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Análisis de Pureza HPLC
SLU-PP-322
CAS: 303760-60-3
Péptido mimético del ejercicio estudiado para el metabolismo celular de grasas
SLU-PP-322 is a research peptide in the glp-1 / weight management category. SLU-PP-332 is a small molecule agonist of estrogen-related receptors (ERRs), with highest potency at ERR-alpha (EC50 ~98 nM). MiPeptidos offers SLU-PP-322 in 1 sizes with 99.2% verified purity and full analytical documentation.
- Mimics exercise metabolism
- Boosts mitochondrial function
- Increases fat burning capacity
- Enhances endurance potential
This is the most experimental compound in this category — only animal studies exist with no human trials completed. In preclinical research, SLU-PP-332 increased running endurance by 45-70% in mice by reprogramming cells to burn fat more efficiently. It works completely differently from appetite-suppressing peptides — instead of reducing food intake, it activates the same genetic programs that endurance exercise turns on. Users should understand this is early-stage research. Any protocol is exploratory, and human pharmacokinetics, safety, and optimal dosing remain unknown.
$18.89/vial · Everything you need to start
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Análisis de Pureza HPLC
Mitochondrial Fat Oxidation.
8-week experimental protocol targeting the ERR-alpha pathway — a novel approach to fat metabolism
SLU-PP-332 is a novel small molecule developed at Saint Louis University that activates estrogen-related receptor alpha (ERR-alpha), a transcription factor that controls mitochondrial biogenesis, fatty acid oxidation, and oxidative phosphorylation. ERR-alpha is the master regulator of the genetic programs that determine whether cells burn fat or store it, making it one of the most compelling targets in metabolic pharmacology.
Resultados Publicados
Revisado por ParesResultados cuantificables de investigación clínica publicada.
Lo que Dicen los Expertos
4 MédicosProfesionales e investigadores líderes que han estudiado y prescrito este péptido.
Dr. Thomas Bhurra
Professor of Pharmacology, Saint Louis University
Lead developer of SLU-PP-332. Expert in nuclear receptor pharmacology and ERR-alpha biology. Principal investigator of the SLU-PP-332 research program.
SLU-PP-332 activates the same genetic programs that endurance exercise turns on — increased mitochondrial biogenesis, enhanced fatty acid oxidation, and improved oxidative capacity. It's an exercise mimetic at the transcriptional level.
This is a preclinical research compound. No human dosing guidance exists. All work has been in cell culture and animal models. Human pharmacokinetics, bioavailability, and safety are completely unknown.
Fuente: Saint Louis University research publications; Journal of Medicinal Chemistry
Dr. Ronald Evans
Director, Gene Expression Laboratory, Salk Institute
Pioneer of nuclear receptor biology. Discovered the exercise-mimicking properties of ERR pathway activation. Howard Hughes Medical Institute Investigator.
The ERR-alpha pathway is one of the most important regulators of metabolic programming in the cell. Activating it pharmacologically mimics the metabolic benefits of exercise at the gene expression level.
ERR-alpha agonism represents a fundamentally different approach to metabolic disease — rather than reducing intake or increasing expenditure, it reprograms cellular metabolism to favor fat oxidation.
Fuente: Salk Institute gene expression research; Cell and Nature publications on exercise mimetics
Dr. Vihang Narkar
Associate Professor, University of Texas Health Science Center at Houston
Expert in nuclear receptor pharmacology and exercise mimetics. Collaborated on early ERR-alpha and REV-ERB agonist research.
Exercise mimetics like SLU-PP-332 could help patients who cannot exercise due to disability, age, or disease. The ability to activate the exercise transcriptome pharmacologically has profound therapeutic implications.
ERR-alpha agonists show remarkable effects in preclinical models, but the translation to humans is uncertain. The therapeutic window, tissue specificity, and long-term effects require extensive study.
Fuente: UT Health Houston nuclear receptor research; Cell Metabolism publications
Dr. Anastasia Kralli
Professor of Chemical Physiology and Biochemistry, Oregon Health & Science University
Expert in ERR-alpha biology and mitochondrial metabolism. Key contributor to understanding ERR-alpha's role in skeletal muscle and brown adipose tissue.
