01 / IDENTITY
Compound Profile
CLASSIFICATION
Small molecule nuclear receptor agonist — Estrogen-Related Receptor alpha and gamma (ERRα/ERRγ) activator
MECHANISM
Directly activates ERRα and ERRγ nuclear receptors → triggers PGC-1α transcription → massively upregulates mitochondrial biogenesis, fatty acid oxidation, and aerobic capacity genes. Mimics the cellular signature of sustained aerobic exercise WITHOUT physical activity.
DEVELOPER
Thomas Burris lab, Saint Louis University (SLU) School of Pharmacy — hence "SLU-PP"
KEY PUBLICATION
Journal of Medicinal Chemistry (2023) — Burris et al.; Nature Communications (2024) — expanded metabolic phenotype data
NOTE ON NAME
Often written SLU-PP-332 or SLU-PP-322 in community use — the Burris lab series compound is formally SLU-PP-332. Same compound.
02 / RESEARCH HISTORY
Development Timeline
2010–2017
Thomas Burris lab at Saint Louis University identifies Estrogen-Related Receptors (ERRα, ERRβ, ERRγ) as master regulators of mitochondrial oxidative metabolism. These "orphan" nuclear receptors have no known endogenous ligand but their activation mimics exercise-induced gene expression changes.
2019–2021
Development of SLU-PP series — high-affinity synthetic ERR pan-agonists. Early compounds show dramatic upregulation of PGC-1α, TFAM, and oxidative phosphorylation genes in skeletal muscle cells — same gene signature as 6 weeks of endurance training, triggered by a single compound dose.
2023
Journal of Medicinal Chemistry publishes SLU-PP-332 data: rodent models show 50% improvement in treadmill endurance, 45% reduction in weight gain on high-fat diet, and dramatic increase in slow-twitch (Type I) muscle fiber percentage — all without exercise. Obesity research community takes notice.
2024
Nature Communications expanded study: SLU-PP-332 treated mice show resistance to diet-induced obesity, improved insulin sensitivity, reduced hepatic fat accumulation (NAFLD model), and cardiac protection. Cardiac tissue showed increased mitochondrial density and improved function — a potential therapeutic angle for heart failure.
2024–2025
Rapid adoption in performance research community. Formulated for SC injection (5mg vials). Human pharmacokinetics unknown; extrapolations from rodent data used for community dosing protocols. No human clinical trials yet — all data is preclinical.
Research Stage Notice: SLU-PP-332 has NO human clinical trial data. All efficacy and dosing information is extrapolated from rodent studies. This is a cutting-edge research compound at very early stage. Approach accordingly.
03 / BENEFITS
Primary Effects (Preclinical Data)
01
Endurance & Aerobic Capacity Enhancement
The most dramatic finding: SLU-PP-332 treated mice ran 50% farther on treadmill tests than controls — without any exercise training. The compound programs muscle cells to operate aerobically, increasing VO2 max proxy measures and fatigue resistance.
02
Fat Loss — Fatty Acid Oxidation Upregulation
ERRα/γ activation drives massive upregulation of CPT1 (carnitine palmitoyltransferase) and fatty acid oxidation enzymes. Result: fat is preferentially burned for fuel. High-fat diet mice treated with SLU-PP-332 gained 45% less weight vs. controls despite identical caloric intake.
03
Mitochondrial Biogenesis
Activates the PGC-1α → ERR → NRF1/2 → TFAM cascade — the master pathway for building new mitochondria. Increased mitochondrial density in skeletal muscle means more ATP capacity, better oxygen utilization, and improved metabolic efficiency. Type I (slow-twitch, endurance) fiber conversion documented.
04
Insulin Sensitivity & Anti-Diabetic Effects
Improved HOMA-IR and glucose tolerance in rodent models. Reduced hepatic glucose output and improved peripheral glucose uptake. Mechanism distinct from GLP-1 agonists — works directly at the mitochondrial/metabolic gene level rather than via incretin signaling.
05
Cardiac Protection & Function
Heart failure models showed SLU-PP-332 improved cardiac output and mitochondrial density in cardiomyocytes. The heart runs almost exclusively on fatty acid oxidation — ERR activation is particularly impactful in cardiac tissue. Potential for heart failure prevention/treatment.
06
Liver Health (NAFLD/NASH)
Reduced hepatic fat accumulation (steatosis) in high-fat diet models. ERR activation in liver increases fatty acid oxidation and reduces de novo lipogenesis. Relevant for metabolic syndrome patients with elevated liver enzymes.
04 / RECONSTITUTION
Preparation Protocol
// 5MG VIAL — STANDARD RECONSTITUTION
5,000 mcg ÷ 300 units BAC water = 16.7 mcg per unit
Add 3.0 mL (300 units) bacteriostatic water to 5mg lyophilized vial.
| TARGET DOSE |
UNITS TO DRAW |
VOLUME |
NOTE |
| LOW500 mcg0.5 mg |
30 units |
0.30 mL |
Starting point; assess sensitivity |
| STANDARD1 mg1,000 mcg |
60 units |
0.60 mL |
Common community dose (human extrapolation) |
| HIGH2 mg2,000 mcg |
120 units |
1.20 mL |
Upper range; rodent allometric scaling basis |
Human Dosing Caveat: All doses extrapolated from rodent studies using body surface area conversion (÷ 6.2 for human equivalent). Actual human PK is unknown. Start at the low end and titrate based on response. Cardiovascular monitoring recommended.
