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SLU-PP-332Small moleculeNo amino acid sequence. Icon reflects category theme only.Also known as: SLU-PP-332, SLUPP332, SLU PP 332
Mice on SLU-PP-332 ran 45% farther and 70% longer without any extra training. This small-molecule ERR agonist (not actually a peptide) flips on the same metabolic gene programs that aerobic exercise triggers, pushing skeletal muscle toward fatty acid oxidation and oxidative fiber types. All published data come from mouse models; zero human trials exist. The community figured this out before formal research caught up, with 20 to 60 Reddit threads tracking mg-level subcutaneous protocols for endurance and fat loss. Cardiac safety remains the open question, given ERR expression in heart tissue and an NFAT activation signal in one 2024 study [1].
Twelve percent body weight gone in 28 days, and the mice weren't even running. SLU-PP-332 (CAS pending; developed at Saint Louis University and Washington University School of Medicine) is a synthetic pan-agonist of the estrogen-related receptors ERRalpha, ERRbeta, and ERRgamma. It activates aerobic exercise gene programs without physical activity. The mechanism is direct. SLU-PP-332 binds the ligand-binding domain of ERRalpha (EC50 = 98 nM) and recruits the coactivator PGC-1alpha. That drives transcription of genes governing mitochondrial biogenesis, fatty acid oxidation, and oxidative phosphorylation. Muscle fibers shift toward the oxidative Type IIa phenotype. Resting energy expenditure climbs within two hours of the first dose in mice. The numbers from Billon et al. [2] are specific: 25% increase in fatty acid oxidation, 12% body weight reduction in diet-induced obese mice, and fat mass gain reduced roughly 10-fold versus untreated controls. A second study from the same group [3] confirmed 45% greater running distance and 70% longer time to exhaustion. Unlike GLP-1 receptor agonists, SLU-PP-332 does not suppress appetite. Community adoption runs ahead of the science. Subcutaneous injection at 10 to 50 mg/day is the current standard, though no human pharmacokinetic data exist. All published in vivo data used intraperitoneal injection in mice at 50 mg/kg twice daily. Formal clinical trials have not been initiated.
SLU-PP-332 is a pan-agonist of the estrogen-related receptors, with highest potency at ERRalpha (EC50 = 98 nM), followed by ERRbeta (EC50 = 230 nM) and ERRgamma (EC50 = 430 nM). It binds a hydrophobic trench adjacent to the ligand-binding domain, interacting with residues Leu345 and Phe377. That stabilizes the receptor in its active conformation. The downstream cascade starts with PGC-1alpha recruitment. PGC-1alpha is a transcriptional coactivator that amplifies expression of genes controlling mitochondrial biogenesis, fatty acid oxidation, and oxidative phosphorylation. Skeletal muscle responds by shifting fiber composition toward the oxidative Type IIa phenotype, the same adaptation seen after weeks of endurance training. SLU-PP-332 also induces DDIT4, a negative regulator of mTORC1. This adds an interesting wrinkle; mTOR suppression could theoretically limit anabolic recovery. Bonanni et al. (Frontiers in Physiology, 2025; DOI 10.3389/fphys.2025.1616693) confirmed ERR pathway activation in human myoblasts in vitro, providing the first human-adjacent data. Whole-body energy expenditure increased within two hours of dosing in mouse models. One concern sits in the cardiac data. Xu et al. (Circulation 2024)[1] found improved ejection fraction and reduced fibrosis in a heart failure mouse model, which looks cardioprotective. The same paper noted NFAT pathway activation in cardiomyocytes. NFAT signaling is a hypertrophic pathway. No cardiac hypertrophy was confirmed at study doses, but the signal warrants monitoring.
Preclinical evidence in mice shows increased fat oxidation, reduced body weight, improved endurance, and improved glucose tolerance. Cardioprotective in heart failure mouse model [1]. First human-adjacent data (in vitro myoblasts, Frontiers 2025) confirms ERR pathway activation. Zero human clinical trials. No established safe or effective human dose.
Billon et al., ACS Chem Biol 2023 (PMID 36988910): ERR-dependent exercise response; Billon et al., JPET 2024 (PMID 37739806): metabolic syndrome; Xu et al., Circulation 2024 (PMID 37961903): cardiac protection; Bonanni et al., Front Physiol 2025 (DOI 10.3389/fphys.2025.1616693): human myoblasts in vitro
All in vivo data from mouse models. Route used in studies (i.p.) is not translatable to humans. No PK/PD data in humans. Long-term toxicity, carcinogenicity, and reproductive safety uncharacterized. NFAT pathway activation in cardiomyocytes noted in Xu et al. 2024: clinical relevance in healthy humans unknown.
