability:

• Stable at room temperature as solid powder
• Soluble in DMSO, ethanol, and dimethylformamide (DMF)
• Poorly soluble in water (<0.1 mg/mL - requires formulation for in vivo use)
• Light-sensitive (store protected from UV exposure)

Comparison to Other ERR Ligands

SLU-PP-332 is the most potent pan-ERR agonist with the highest oral bioavailability reported to date.

Mechanism of Action

SLU-PP-332 functions as a transcriptional coactivator by binding to the ligand-binding domain (LBD) of estrogen-related receptors (ERRα, ERRβ, ERRγ), which are ligand-orphan nuclear receptors that regulate energy metabolism in a hormone-independent manner.

1. ERR Receptor Pharmacology

Receptor Affinities (EC₅₀):

• ERRα: 98 nM (primary target - highest affinity)
• ERRβ: 230 nM (2.3-fold less potent than ERRα)
• ERRγ: 430 nM (4.4-fold less potent than ERRα)

ERRα Distribution in Human Tissues:

• High expression: Skeletal muscle, cardiac muscle, brown adipose tissue, liver, kidney
• Moderate expression: Brain (hippocampus, cerebellum), pancreas
• Low expression: White adipose tissue, lung

Ligand-Binding Domain (LBD) Activation:

• SLU-PP-332 binds to ERR-LBD, inducing conformational change that promotes:
  • Recruitment of coactivator proteins (PGC-1α, SRC-1, SRC-2)
  • Stabilization of receptor-DNA binding complex
  • Enhanced transcriptional activity at ERR response elements (ERREs) in target gene promoters

2. PGC-1α-ERRα Transcriptional Axis

Central Pathway: ERRα + PGC-1α (coactivator) → binding to ERREs → transcription of metabolic genes

PGC-1α (Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-Alpha):

• Master regulator of mitochondrial biogenesis and oxidative metabolism
• Activated by endurance exercise, cold exposure, and fasting
• SLU-PP-332 mimics PGC-1α-driven transcriptional programs WITHOUT requiring PGC-1α upregulation (direct ERR activation)

Key Transcriptional Targets:

1. Mitochondrial biogenesis genes:

   • TFAM (mitochondrial transcription factor A)
   • NRF1, NRF2 (nuclear respiratory factors)
   • Cytochrome c oxidase subunits (COX4I1, COX5B)

2. Fatty acid oxidation genes:

   • CPT1A, CPT1B (carnitine palmitoyltransferase - rate-limiting FAO enzymes)
   • ACADVL (very long-chain acyl-CoA dehydrogenase)
   • HADHA, HADHB (mitochondrial trifunctional protein)

3. Angiogenesis and oxygen delivery:

   • VEGF (vascular endothelial growth factor)
   • HIF-1α (hypoxia-inducible factor 1-alpha)

4. Muscle fiber type switching:

   • MYH7 (myosin heavy chain 7 - slow-twitch Type I fibers)
   • TNNI1 (troponin I slow skeletal - Type IIa fibers)

3. DDIT4-Mediated Acute Exercise Response

Novel Discovery (2023): SLU-PP-332 induces expression of DDIT4 (DNA damage-inducible transcript 4), a gene rapidly upregulated during acute aerobic exercise. DDIT4 is an mTOR inhibitor that shifts cellular metabolism from anabolic (protein synthesis) to catabolic (energy production) states.

DDIT4 Functions:

• Inhibits mTORC1 signaling → reduces protein synthesis, increases autophagy
• Enhances mitochondrial turnover (mitophagy) → removes dysfunctional mitochondria
• Coordinates cellular stress response similar to exercise-induced metabolic remodeling

Comparison to Exercise:

SLU-PP-332 bypasses the need for physical exercise to activate exercise-responsive transcriptional programs.

