⁠SLU-PP-322 50MG

$150.00MG

SLU-PP-332 is a synthetic small-molecule agonist of the estrogen-related receptor (ERR) family — a class of orphan nuclear receptors that regulate mitochondrial biogenesis, oxidative phosphorylation, and cellular energy homeostasis.

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SKU: ⁠SLU-PP Category:
Description

Overview

SLU-PP-332 is a synthetic small-molecule agonist of the estrogen-related receptor (ERR) family — a class of orphan nuclear receptors that regulate mitochondrial biogenesis, oxidative phosphorylation, and cellular energy homeostasis. Developed at Saint Louis University School of Medicine, SLU-PP-332 activates all three ERR isoforms (ERRα, ERRβ, and ERRγ) with preferential potency at ERRα (EC50 = 98 nM), making it one of the most well-characterized pan-ERR agonists available for laboratory research.

As a pharmacological exercise mimetic, SLU-PP-332 has attracted significant interest from researchers investigating metabolic pathways, mitochondrial function, and the molecular mechanisms underlying exercise adaptation. The compound reproduces many of the gene-expression changes associated with aerobic exercise in preclinical models, offering investigators a controlled tool for studying these pathways without the confounding variables of physical activity protocols.

This product is strictly for research purposes only. Not approved for human or animal use.

Key Characteristics

MOLECULAR PROFILE

PHYSICAL PROPERTIES

How It Works

MOTS-c operates like a master switch for cellular metabolism, activating multiple pathways that help cells use energy more efficiently. When released from mitochondria, this peptide travels throughout the cell and even into the bloodstream, where it can influence metabolism on a whole-body level.

Primary Mechanisms

AMPK Pathway Activation

Acts as your cells’ fuel gauge sensor. When AMPK is activated, cells become more efficient at burning fat for energy and maintaining healthy insulin sensitivity.

Metabolic Regulation

Influences glucose uptake from the bloodstream and optimizes cellular energy utilization across all systems.

Secondary Effects

Gene Expression Modulation

Influences gene expression related to metabolism and aging, potentially helping cells maintain their youthful function longer.

Multi-Level Approach

This comprehensive mechanism makes MOTS-c a fascinating subject for metabolic and longevity research.

Research Findings

Laboratory investigations have revealed multiple areas where MOTS-c demonstrates significant research potential.

Metabolic Health Enhancement

Laboratory studies have shown significant improvements in metabolic parameters.

Cellular Energy Optimization

Research indicates enhanced mitochondrial function and energy production.

Neuroprotective Properties

Emerging research suggests protective effects on brain cells.

Longevity and Healthy Aging

Emerging research suggests protective effects on brain cells.

Cardiovascular Support

Preliminary studies suggest cardiovascular protective properties.

Potential Side Effects in Research

Current research has reported remarkably few adverse effects associated with MOTS-c in laboratory settings. However, as with any research compound, careful monitoring is essential.
Metabolic Monitoring

Potential changes in blood glucose levels requiring monitoring in diabetic research models

Drug Interactions

Limited data on interactions with other compounds or medications

Administration Effects

Possible mild injection site reactions in animal studies

Long-term Considerations

Theoretical concerns about long-term metabolic adaptations that require further investigation

Most research has been conducted in cell cultures and animal models, with human studies still in early stages. Researchers should maintain detailed records of any observed effects during their investigations.
IMPORTANT: This product is exclusively for laboratory research purposes and is not approved for human or veterinary use.

References

  1. Billon C, Sitaula S, Burris TP. “Inhibition of RORα/γ suppresses atherosclerosis via inhibition of both cholesterol absorption and inflammation.” Mol Metab. 2016;5(10):997–1005.
  2. Billon C, et al. “SLU-PP-332 activates an ERR-dependent exercise gene program and increases exercise endurance.” Reported in Wansapura et al. 2024 (reference therein).
  3. Wansapura J, et al. “A Synthetic ERR Agonist Alleviates Metabolic Syndrome.” J Pharmacol Exp Ther. 2024;388(2):232–240. PMID: 37739806. DOI: 10.1124/jpet.123.001733.
  4. Shahien AA, et al. (2020). Development of pan-ERR agonists. Referenced in Wansapura et al. 2024.
  5. Mao L, et al. (2022). ERRα activation via a synthetic agonist improved fatty liver disease in vivo. Referenced in Wansapura et al. 2024.
  6. “Novel Pan-ERR Agonists Ameliorate Heart Failure Through Enhanced Cardiac Fatty Acid Metabolism.” Circulation. 2023. DOI: 10.1161/CIRCULATIONAHA.123.066542.
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