Cautious optimism. mg-level SC injection community reports improved endurance, subjective fat loss, and anecdotal bloodwork improvement (LDL, A1C, eGFR). Significant early dosing confusion (mcg vs mg) meant many users saw zero effect. Cardiac concern is discussed but not based on confirmed human adverse events.
Community protocols directionally follow the mouse mechanism (ERR agonism → fat oxidation + endurance). BSA allometric scaling from 50 mg/kg mouse dose gives theoretical rationale for mg-level SC dosing. However, route (SC vs. i.p.), dose magnitude, and human safety profile are entirely unvalidated. Science is mouse-only; community outcomes cannot be confirmed or denied by published data.
| Level | Dose / Injection | Frequency |
|---|---|---|
| Beginner | 10mg | Daily |
| Moderate | 25mg | Daily |
| Aggressive | 50mg | Daily |
This is a small molecule, not a peptide. Reconstitution math depends on your vial and solvent choice. SLU-PP-332 dissolves in DMSO or can be reconstituted with bacteriostatic water for subcutaneous injection. For a 25 mg vial reconstituted with 1 mL bacteriostatic water: concentration is 25 mg/mL. A 10 mg dose is 40 IU on a U100 insulin syringe (0.4 mL). A 25 mg dose uses the full syringe (100 IU / 1.0 mL); consider splitting across two injection sites at that volume. For a 10 mg vial reconstituted with 0.5 mL: concentration is 20 mg/mL. A 10 mg dose is 50 IU (0.5 mL). The mcg versus mg confusion tripped up a lot of early adopters. If you're dosing in the 250 to 1,500 mcg range, you're almost certainly too low. Community consensus settled on 10 to 50 mg/day subcutaneous as the effective range. Oral bioavailability is widely described as "nearly useless" for hitting meaningful plasma levels. Get an ECG before your first cycle. That's the single most important safety step given the cardiac data.
No established cycling protocol for humans. Animal studies used continuous 28-day dosing. Extended use beyond study durations has not been evaluated.
No evidence-based cycling rationale exists for SLU-PP-332. Published mouse studies used continuous 28-day dosing without cycling. Community cycling conventions (4–8 weeks on / 4–8 weeks off) are borrowed from GW501516 (Cardarine) community protocols as a precautionary measure. No receptor desensitization, antibody formation, or hormonal axis disruption has been documented in any species. Cycling is precautionary in the absence of long-term safety data.
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Expected: Mouse data: 12% body weight reduction, improved glucose tolerance over 28 days. Community: subtle fat loss, improved metabolic bloodwork (anecdotal only, no controlled human data).
Monitor: Baseline and end-of-cycle: ECG (cardiac monitoring), ALT/AST, lipid panel, HbA1c/fasting glucose
Common sizes are 10 mg and 25 mg. Verify lot-specific certificate of analysis (COA) with HPLC purity of 99% or higher.
For a 25 mg vial, add 1 mL. For a 10 mg vial, add 0.5 mL. Swirl gently until fully dissolved. Do not inject if any visible powder or particles remain; injection site lumps come from undissolved material.
For a 10 mg dose from a 25 mg/1 mL vial: draw to 40 IU on a U100 insulin syringe (0.4 mL). For a 25 mg dose from the same vial: draw the full 100 IU (1.0 mL) and consider splitting across two injection sites.
Inject subcutaneously using a 27 to 29 gauge needle at a 45 degree angle into abdominal or thigh fat. Rotate sites.
Timing: 60 to 90 minutes before exercise or with your first meal in the morning.
Use within 2 weeks.
Liver enzymes (ALT, AST) and lipid panel at baseline and end of cycle. Stop immediately if you experience palpitations, chest tightness, or shortness of breath.
Consumer products are typically 250–500 mcg/capsule. Achieving 10 mg orally requires 20–40 capsules/day at ~$667–$1,334/day (Loti Labs pricing). No published oral bioavailability data in any species.
Community consensus: oral bioavailability is very low: widely described as "nearly useless" for achieving effective plasma levels. All published mouse PK used i.p. administration. Some users report mild effects at 1–2 mg oral; almost universally reported as underdosed vs. SC injection.
Same mg dose as community standard. Volume challenge: 10 mg dose requires 0.4–1.0 mL depending on reconstitution concentration. No IP-to-SC bioavailability equivalence data.