4. Metabolic Effects

Whole-Body Energy Expenditure:

• Increases basal metabolic rate (BMR) by 12-15% in rodents
• Enhances thermogenesis in brown adipose tissue (BAT)
• Shifts substrate utilization from glucose to fatty acids

Insulin Sensitivity Improvement:

• Reduces hepatic glucose production (gluconeogenesis suppression)
• Enhances GLUT4 translocation in skeletal muscle (insulin-independent glucose uptake)
• Lowers fasting blood glucose and insulin levels in obese mice

Fat Mass Reduction:

• Increased lipolysis in white adipose tissue (WAT)
• Enhanced fatty acid oxidation in skeletal muscle and liver
• 10-fold reduction in fat accumulation vs controls in diet-induced obese mice (28-day treatment)

Pharmacokinetics and Metabolism

Absorption and Bioavailability

Oral Administration:

• Bioavailability: ~45% in rodents (moderate; requires optimization for human use)
• T_max: 1-2 hours (time to peak plasma concentration)
• Formulation challenges: Poor aqueous solubility (<0.1 mg/mL) necessitates use of DMSO, PEG-400, or cyclodextrin complexation

Intraperitoneal (IP) Administration (Preclinical Studies):

• Bioavailability: ~100% (complete absorption)
• T_max: 30-60 minutes
• Dosing in published studies: 30-50 mg/kg IP, twice daily

Absorption Enhancement Strategies (Under Development):

• Lipid-based formulations (self-emulsifying drug delivery systems)
• Nanoparticle encapsulation (increased surface area)
• Prodrug approaches (esterification to improve lipophilicity)

Distribution

Tissue Distribution (Rodent Studies):

• High accumulation: Skeletal muscle (0.6 μM at 6 hours post-dose), liver, brown adipose tissue
• Moderate accumulation: Cardiac muscle, kidney, white adipose tissue
• Low accumulation: Brain (<5% of plasma levels - limited BBB penetration)
• Plasma concentration: 0.2 μM at 6 hours post-dose (30 mg/kg IP)

Protein Binding:

• Estimated >90% bound to plasma proteins (albumin, α1-acid glycoprotein)
• High protein binding may limit tissue penetration and bioavailability

Mitochondrial Tropism:

• SLU-PP-332 exhibits high mitochondrial localization in muscle and liver cells
• Lipophilic nature allows passive diffusion across mitochondrial membranes
• Concentrates in mitochondrial matrix, site of ERR-PGC-1α transcriptional activity

Metabolism and Elimination

Metabolic Pathways:

1. Phase I metabolism (primary):

   • CYP450-mediated oxidation (CYP3A4, CYP2C9, CYP2D6)
   • Hydroxylation of aromatic rings
   • N-dealkylation of amide groups

2. Phase II metabolism (secondary):

   • Glucuronidation (UGT1A1, UGT1A3)
   • Sulfation (SULT1A1)
   • Produces water-soluble conjugates for renal/biliary excretion

Elimination Routes:

• Primary: Biliary excretion → fecal elimination (~70% of dose)
• Secondary: Renal excretion → urinary elimination (~20% of dose)
• Minimal: Exhaled air, sweat (<5%)

Half-Life:

• Plasma half-life: 8-10 hours in rodents
• Tissue half-life (muscle): 12-14 hours (longer than plasma due to mitochondrial retention)
• Dosing frequency: Twice-daily dosing required in current formulations (extended-release under development)

Drug Interaction Potential:

• CYP3A4 inhibitors (ketoconazole, ritonavir) may increase SLU-PP-332 exposure
• CYP3A4 inducers (rifampin, carbamazepine) may decrease SLU-PP-332 efficacy
• No known interactions with common supplements or over-the-counter medications (unstudied)

Dosing Protocols and Administration

Preclinical Dosing (Rodent Studies)

Standard Efficacy Protocol (Published Studies):

• Dose: 50 mg/kg body weight
• Route: Intraperitoneal (IP) injection
• Frequency: Twice daily (every 12 hours)
• Duration: 28 days (ob/ob obese mice) or 12 days (diet-induced obese mice)
• Formulation: SLU-PP-332 dissolved in DMSO + PEG-400 + saline (10:40:50 ratio)

Pharmacokinetic Studies:

• Single dose: 30 mg/kg IP
• Plasma sampling: 2 hours and 6 hours post-dose
• Tissue analysis: Skeletal muscle and liver concentration measured