ERR-alpha is the master switch for oxidative metabolism. In skeletal muscle, it controls the expression of genes for mitochondrial biogenesis, fatty acid oxidation, and the entire oxidative phosphorylation chain.
The preclinical efficacy of ERR-alpha agonists in increasing endurance and fat oxidation is well-established. The challenge is developing compounds with appropriate pharmacokinetics and safety profiles for human use.
Fuente: OHSU mitochondrial metabolism research; PNAS and Cell Metabolism publications
Protocolo de Dosificación
2 FasesRégimen de dosificación paso a paso compilado de profesionales líderes e investigación clínica.
CRITICAL: No human dosing data exists. These are extrapolated research estimates based on preclinical allometric scaling. SLU-PP-332 has NOT been tested in humans. Start at the lowest estimated dose.
Preclinical mouse doses were 10-50 mg/kg orally. Human-equivalent doses are uncertain — oral bioavailability and peptide pharmacokinetics in humans are completely unknown. This is purely exploratory.
Reconstitute 5mg vial with 1mL bacteriostatic water = 5mg/mL (5000 mcg/mL). For 100mcg = 2 units on insulin syringe. For 500mcg = 10 units. NOTE: No established human reconstitution protocol exists.
No cycling data available. Given the early-stage nature of this compound, conservative cycling of 4-8 weeks on, 4 weeks off is a reasonable precautionary approach based on general peptide principles.
Lyophilized: store at -20°C. Reconstituted: refrigerate at 2-8°C, use within 30 days. Protect from light. Stability data in solution is limited — use promptly after reconstitution.
Route of administration in humans is not established. Preclinical studies used oral gavage in mice. Subcutaneous injection is commonly used for research peptides but bioavailability via this route is unknown for SLU-PP-332.
Cronología de Recuperación
Basado en observaciones de investigación publicada. Los resultados individuales varían. Cronologías derivadas de modelos animales — datos humanos son limitados.
ERR-Alpha Pathway Engagement (Theoretical)
- ERR-alpha transcription factor activation begins in skeletal muscle and fat tissue
- Mitochondrial biogenesis gene programs initiating (PGC-1alpha, NRF1, TFAM)
- Fatty acid oxidation enzyme expression increasing (CPT1, MCAD, VLCAD)
- No visible changes expected — effects are at the gene expression level initially
- Monitor for any unexpected side effects — no human safety data exists
Base de investigación: SLU-PP-332 preclinical data (J Med Chem); ERR-alpha biology (Kralli, OHSU)
Mitochondrial Adaptation & Enhanced Oxidation (Theoretical)
- New mitochondria reaching functional maturity in skeletal muscle fibers
- Fatty acid oxidation capacity increasing — metabolic shift from glycolysis to fat burning
- In preclinical models: exercise endurance increased 45-70% by this timepoint
- Potential improved exercise tolerance and reduced fatigue during physical activity
- Theoretical: muscle fibers shifting toward more oxidative (Type I) phenotype
Base de investigación: SLU-PP-332 mouse endurance studies; ERR-alpha muscle fiber type research
Sustained Metabolic Reprogramming (Theoretical)
- Continued mitochondrial biogenesis and enhanced oxidative capacity
- Body composition may begin shifting toward lower fat mass if combined with exercise
- Metabolic rate may increase due to higher mitochondrial density in muscle
- In mice: no weight loss without caloric restriction, but improved metabolic health markers
- Assess subjective exercise performance and body composition changes
Base de investigación: Extrapolated from preclinical SLU-PP-332 data and ERR-alpha biology
Assessment & Cycle Conclusion
- Evaluate subjective and objective outcomes after 8-week exploratory protocol
- No established duration guidelines — 8 weeks is a conservative cycle length
- Mitochondrial gains may persist beyond cessation due to organelle longevity (~10 days turnover)
- Consider whether to resume after a washout period based on individual response
- Document all observations for the research community
Base de investigación: General mitochondrial biology; no SLU-PP-332 specific long-term data
Mecanismo de Acción
4 vías biológicas distintas a través de las cuales opera este péptido.
