For research purposes only — not for human consumption — 18+ only

MOTS-c 20mg

$100.00

Mitochondrial-derived peptide. Research in metabolic health insulin sensitivity and exercise mimicry.

SKU: MS20 Category:

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MOTS-c (Mitochondrial Open Reading Frame of the 12S rRNA type-c) is a mitochondria-derived peptide encoded within the mitochondrial genome itself — a highly unusual origin for a bioactive peptide. It functions as a mitochondrial stress signal that translocates to the nucleus in response to metabolic stress, directly regulating nuclear gene expression and systemic metabolism. Discovered in 2015, MOTS-c has rapidly emerged as a major research target in metabolic disease, exercise biology, and ageing, functioning as a hormone-like molecule that mediates communication between mitochondria and the rest of the body.

Molecular Data

Sequence: MRWQEMGYIFYPRKLR | Molecular Formula: C110H187N35O28S | Molecular Weight: 2681.0 g/mol

AMPK Activation and Metabolic Regulation

MOTS-c activates AMPK (AMP-activated protein kinase), a master regulator of cellular energy homeostasis. It inhibits the folate cycle and de novo purine biosynthesis, increasing AICAR — an endogenous AMPK activator. In skeletal muscle, this drives glucose uptake independently of insulin signalling, making MOTS-c of particular research interest in insulin resistance and type 2 diabetes models.

Exercise Mimicry

One of MOTS-c's most studied properties is its ability to replicate aspects of the metabolic response to exercise. Administration of MOTS-c to sedentary mice produces improvements in glucose tolerance, insulin sensitivity, and physical performance comparable to those induced by regular exercise. This exercise-mimetic property has generated significant interest in the context of metabolic disease, sarcopenia, and conditions where exercise capacity is limited.

Age-Related Decline

Circulating MOTS-c levels decline significantly with age and obesity in both animal and human studies. This decline correlates with deteriorating insulin sensitivity and metabolic flexibility. Research suggests that declining MOTS-c may be a mediating factor in age-related metabolic dysfunction, positioning MOTS-c replacement or augmentation as a potential research strategy for metabolic ageing.

Systemic Signalling

Unlike most mitochondrial proteins that remain within cells, MOTS-c is secreted into the bloodstream and acts as a hormone-like systemic signal. Studies show MOTS-c regulates whole-body glucose homeostasis and responds dynamically to metabolic stressors, exercised, and fasting. This systemic role distinguishes it from conventional mitochondrial peptides and opens new avenues in inter-organ communication research.

Future Research

MOTS-c is an active area of investigation in metabolic disease, exercise biology, longevity, and inter-organ communication research. Its unique mitochondrial origin and systemic hormonal activity make it a novel class of research compound with broad potential applications.

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