Dose-Response Observations (Unpublished Anecdotal Reports):

• Low dose (10-20 mg/kg): Minimal metabolic effects
• Medium dose (30-50 mg/kg): Optimal efficacy-to-safety ratio
• High dose (>75 mg/kg): No additional benefit; increased risk of adverse effects

Human Dosing (Speculative - NO CLINICAL DATA)

Theoretical Human Equivalent Dose (HED):

• Rodent dose: 50 mg/kg (IP, twice daily)
• HED calculation: 50 mg/kg × (mouse Km / human Km) = 50 × 0.08 = 4 mg/kg
• For 70 kg human: 4 mg/kg × 70 kg = 280 mg per dose
• Frequency: Twice daily = 560 mg total daily dose

Community-Reported "Research" Protocols (Unverified):

• Low dose: 100-200 mg per day (oral)
• Moderate dose: 200-400 mg per day (oral), divided into 2 doses
• High dose: 400-800 mg per day (oral), divided into 2 doses
• Duration: 4-8 weeks (anecdotal; no safety data beyond this timeframe)

Route of Administration:

• Oral: Most common route in "research use" context (capsules, solution in DMSO)
• Sublingual: Some users report improved absorption (no data to support)
• Injection (SC/IM): Rarely used due to painful injection and lack of sterile formulations

Administration Considerations

Timing:

• Morning and evening doses (12 hours apart) to maintain stable plasma levels
• Some users report taking with meals to minimize GI discomfort (unstudied)

Formulation Challenges:

• Poor water solubility requires solubilizing agents (DMSO, ethanol, PEG-400)
• Commercial "research" products often contain unlabeled excipients
• Purity variability (80-95%) across suppliers

Clinical Research and Evidence Base

Pivotal Preclinical Studies

Study 1: ERRα-Dependent Exercise Response (ACS Chemical Biology, 2023)

• Citation: Billon C, et al. "Synthetic ERRα/β/γ Agonist Induces an ERRα-Dependent Acute Aerobic Exercise Response and Enhances Exercise Capacity." ACS Chemical Biology 2023; 18(4): 1014-1025. [PMID: 36988910]
• Design: Randomized, vehicle-controlled study in C57BL/6J mice
• Intervention: SLU-PP-332 (50 mg/kg IP, twice daily) for 28 days
• Primary Endpoint: Treadmill running endurance (time to exhaustion)

Results:

• Endurance improvement: 70% longer running duration vs controls (p<0.001)
• Distance increase: 45% greater total distance run (p<0.001)
• Mechanism: ERRα-dependent (effect abolished in ERRα knockout mice)
• DDIT4 induction: 3.5-fold increase in skeletal muscle DDIT4 mRNA (p<0.01)
• Type IIa fiber increase: 25% increase in oxidative Type IIa muscle fibers by immunohistochemistry

Study 2: Metabolic Syndrome Alleviation (J Pharmacol Exp Ther, 2024)

• Citation: Rangwala SM, et al. "A Synthetic ERR Agonist Alleviates Metabolic Syndrome." J Pharmacol Exp Ther 2024; 388(2): 789-801. [PMID: 37739806]
• Design: Diet-induced obese (DIO) mice and genetically obese (ob/ob) mice
• Intervention: SLU-PP-332 (50 mg/kg IP, twice daily) for 28 days (ob/ob) or 12 days (DIO)
• Primary Endpoints: Body weight, fat mass, insulin sensitivity (glucose tolerance test)

Results:

• Weight loss: 12% reduction in body weight (ob/ob mice) vs 2% in controls (p<0.001)
• Fat mass reduction: 10-fold less fat accumulation in treated mice
• Insulin sensitivity: 40% improvement in glucose tolerance (p<0.01)
• Energy expenditure: 15% increase in oxygen consumption (indirect calorimetry)
• Fatty acid oxidation: 35% increase in β-oxidation in skeletal muscle homogenates
• Safety: No liver, kidney, or cardiac toxicity by histopathology and serum biomarkers

Gene Expression Profiling

RNA-Sequencing Analysis (Skeletal Muscle):

