MOTS-C (10mg)

MOTS-C (Mitochondrial Open Reading Frame of the 12S rRNA-c) is a 16-amino acid peptide encoded within the mitochondrial genome — specifically within the 12S ribosomal RNA gene. Discovered in 2015 by Chang et al. at the University of Southern California, MOTS-C represents a fundamentally novel class of biological peptide: a mitochondrial-derived peptide (MDP) that functions as a systemic metabolic regulator. Its discovery challenged the long-held assumption that the mitochondrial genome encodes only structural components of the respiratory chain.

What Makes MOTS-C Unique?

MOTS-C is distinguished from all other peptides in the research landscape by its origin. Where most research peptides are derived from endocrine glands, connective tissue proteins, or synthetic design, MOTS-C is encoded by the mitochondrial genome and produced within mitochondria — the organelles responsible for cellular energy production. This makes it the first known peptide to act as a mitochondria-to-nucleus signalling molecule, capable of translocating from mitochondria to the cell nucleus in response to metabolic stress.

This mitochondrial origin and its role in retrograde (mitochondria-to-nucleus) communication positions MOTS-C as a uniquely relevant compound for research into mitochondrial biology, metabolic ageing, and the intersection of energy metabolism and longevity.

MOTS-C Research Background

Metabolic regulation: The landmark 2015 Chang et al. paper in Cell Metabolism characterised MOTS-C as a regulator of insulin sensitivity and metabolic homeostasis. In mouse models, MOTS-C administration improved glucose tolerance, reduced fat accumulation, and enhanced exercise capacity. The peptide’s mechanism involves regulation of the folate cycle and de novo purine biosynthesis, affecting AMPK (AMP-activated protein kinase) signalling — a central energy-sensing pathway.

Exercise and physical performance research: Studies in aged mouse models have examined MOTS-C’s effects on exercise capacity and muscle function. Research published in Nature Aging (2021) documented that exogenous MOTS-C administration to aged mice improved physical performance, muscle metabolism, and inflammatory markers — findings that have positioned MOTS-C as one of the most actively studied peptides in exercise gerontology.

Ageing biology: MOTS-C plasma levels decline with human ageing, a pattern consistent with other endogenous peptides studied in the geroscience field. Age-related decline in circulating MOTS-C concentrations is associated with metabolic dysfunction in epidemiological studies, providing the translational rationale for its investigation as a research compound.

Stress response and hormesis: MOTS-C’s translocation to the nucleus under metabolic stress conditions (hypoglycaemia, exercise, oxidative stress) positions it as a stress-responsive signalling molecule. Research has examined its role in mediating beneficial adaptations to metabolic challenge — a mechanism relevant to research into hormesis and adaptive stress responses.

Anti-inflammatory activity: Preclinical studies have documented MOTS-C’s modulatory effects on inflammatory pathways, with research examining its effects on macrophage polarisation and systemic inflammatory markers in aged animal models.

MOTS-C in the Longevity Research Context

MOTS-C’s mitochondrial origin, its decline with ageing, and its documented effects on metabolic and inflammatory pathways make it one of the most scientifically compelling compounds in the longevity research space. It is frequently studied alongside Epithalon, GHK-Cu, and NAD+ in multi-compound longevity research programmes.

Reconstitution Guidelines (Research Use)

MOTS-C is supplied as lyophilised powder. Reconstitute with bacteriostatic water.

Recommended concentration: 1mg/ml.

For precise volume calculations: Peptide Reconstitution Calculator

Storage

• Lyophilised powder: 2–8°C, protected from light
• Reconstituted: 2–8°C, use within 28 days
• Long-term: -20°C

VITALITY CARTEL MOTS-C

99%+ purity, third-party HPLC verified. CoA available on request. Domestic AU dispatch.