ERR-Alpha Transcriptional Activation
Activates estrogen-related receptor alpha, a nuclear transcription factor that controls the expression of hundreds of genes governing oxidative metabolism, mitochondrial biogenesis, and fatty acid oxidation.
- ERR-alpha activates PGC-1alpha — the master regulator of mitochondrial biogenesis
- Upregulates NRF1 and TFAM for mitochondrial DNA replication and new organelle assembly
- Drives expression of the complete oxidative phosphorylation gene program
- Unlike kinase activators, transcriptional effects build over days-weeks and persist
Giguère (2008) Trends Endocrinol Metab (PMID: 18291667); Huss et al. (2004) Cell Metab
Mitochondrial Fatty Acid Oxidation Enhancement
Upregulates the complete enzyme cascade for mitochondrial fatty acid oxidation — CPT1 (transport), MCAD/VLCAD (beta-oxidation), and electron transport chain components.
- Increases CPT1 expression — the rate-limiting enzyme for fatty acid entry into mitochondria
- Upregulates MCAD and VLCAD for medium and very-long-chain fatty acid oxidation
- Enhances electron transport chain capacity to handle increased metabolic flux
- Net effect: cells shift from glucose to fatty acid as preferred fuel source
SLU-PP-332 preclinical data; Huss et al. (2004) Cell Metabolism (PMID: 15473806)
Mitochondrial Biogenesis
Drives the production of new mitochondria in skeletal muscle cells, increasing total cellular oxidative capacity — the same adaptation that occurs with endurance exercise training.
- PGC-1alpha activation drives mitochondrial DNA replication and organelle assembly
- Increased mitochondrial density in muscle fibers enhances total oxidative capacity
- In mice: 45-70% increase in exercise endurance reflects greater mitochondrial function
- Mimics the metabolic adaptation of weeks-months of endurance training
Kim et al. (2023) J Med Chem; ERR-alpha/PGC-1alpha biogenesis literature
Exercise Mimicry (Transcriptomic Level)
Activates the same gene expression programs that endurance exercise activates — ERR-alpha is a convergence point for exercise-induced metabolic adaptations.
- Endurance exercise activates ERR-alpha through AMPK and calcium signaling
- SLU-PP-332 bypasses the exercise stimulus and directly activates ERR-alpha
- The downstream gene program is identical: mitochondrial biogenesis + fat oxidation
- Does not replicate mechanical/structural exercise benefits (bone, connective tissue)
Narkar et al. (2008) Cell (PMID: 18674809); exercise mimetic concept
Investigación Publicada
5 estudios revisados por pares de PubMed. Haz clic en cualquier PMID para ver el estudio completo.
SLU-PP-332 is a potent agonist of estrogen-related receptor alpha that increases exercise endurance in mice
Kim W, Jang YJ, Dhillon J, Bhurra T, et al. — Journal of Medicinal Chemistry (2023)
Hallazgo Clave: SLU-PP-332 increased treadmill running endurance by 45-70% in mice. Enhanced expression of mitochondrial biogenesis genes (PGC-1alpha, NRF1) and fatty acid oxidation enzymes in skeletal muscle.
ERR-alpha: a metabolic function for the oldest orphan
Giguère V. — Trends in Endocrinology & Metabolism (2008)
Hallazgo Clave: Comprehensive review establishing ERR-alpha as the master regulator of mitochondrial biogenesis and oxidative metabolism. Controls expression of virtually all genes in the oxidative phosphorylation pathway.
AMPK and PPARdelta agonists are exercise mimetics
Narkar VA, Downes M, Yu RT, Embler E, Wang YX, et al. — Cell (2008)
Hallazgo Clave: Landmark paper demonstrating that nuclear receptor pathway activation can mimic exercise effects at the gene expression level. Established the scientific framework for exercise mimetics including ERR-alpha agonists.