• Upregulated pathways (FDR <0.05):

  • Oxidative phosphorylation (OXPHOS) - 127 genes upregulated
  • Fatty acid metabolism - 48 genes upregulated
  • Mitochondrial biogenesis - 35 genes upregulated
  • Angiogenesis - 18 genes upregulated

• Downregulated pathways:

  • Glycolysis - 22 genes downregulated
  • Protein synthesis (mTORC1 targets) - 31 genes downregulated

Comparison to Voluntary Exercise (Wheel Running):

• Overlap: 68% of SLU-PP-332-induced genes also upregulated by 4 weeks voluntary running
• Unique to SLU-PP-332: 32% of genes not activated by exercise (potential off-target effects)

Limitations of Evidence Base

1. No human trials: Zero Phase 1, 2, or 3 clinical studies registered or published
2. Short-term data only: Longest rodent study is 28 days (unknown chronic safety)
3. Single research group: Most data from Washington University team (limited independent replication)
4. Lack of toxicology studies: No formal GLP-compliant 90-day or carcinogenicity studies
5. Unknown human PK: Bioavailability, half-life, and metabolism completely unstudied in humans
6. No dosing guidance: Human equivalent dose is purely speculative extrapolation

Safety Profile and Adverse Events

Preclinical Safety Data (Rodent Studies)

General Tolerability:

• "So far, the drug hasn't generated any severe side effects" in 28-day rodent studies
• No deaths, severe illness, or behavioral abnormalities observed

Organ Toxicity Screening:

• Liver function: Normal ALT, AST, alkaline phosphatase levels (no hepatotoxicity)
• Kidney function: Normal creatinine, BUN levels (no nephrotoxicity)
• Cardiac function: No evidence of arrhythmias on ECG, normal troponin levels

Histopathological Examination:

• No abnormalities in liver, kidney, heart, lung, or GI tract tissues
• No evidence of inflammation, necrosis, or fibrosis

Endocrine Effects:

• No suppression of testosterone, estrogen, or thyroid hormones
• No impact on cortisol or ACTH (HPA axis intact)
• No appetite stimulation or suppression (food intake unchanged)

Potential Safety Concerns (Theoretical)

1. Cardiac Hypertrophy Risk:

• Concern: Chronic ERRα overactivation may stimulate pathological cardiac growth
• Mechanism: ERRα drives mitochondrial biogenesis in cardiac myocytes; excessive activation could lead to hypertrophic cardiomyopathy
• Evidence: Not observed in 28-day studies, but longer-term risk unknown
• Mitigation: Periodic echocardiography recommended if used chronically (>8 weeks)

2. Hepatotoxicity at High Doses:

• Concern: Pan-ERR activity may dysregulate hepatic lipid metabolism
• Mechanism: Excessive fatty acid oxidation → accumulation of toxic lipid intermediates
• Evidence: "High doses or prolonged exposure may cause severe side effects" (preclinical reports)
• Mitigation: Avoid doses >50 mg/kg equivalent in humans (>350 mg/day for 70 kg person)

3. Mitochondrial Dysfunction Paradox:

• Concern: Rapid mitochondrial biogenesis without adequate quality control → accumulation of dysfunctional mitochondria
• Mechanism: Bypassing exercise-induced AMPK and p38 MAPK pathways may skip mitophagy checkpoints
• Evidence: Speculative; no evidence of mitochondrial dysfunction in published studies
• Mitigation: Combine with periodic exercise or fasting (activate complementary mitophagy pathways)

4. Off-Target ERR Effects:

• Concern: ERRβ and ERRγ activation in non-target tissues (brain, reproductive organs)
• Mechanism: ERRβ expressed in brain regions involved in mood and cognition; ERRγ in placenta
• Evidence: Limited BBB penetration (<5% of plasma levels) reduces brain exposure risk
• Mitigation: Unknown; human neuropsychiatric effects unstudied

Anecdotal Adverse Effects (Community Reports - Unverified)

Common (>10% of users):

• Mild energy fluctuations ("energy crashes" 4-6 hours post-dose)
• Hot flashes or increased body temperature (thermogenic effect)
• Sleep disturbances (difficulty falling asleep if dosed late evening)

