MOTS-C 10mg

MOTS-C (Mitochondrial Open Reading frame of the Twelve S rRNA-c) is an endogenous 16-amino-acid peptide encoded within the human mitochondrial genome, specifically in the 12S ribosomal RNA subunit. Identified in 2015 by the Pinchas Cohen team at the University of Southern California, it represents a new class of mitochondria-derived peptides with systemic regulatory function.

Molecular structure:

• Secuencia: MRWQEMGYIFYPRKLR
• Peso molecular: aproximadamente 2,174 Da
• Biological origin: derived from human mitochondrial DNA
• Endogenous presence: detectable in human plasma, levels decreasing with age

The discovery of MOTS-C changed the classical understanding of the mitochondrion as a purely energetic organelle, revealing its role as a metabolic signaling node that communicates cellular state to the rest of the organism.

MOTS-C exerts its effects through multiple metabolic signaling pathways:

AMPK Activation:

The peptide directly activates AMPK (AMP-activated protein kinase), the cell's master energy sensor. AMPK activation triggers cascades that favor fatty acid oxidation, improve insulin-independent glucose uptake, and increase mitochondrial biogenesis.

Folate pathway regulation:

Modulates folate metabolism and the methionine cycle, impacting DNA methylation and epigenetic regulation associated with cellular aging.

Nuclear translocation under stress:

Under metabolic stress conditions (fasting, exercise, caloric restriction), MOTS-C translocates from the mitochondria to the nucleus, where it modulates the expression of adaptive genes as an integrated stress response.

Improvement of mitochondrial function:

Increases electron transport chain activity, improves coupling between oxidative phosphorylation and ATP production, and reduces mitochondrial reactive oxygen species (ROS) generation.

Active research lines with MOTS-C:

• Resistencia a la insulina: studies in murine models show a 30 to 50% improvement in insulin sensitivity with chronic treatment
• Obesidad inducida por dieta: protection against weight gain in high-fat diet models
• Capacidad aeróbica y ejercicio: increased muscle oxidative capacity, a phenomenon described as “exercise in an injection” in preclinical literature
• Envejecimiento metabólico: endogenous levels decline with age, which correlates with metabolic decline
• Fatty liver disease Reduced hepatic lipid content in NAFLD models
• Cardioprotección: effects on myocardial ischaemia-reperfusion
• Neuroprotection investigaciones preliminares sobre Parkinson y enfermedad de Alzheimer

Reference volumetric data for solution preparation in the laboratory. For calculation reference only; does not constitute usage instruction.

Reconstitution with bacteriostatic water:

The 10 mg vial can be reconstituted with 2 to 4 ml of bacteriostatic water.

• With 2 ml: 20,000 mcg/ml concentration (200 mcg per unit on U-100 scale)
• With 4 ml: 10,000 mcg/ml concentration (100 mcg per unit on U-100 scale)

The U-100 scale is included solely as a laboratory volumetric reference for calculating aliquots. Keep refrigerated after reconstitution.

In preclinical studies and in the first human trials documented in the literature, the safety profile of MOTS-C is notably clean, given that it is an endogenous peptide. Adverse events reported in that literature:

• Reacciones locales leves
• Cefalea ocasional en fases iniciales
• Mild hypoglycaemia in subjects with advanced insulin resistance on antidiabetic medication

The literature describes that, because of its mechanism of improving insulin sensitivity, studies typically monitor blood glucose in subjects on sulfonylureas or insulin. This information is presented as scientific context and not as usage guidance.

Combinations documented or explored in the research literature:

• Eje metabólico: MOTS-C alongside incretin agonists, studied for the possible synergy between the incretin axis and mitochondrial signalling
• Longevidad celular: MOTS-C with NAD+ and Epithalon, explored as a set of interest in cellular ageing research
• Capacidad oxidativa: MOTS-C con secretagogos de GH, estudiado en modelos de capacidad oxidativa
• Metabolismo hepático: MOTS-C with metabolic agonists, researched in visceral and hepatic fat models
• Soporte mitocondrial: MOTS-C with NAD+ in mitochondrial function research

1. Lee C, Zeng J, Drew BG, et al. The mitochondrial-derived peptide MOTS-c promotes metabolic homeostasis and reduces obesity and insulin resistance. Cell Metab. 2015;21(3):443-454.
2. Reynolds JC, Lai RW, Woodhead JST, et al. MOTS-c is an exercise-induced mitochondrial-encoded regulator of age-dependent physical decline and muscle homeostasis. Nat Commun. 2021;12:470.
3. Kim KH, Son JM, Benayoun BA, Lee C. The mitochondrial-encoded peptide MOTS-c translocates to the nucleus to regulate nuclear gene expression. Cell Metab. 2018;28(3):516-524.
4. Yang Y, Gao H, Zhou H, et al. The role of mitochondrial-derived peptide MOTS-c in metabolic homeostasis. Pharmacol Res. 2019;143:166-171.
5. Merry TL, Chan A, Woodhead JST, et al. Mitochondrial-derived peptides in energy metabolism. Am J Physiol Endocrinol Metab. 2020;319(4):E659-E666.

Product intended exclusively for scientific research purposes.