MOTS-c is strictly for laboratory research and is commonly employed in the following investigational areas:

Metabolic Homeostasis and Obesity

MOTS-c is a primary reagent in obesity and diabetes research. Studies utilize the peptide to investigate the regulation of insulin sensitivity and lipid metabolism. It is observed to suppress weight gain in high-fat diet models and regulate adipose homeostasis, specifically in preventing metabolic dysfunction associated with ovariectomy.

Muscle Physiology and Physical Performance

Researchers employ MOTS-c to study age-dependent physical decline. It is investigated for its ability to enhance physical performance and reduce muscle atrophy signaling (myostatin downregulation) in aged models, validating its classification as an exercise-induced mitochondrial regulator.

Neuroprotection and Cognitive Function

In neuroscience, MOTS-c is used to explore mechanisms of neuroprotection. Models of Traumatic Brain Injury (TBI) and neurodegeneration (Alzheimer’s-like pathology) utilize MOTS-c to assess its ability to inhibit neuroinflammation, reduce beta-amyloid toxicity, and improve memory via transcriptomic and metabolomic modulation.

Longevity and Aging

Given its mitochondrial origin and metabolic effects, MOTS-c is studied in the context of exceptional longevity. Research investigates the correlation between MOTS-c polymorphism/levels and healthy aging phenotypes.

Pathway / Mechanistic Context

The primary mechanisms of action for MOTS-c in research settings involve AMPK activation and nuclear gene regulation.

• Folate Cycle Inhibition: MOTS-c inhibits the folate cycle, leading to an accumulation of AICAR (5-aminoimidazole-4-carboxamide ribonucleotide).
• AMPK Activation: Increased AICAR levels trigger the activation of Adenosine Monophosphate-Activated Protein Kinase (AMPK), a master regulator of cellular energy homeostasis that promotes glucose uptake and fatty acid oxidation.
• Nuclear Regulation: In response to stress, MOTS-c translocates to the nucleus to bind to Adaptive Antioxidant Response Elements (ARE), regulating the expression of genes involved in stress resistance and metabolism.

Preclinical Research Summary

Published preclinical literature documents investigations of MOTS-c across multiple experimental models:

• Insulin Resistance: In mice fed a high-fat diet, MOTS-c administration was shown to prevent the development of insulin resistance and diet-induced obesity, mirroring the effects of exercise.
• Muscle Regeneration: Research in aged mice indicates that MOTS-c treatment significantly improves physical capacity and skeletal muscle health, potentially by suppressing myostatin expression.
• Cognitive Recovery: In models of TBI and LPS-induced inflammation, MOTS-c demonstrated neuroprotective properties, reducing neuronal apoptosis and improving cognitive outcomes through the suppression of pro-inflammatory cytokines.
• Post-Menopausal Metabolism: In ovariectomized mice, MOTS-c treatment prevented brown adipose tissue inflammation and visceral fat accumulation, suggesting a role in managing hormonal metabolic shifts.

Form & Analytical Testing

This material is produced via robust solid-phase peptide synthesis and supplied as a lyophilized (freeze-dried) powder.

• Lyophilization: Removes water content under vacuum to maintain peptide integrity and extend shelf-life.
• Identity Verification: Each lot undergoes Mass Spectrometry (MS) to confirm molecular weight and identity.
• Purity Verification: High-Performance Liquid Chromatography (HPLC) is performed to ensure the product meets the ≥99% purity standard required for reproducible research data.

Referenced Citations

References are provided for informational purposes only and are not clinical claims.

• Kim, K., Son, J., Benayoun, B., & Lee, C. (2018). The Mitochondrial-Encoded Peptide MOTS-c Translocates to the Nucleus to Regulate Nuclear Gene Expression in Response to Metabolic Stress. Cell metabolism, 28 3, 516-524.e7. https://doi.org/10.1016/j.cmet.2018.06.008.
• Lu, H., Wei, M., Zhai, Y., Li, Q., Ye, Z., Wang, L., Luo, W., Chen, J., & Lu, Z. (2019). MOTS-c peptide regulates adipose homeostasis to prevent ovariectomy-induced metabolic dysfunction. Journal of Molecular Medicine, 97, 473 – 485. https://doi.org/10.1007/s00109-018-01738-w.
• Lee, C., Zeng, J., Drew, B., Sallam, T., Martín-Montalvo, A., Wan, J., Kim, S., Mehta, H., Hevener, A., De Cabo, R., & Cohen, P. (2015). The mitochondrial-derived peptide MOTS-c promotes metabolic homeostasis and reduces obesity and insulin resistance. Cell metabolism, 21 3, 443-54. https://doi.org/10.1016/j.cmet.2015.02.009.
• Li, F., Jia, Y., Fang, J., Gong, L., Zhang, Y., Wei, S., Wu, L., & Jiang, P. (2024). Neuroprotective Mechanism of MOTS-c in TBI Mice: Insights from Integrated Transcriptomic and Metabolomic Analyses. Drug Design, Development and Therapy, 18, 2971 – 2987. https://doi.org/10.2147/DDDT.S460265.
• Jiang, J., Chang, X., Nie, Y., Shen, Y., Liang, X., Peng, Y., & Chang, M. (2021). Peripheral Administration of a Cell-Penetrating MOTS-c Analogue Enhances Memory and Attenuates Aβ1-42- or LPS-Induced Memory Impairment through Inhibiting Neuroinflammation. ACS chemical neuroscience. https://doi.org/10.1021/acschemneuro.0c00782.
• Reynolds, J., Lai, R., Woodhead, J., Joly, J., Mitchell, C., Cameron-Smith, D., Lu, R., Cohen, P., Graham, N., Benayoun, B., Merry, T., & Lee, C. (2021). MOTS-c is an exercise-induced mitochondrial-encoded regulator of age-dependent physical decline and muscle homeostasis. Nature Communications. https://doi.org/10.1038/s41467-020-20790-0.
• Kumagai, H., Coelho, A., Wan, J., Mehta, H., Yen, K., Huang, A., Zempo, H., Fuku, N., Maeda, S., Oliveira, P., Cohen, P., & Kim, S. (2021). MOTS-c reduces myostatin and muscle atrophy signaling. American journal of physiology. Endocrinology and metabolism. https://doi.org/10.1152/ajpendo.00275.2020.
• Mohtashami, Z., Singh, M., Salimiaghdam, N., Ozgul, M., & Kenney, M. (2022). MOTS-c, the Most Recent Mitochondrial Derived Peptide in Human Aging and Age-Related Diseases. International Journal of Molecular Sciences, 23. https://doi.org/10.3390/ijms231911991.
• Fuku, N., Pareja-Galeano, H., Zempo, H., Alis, R., Arai, Y., Lucia, A., & Hirose, N. (2015). The mitochondrial‐derived peptide MOTS‐c: a player in exceptional longevity?. Aging Cell, 14, 921 – 923. https://doi.org/10.1111/acel.12389.

• Stable at room temperature for up to 90 days. For long-term storage, keep at -20°C (-4°F) or colder.
• Once mixed with a solvent (e.g., bacteriostatic water), the solution must be stored at 4 °C (39°F) and utilized within 30 days. Avoid repeated freeze-thaw cycles, as this degrades the peptide structure.

RESEARCH USE ONLY

This product is intended strictly for laboratory research use only. It is not for human or veterinary use. It is not intended for diagnosis, treatment, cure, or prevention of any disease. All purchases are subject to our Terms of Service and Purity Guarantee.

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