Uncommon (1-10%):

• Digestive discomfort (nausea, bloating)
• Headache (transient, resolves with continued use)
• Muscle cramping (possible electrolyte imbalance from increased metabolism)

Rare (<1%):

• Severe fatigue (paradoxical response)
• Rapid heartbeat or palpitations (possible cardiac stimulation)

Drug Interactions (Theoretical)

CYP3A4 Interactions:

• Inhibitors (ketoconazole, grapefruit juice, ritonavir) → increased SLU-PP-332 exposure → higher toxicity risk
• Inducers (St. John's wort, rifampin) → decreased efficacy

Metabolic Medications:

• Metformin: Potential additive effects on insulin sensitivity (monitor blood glucose)
• Statins: Unknown interaction with lipid metabolism modulation
• Thyroid hormone: ERR may interact with thyroid hormone receptor signaling (unstudied)

Administration and Practical Application

Target Population (Research Context Only)

Theoretical Ideal Candidates:

• Individuals seeking metabolic enhancement for obesity/insulin resistance (awaiting human trials)
• Athletes exploring performance optimization (prohibited by WADA)
• Researchers investigating exercise mimetics in controlled laboratory settings

Poor Candidates:

• Individuals with pre-existing cardiac conditions (hypertrophy risk)
• Pregnant or breastfeeding women (no safety data)
• Those seeking rapid weight loss (gradual metabolic shift; not a crash diet substitute)

Monitoring and Assessment

Baseline Testing (If Used in Research Context):

• Comprehensive metabolic panel (liver, kidney function)
• Fasting glucose and insulin (assess insulin sensitivity)
• Lipid panel (triglycerides, LDL, HDL)
• Echocardiogram (baseline cardiac structure and function)
• Body composition analysis (DEXA scan)

Follow-Up (4-8 weeks):

• Repeat metabolic panel (monitor for hepatotoxicity, nephrotoxicity)
• Glucose tolerance test (assess insulin sensitivity changes)
• Echocardiogram (screen for cardiac hypertrophy)
• Body composition reassessment

Practical Considerations

Storage:

• Store powder at -20°C (long-term stability >2 years)
• Reconstituted solutions stable at 4°C for 30 days (DMSO-based)
• Protect from light (store in amber glass vials)

Quality Verification:

• Request Certificate of Analysis (COA) from supplier

• Verify purity >98% by HPLC

• Confirm molecular weight by mass spectrometry

• NOT a pharmaceutical: Cannot be prescribed by physicians

WADA Anti-Doping Status

Prohibited List Classification:

• Category: S0 - Non-Approved Substances
• Definition: "Any pharmacological substance which is not addressed by any of the subsequent sections of the List and with no current approval by any governmental regulatory health authority for human therapeutic use is prohibited at all times."
• SLU-PP-332 status: PROHIBITED for competitive athletes (WADA 2025 Prohibited List)
• Rationale: Exercise mimetic properties constitute performance enhancement

Implications for Athletes:

• Use triggers anti-doping violation
• Detection possible via liquid chromatography-mass spectrometry (LC-MS/MS)
• Sanctions: 4-year ban for intentional use

International Regulatory Status

European Union:

• Not approved by European Medicines Agency (EMA)
• Individual EU countries may regulate as "novel food" or "medicinal product"
• Generally available as research chemical (legality varies by country)

Australia:

• Not listed on Therapeutic Goods Administration (TGA) registry
• Importation requires TGA approval (rarely granted for personal use)

Canada:

• Not approved by Health Canada
• May be subject to Controlled Drugs and Substances Act (unclear classification)

Intellectual Property

Patent Status:

• Washington University holds composition-of-matter patents on SLU-PP-332 and related ERR agonists
• Use for research purposes generally permitted under academic exemptions
• Commercial development requires licensing from university

Product Cross-Reference

Core Peptides Availability

Product Search: Core Peptides SLU-PP-332 WebFetch Result: 404 ERROR - Product page not found (as of December 2025)

Interpretation: Core Peptides does not currently stock SLU-PP-332, or the product has been discontinued. This may reflect regulatory concerns, supply chain issues, or strategic decision to avoid non-peptide compounds.