All published studies used i.p. injection in mice. SC adopted by community as closest feasible human analog. Injection site lumps reported with improper reconstitution. Splitting doses across 2 sites recommended if volume >0.5 mL.
BSA-scaled human equivalent of mouse 50 mg/kg i.p. dose ≈ 650 mg/day for 80 kg human: far above community SC protocols of 10–50 mg/day.
I.P. is standard preclinical methodology. Not appropriate for self-administration. The extreme dose gap between BSA-scaled theoretical equivalent (650 mg) and community practice (10–50 mg) underscores the complete absence of human dose-finding data.
Both exercise mimetics targeting mitochondrial biogenesis. Hypothetically complementary pathways (ERR agonism vs AMPK). Community stack for amplified metabolic and endurance effect.
Another exercise mimetic via AMPK activation. Community "double exercise mimetic" stack. Combined risks completely unknown. Both compounds are WADA-prohibited in competitive sport.
Fat loss synergy hypothesis: AOD-9604 lipolysis via GH fragment mechanism; SLU-PP-332 via fatty acid oxidation upregulation. Community body recomposition combination.
Mitochondrial support stack. Both target mitochondrial biogenesis via different pathways (ERR vs sirtuins/PARP1). Anti-aging and metabolic optimization rationale.
Community "max metabolic" combination but carries uncharacterized additive cardiovascular and carcinogenic risk. GW501516 was abandoned in human trials after multi-organ tumorigenesis in animal carcinogenicity studies. Combined ERR + PPARδ agonism has not been studied in any model.
SLU-PP-332 upregulates DDIT4, a negative regulator of mTORC1. Combined mTOR suppression could impair muscle protein synthesis and anabolic recovery.
SLU-PP-332 activates ERRs highly expressed in cardiac tissue. Combined effects on cardiac energy metabolism and rate control are completely unknown. Theoretical arrhythmia risk.
SLU-PP-332 improves insulin sensitivity and glucose tolerance in animal models. Additive glucose-lowering effect with antidiabetic medications could cause clinically significant hypoglycemia.
Pricing updated 2026-04-09
The most serious concern with SLU-PP-332 is cardiac. ERR receptors are highly expressed in heart tissue, and Xu et al. (Circulation 2024)[1] identified NFAT pathway activation in cardiomyocytes. NFAT is a hypertrophic signaling pathway. No cardiac hypertrophy was observed at study doses in mice, but the clinical relevance in healthy human hearts is entirely unknown. An ECG baseline before starting is not optional for anyone considering this compound. Zero human safety data exist. That bears repeating: no Phase 1 trial, no formal toxicology in humans, no dose-finding study. Everything below comes from mouse models or community self-reports. In published animal studies, Billon et al. [2] noted minor elevations in plasma cholesterol and liver enzymes. These were described as relatively minor changes, but "minor" in a 28-day mouse study does not predict what happens in a human over months. Liver function monitoring (ALT, AST) at baseline and end of cycle is the minimum standard. Long-term toxicity has not been assessed. Carcinogenicity studies have not been conducted. Reproductive safety is completely uncharacterized. The community draws comfort from SLU-PP-332 working through ERR (not PPARdelta like Cardarine/GW501516, which caused multi-organ tumors in animal carcinogenicity studies). That distinction is mechanistically valid but does not constitute a safety endorsement. Injection site lumps and nodules are the most commonly reported issue in community forums. These result from incomplete reconstitution or suspension formulations not designed for subcutaneous administration. Ensuring complete dissolution before drawing prevents most occurrences. Using a 27 to 29 gauge needle at a 45 degree angle into subcutaneous fat and rotating sites helps. Source quality is a real problem. Counterfeit and underdosed supply has been flagged across community forums. Consumer oral capsules at mcg doses are not appropriate for mg-level subcutaneous protocols. Contraindications include pregnancy or breastfeeding (reproductive safety unassessed in any species), liver disease (given the enzyme elevation signal), hormone-sensitive conditions (ERR receptors interact with estrogen-related pathways), and anyone on rate-controlling cardiac medications. Children and adolescents should not use this compound. When to stop: any new cardiac symptom (palpitations, chest tightness, dyspnea). ALT or AST above 2x the upper limit of normal. Unexplained injection site reactions beyond a transient lump.