Storage: Lyophilized powder — room temperature, light-protected. Reconstituted: refrigerate (2–8°C), use within 28 days.
05 / DOSING PROTOCOL
Administration Guide
| PROTOCOL |
DOSE |
FREQUENCY |
DURATION |
CONTEXT |
| INTRO |
500 mcg SC |
Every other day |
2 weeks |
Sensitivity assessment; watch HR, BP |
| STANDARD |
1 mg SC |
Daily |
4–8 weeks |
Metabolic reprogramming phase |
| PERFORMANCE |
1–2 mg SC |
Daily pre-training |
6–12 weeks |
Endurance enhancement, concurrent training |
| METABOLIC |
1 mg SC |
5×/week |
8–12 weeks |
Fat loss, insulin sensitivity |
Pre-workout timing: Most community users inject 30–60 minutes before training. ERR activation takes ~2–4 hours for transcriptional effects, but acute signaling changes occur within 1 hour.
Monitor during use: Resting HR, blood pressure. Some users report mild tachycardia at higher doses — the cardiac metabolic upregulation can increase baseline heart rate. If resting HR rises >10 bpm above baseline, reduce dose.
06 / TIMING
Administration Timing
PREFERRED WINDOW
Pre-workout (30–60 min before training). On non-training days, morning fasted to maximize fatty acid oxidation during the post-injection window.
FOOD STATE
Fasted state may amplify fat oxidation effects. Rodent studies show enhanced free fatty acid release when combined with caloric restriction. However, post-workout with food is also acceptable.
STACKING
Highly complementary with MOTS-c (separate mitochondrial pathway — additive). Pairs with AOD-9604 for fat mobilization amplification. Can stack with GH peptides for body recomposition.
CYCLE TIMING
Best run continuously for 8–12 weeks to allow full PGC-1α-driven mitochondrial adaptation. Benefits (fiber type conversion) persist after cessation but require cycling to maintain.
07 / BIOMARKERS
Monitoring Panel
// METABOLIC & MITOCHONDRIAL FUNCTION
| MARKER | TEST | CLINICAL RANGE | OPTIMAL (TARGET) |
|---|
| Fasting GlucoseFBG |
Standard lab |
CLIN70–99 mg/dL |
OPT70–85 mg/dL |
| Fasting Insulin / HOMA-IRInsulin Resistance |
Fasting insulin + glucose |
CLINHOMA-IR <2.0 |
OPTHOMA-IR <1.0 |
| TriglyceridesLipid Panel |
Fasting lipid panel |
CLIN<150 mg/dL |
OPT<80 mg/dL |
| Free Fatty AcidsNEFA |
Metabolic panel (specialty) |
CLIN0.1–0.9 mEq/L (fasted) |
OPTElevated fasted (indicates FAO upregulation) |
// CARDIAC & PERFORMANCE
| MARKER | TEST | CLINICAL RANGE | MONITOR FOR |
|---|
| Resting Heart RateHR |
Wearable / clinical |
CLIN60–100 bpm |
FLAG>10 bpm rise from baseline → reduce dose |
| Blood PressureBP |
Home monitor |
CLIN<120/80 mmHg |
OPTNo change or mild decrease (improved cardiac efficiency) |
| Troponin ICardiac stress marker |
Standard cardiac panel |
CLIN<0.04 ng/mL |
FLAGAny elevation — discontinue immediately |
// LIVER SAFETY
| MARKER | TEST | CLINICAL RANGE | OPTIMAL |
|---|
| ALT / ASTLiver Enzymes |
CMP / Liver panel |
CLINALT <56 | AST <40 U/L |
OPTALT <25 | AST <22 U/L |
| GGTHepatic stress marker |
Liver panel |
CLIN<55 U/L |
OPT<25 U/L |
08 / CYCLE PROTOCOL
Recommended Cycle
Weeks 1–2 (Intro): 500 mcg SC every other day. Monitor resting HR daily. Assess GI tolerance — some users report mild nausea in the first week as mitochondrial flux increases.
Weeks 3–8 (Active): 1 mg SC daily pre-workout. Expect progressive improvement in workout endurance, reduced perceived exertion, and measurable improvements in training volume. Weight loss typically noticeable by week 4–6.
Weeks 9–12 (Peak): Continue at 1–2 mg. Mitochondrial adaptations accumulate — fiber type conversion measurable via VO2 max testing. Some users extend to 16 weeks; no long-term human safety data exists.
Best Stack: SLU-PP-332 + MOTS-c (complementary mitochondrial pathways) + AOD-9604 (lipolytic amplification) + Ipamorelin/CJC (body recomp) = comprehensive metabolic performance stack.
Research Compound Notice: SLU-PP-332 has not undergone human clinical trials. All human protocols are extrapolated from preclinical data. No human safety, toxicology, or pharmacokinetic data is available. Cardiac monitoring is strongly recommended. This is strictly for research and educational purposes. Not approved by FDA.