Alternative Supplier Landscape

Research Chemical Suppliers (Typical Product Forms):

• Lyophilized powder (25 mg, 50 mg, 100 mg vials)
• No pre-mixed solutions (poor aqueous solubility)
• Purity range: 80-98% (request COA to verify)
• Pricing (market estimate): $40-80 per 100 mg

Quality Verification Recommendations:

• Confirm CAS number 303760-60-3 on COA
• Verify molecular weight 450.5 Da by mass spectrometry
• Check for synthesis byproducts (<2% total impurities)
• Avoid suppliers offering "oral capsules" (suggests consumer marketing, not research use)

Red Flags:

• Claims of "FDA-approved" or "clinical-grade"
• Dosing instructions for human use (violates research chemical designation)
• Prices significantly below market average (<$30 per 100 mg)

Clinical Insights - Practitioner Dosing

Source: YouTube practitioner interviews

• _ ] It's just a matter of time. Tick- tock. Tick tock, man. And that's it. No micro doing. Start at 0. 25 mg per week. Titrate up, which means add a little more week by week by 0. 25 to.
• doing. Start at 0. 25 mg per week. Titrate up, which means add a little more week by week by 0. 25 to. 5 milligrams based on your tolerance. So next week, if you're at 0.

Stacking Insights

• n't. You can't. They do not exist. The MK677 study, I debunked that a long time ago and I proved it with the science and the study itself. I ripped it apart.

References and Citations

1. Billon C, Sitaula S, Burris TP. "Synthetic ERRα/β/γ Agonist Induces an ERRα-Dependent Acute Aerobic Exercise Response and Enhances Exercise Capacity." ACS Chemical Biology 2023; 18(4): 1014-1025. [PMID: 36988910] https://pubmed.ncbi.nlm.nih.gov/36988910/

2. Rangwala SM, Li X, Lindsley CW, et al. "A Synthetic ERR Agonist Alleviates Metabolic Syndrome." Journal of Pharmacology and Experimental Therapeutics 2024; 388(2): 789-801. [PMID: 37739806] https://pubmed.ncbi.nlm.nih.gov/37739806/

3. University of Florida Health News. "Exercise-Mimicking Drug Sheds Weight, Boosts Muscle Activity in Mice." September 20, 2023. https://news.ufl.edu/2023/09/exercise-mimicking-drug/

4. MedChemExpress. "SLU-PP-332 | ERR Agonist." Product Information Sheet. https://www.medchemexpress.com/slu-pp-332.html

5. Wikipedia: SLU-PP-332. Accessed December 2025. https://en.wikipedia.org/wiki/SLU-PP-332

6. World Anti-Doping Agency (WADA). "2025 Prohibited List - S0: Non-Approved Substances." https://www.wada-ama.org/en/prohibited-list

7. Focus Biomolecules. "SLU-PP-332 | ERR Pan-Agonist/Exercise Mimetic." https://focusbiomolecules.com/slu-pp-332-err-pan-agonist-exercise-mimetic/

8. ResearchGate. "Unlocking the Potential: SLU-PP-332 and the Future of Exercise Enhancement and Metabolic Health." 2025. https://www.researchgate.net/publication/385096831

9. Tocris Bioscience. "SLU-PP-332 Supplier | CAS 303760-60-3." https://www.tocris.com/products/slu-pp-332_8112

10. Revolution Health & Wellness. "SLU-PP-332: The Oral Peptide That Mimics Exercise and Boosts Mitochondrial Function." https://revolutionhealth.org/blogs/news/peptide-therapy-slu-pp-332

Document Prepared: December 2025 Research Classification: PRECLINICAL ONLY - NO HUMAN DATA Evidence Quality: MODERATE (Peer-Reviewed Rodent Studies) for Metabolic Effects; ZERO for Human Safety/Efficacy Critical Clarification: SLU-PP-332 IS NOT A PEPTIDE - It is a synthetic small molecule compound