Verify SLU-PP-332 dosing and safety with a second opinion
Novel small-molecule with multi-step synthesis: higher purity variability than standard peptides. No pharmacopoeial standards exist. Counterfeit and underdosed supply flagged in community forums. Consumer oral capsule products at mcg doses are not validated for SC injection use. No regulated pharmaceutical supply chain.
| Test | When | Target |
|---|---|---|
| ECG (12-lead) | Baseline before first cycle; end of each cycle | Normal sinus rhythm; no new conduction abnormalities or QTc prolongation |
| Liver enzymes (ALT, AST) | Baseline; end of cycle | Within normal limits; hold if >2x ULN |
| Lipid panel (LDL, HDL, triglycerides) | Baseline; end of cycle | — |
| Fasting glucose / HbA1c | Baseline; end of cycle | — |
ERRs are highly expressed in cardiac tissue. Xu et al. Circulation 2024 (PMID 37961903) noted NFAT pathway activation in cardiomyocytes: a hypertrophic signaling pathway. No hypertrophy confirmed at study doses in animals, but baseline cardiac assessment is the primary safety step.
Minor liver enzyme elevations observed in animal studies (Billon et al. JPET 2024). No human liver safety data.
Minor plasma cholesterol changes seen in animal studies. Community anecdotally reports LDL improvement. Monitor for unexpected adverse lipid changes.
SLU-PP-332 improves insulin sensitivity in obese mouse models. Monitor for additive hypoglycemia risk in users on antidiabetic medications.
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.
Day 1 to 2: Mouse data show a metabolic shift within two hours of the first dose. Respiratory exchange ratio drops, signaling a switch from carbohydrate to fatty acid oxidation. Resting energy expenditure increases. Community users report little to nothing subjectively at this stage; some mention mild warmth or energy. Injection site lumps can occur if reconstitution was incomplete. Week 1: Mitochondrial biogenesis gene expression ramps up in skeletal muscle (mouse data). Whole-body energy expenditure continues to rise. Community reports start showing subtle improvements in cardiovascular training performance and lower perceived exertion during aerobic work. Weeks 2 to 3: This is where the mouse endurance data get interesting. Treated mice ran 45% farther and 70% longer than controls. Muscle fiber-type shift toward oxidative Type IIa fibers becomes detectable. Most community users report their peak subjective endurance response in this window: improved aerobic capacity, faster recovery between sessions, higher training volume tolerance. Week 4: The full metabolic picture emerges in mouse data. Obese mice lost 12% body weight. Fat mass gain was reduced roughly 10-fold. Fasting glucose improved and insulin sensitivity increased. Community users finishing 4-week cycles report anecdotal fat loss and improved bloodwork numbers (LDL, HbA1c, eGFR), though none of these outcomes are confirmed by controlled human studies.
Decreased respiratory exchange ratio within 2 hours of first dose in mice: shift from carbohydrate to fatty acid oxidation. Raised resting energy expenditure. (Mouse data only)
No reliable acute subjective effects reported at day 1–2. Some users report mild increase in energy or warmth.
Increased mitochondrial biogenesis gene expression in skeletal muscle. Measurable increase in whole-body energy expenditure in mouse models. (Mouse data only)
Subtle improvement in cardiovascular training performance. Reduced perceived exertion during aerobic work reported by some users.
Mice ran 45% farther and 70% longer. Shift toward Type IIa oxidative muscle fibers detectable by week 3. This fiber-type shift is the mechanistic basis for sustained endurance gains. (Mouse data only)
Most users report peak subjective endurance effects in this window. Improved aerobic capacity, faster recovery between sets, higher training volume tolerance.
12% body weight reduction in obese mice vs. controls. Fat mass gain reduced ~10-fold. Improved fasting glucose and insulin sensitivity. (Mouse data only)
Anecdotal fat loss and improved bloodwork (LDL, HbA1c, eGFR) reported at end of 4-week cycles. No controlled human data. Weight loss outcomes are not confirmed in human community reports.
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.
SLU-PP-332 is classified as a research chemical. It has no FDA approval, no investigational new drug (IND) application on file, and no regulatory pathway in progress anywhere in the world. It is sold by chemical suppliers labeled "for research use only, not for human consumption." WADA has taken interest. A 2026 metabolite identification paper (DOI 10.1002/dta.70035) specifically characterized SLU-PP-332 metabolites for anti-doping detection. Competitive athletes should assume this compound is prohibited or soon will be. No compounding pharmacy produces SLU-PP-332. Supply comes from bulk chemical vendors (Carolina Chemical being the most commonly cited for purity-verified product). No pharmaceutical-grade supply chain exists. This content is for educational and research purposes only. SLU-PP-332 is not approved for human use. Consult a licensed physician before considering any research compound. Peptide Schedule does not sell, distribute, or endorse the use of any unapproved substance.
Peptide Schedule Research TeamReviewed Apr 20267 Citations