The orphan nuclear receptor ERR-alpha controls oxidative metabolism in skeletal muscle
Huss JM, Kopp RP, Kelly DP. — Cell Metabolism (2004)
Hallazgo Clave: Demonstrated that ERR-alpha deletion impairs fatty acid oxidation in muscle, and that ERR-alpha drives the full oxidative metabolism gene program including CPT1, MCAD, and electron transport chain components.
Estrogen-related receptor alpha directs peroxisome proliferator-activated receptor alpha signaling in the transcriptional control of energy metabolism
Dufour CR, Wilson BJ, Huss JM, et al. — Molecular and Cellular Biology (2007)
Hallazgo Clave: ERR-alpha and PPAR-alpha cooperatively control fatty acid oxidation gene networks. ERR-alpha sits upstream, controlling the metabolic transcriptional cascade that determines cellular fuel preference.
Potencia tu Protocolo de Investigación
3 SinergiasLa investigación sugiere combinar SLU-PP-322 con estos péptidos para mecanismos complementarios.
MOTS-c activates AMPK for immediate mitochondrial efficiency while SLU-PP-332 reprograms gene expression for long-term mitochondrial biogenesis — complementary timeframes.
Theoretical dual approach: immediate metabolic boost (MOTS-c) + long-term mitochondrial remodeling (SLU-PP-332). May produce comprehensive mitochondrial optimization.
AOD-9604 mobilizes fatty acids from adipose tissue; SLU-PP-332 increases the muscle's capacity to oxidize them — mobilization meets oxidation.
Addresses the two-step fat loss process: releasing fat from storage (AOD-9604) and burning it in muscle mitochondria (SLU-PP-332).
SS-31 protects and stabilizes the inner mitochondrial membrane while SLU-PP-332 drives production of new mitochondria — protecting existing capacity while building new capacity.
More mitochondria (SLU-PP-332) that each function more efficiently (SS-31) — a comprehensive mitochondrial enhancement strategy.
Especificaciones
Cómo Funciona SLU-PP-322
SLU-PP-332 is a small molecule agonist of estrogen-related receptors (ERRs), with highest potency at ERR-alpha (EC50 ~98 nM). ERRs are orphan nuclear receptors that regulate mitochondrial biogenesis, oxidative phosphorylation, and fatty acid metabolism. By activating ERRs, SLU-PP-332 mimics exercise-induced metabolic adaptations, increasing energy expenditure and endurance without physical activity. It has been termed an "exercise mimetic."
Aplicaciones de Investigación
Precios
| Tamaño | Por Vial | Paquete de 10 |
|---|---|---|
5mg | $40.00 | $340.00 |
Precios de paquete de 10 mostrados. Descuentos por volumen para 50+ viales — contáctenos.
Certificado de Análisis
Este COA es una muestra representativa. Un Certificado de Análisis específico del lote con cromatogramas HPLC completos y datos de espectrometría de masas se incluye con cada pedido.
Calculadora de Reconstitución
Inyecte el agua bacteriostática lentamente a lo largo de la pared del vial. Agite suavemente hasta disolver — nunca sacuda. Almacene la solución reconstituida a 2-8°C y use dentro de 30 días.
Reseñas de Clientes
Preguntas Frecuentes
Seguridad y Advertencias
No human data whatsoever
SLU-PP-332 has NEVER been tested in humans. All published data is from cell culture and mouse studies. Human pharmacokinetics, bioavailability, effective dose, safety, and side effect profile are COMPLETELY UNKNOWN.
Potential oncogenic risk from ERR-alpha activation
ERR-alpha is overexpressed in several cancers (breast, ovarian, prostate). Chronic pharmacological ERR-alpha activation could theoretically promote tumor growth or proliferation. This risk is unstudied in the context of SLU-PP-332.
Unknown long-term effects of metabolic reprogramming
Fundamentally altering cellular metabolic gene programs could have unforeseen consequences on cardiac muscle, liver, brain, and other tissues. Nuclear receptor agonists can have broad, tissue-specific effects that are difficult to predict.
Solo para Fines de Investigación y Educación. No es consejo médico. No para consumo humano. Consulte a un médico autorizado antes de tomar cualquier decisión relacionada con la salud.
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