MOTS-c

MOTS-c (Mitochondrial Open Reading Frame of the Twelve-S rRNA, type c) is a naturally occurring mitochondrial-derived peptide investigated for its involvement in metabolic regulation, cellular energy signalling and biological responses to physiological stress. Unlike most peptides encoded by nuclear DNA, MOTS-c originates from a short open reading frame within the mitochondrial genome — making it an important compound in research exploring how mitochondria communicate with other parts of the cell. Since its identification in 2015, published studies have investigated MOTS-c in relation to AMPK activation, glucose metabolism, skeletal muscle physiology, exercise-associated responses and ageing-related biological changes. There is insufficient clinical evidence to establish that externally administered MOTS-c improves human metabolism, physical performance or longevity.

Sequence MRWQEMGYIFYPRKLR

MOTS-c has been investigated through several interconnected molecular pathways. The original 2015 research programme reported AMPK activation linked to changes in the folate–methionine cycle and de novo purine biosynthesis — a mechanism distinct from GLP-1 or other endocrine signalling pathways. Under metabolic stress conditions, experimental studies have reported nuclear translocation of MOTS-c and potential involvement in stress-responsive gene expression, a process described as mitochondrial-to-nuclear retrograde signalling. Research has also examined glucose uptake and insulin-associated metabolic responses, with a 2015 study reporting effects on glucose metabolism in cultured cells and mouse models.

Since its identification in 2015, MOTS-c has accumulated a research base spanning molecular experiments, animal studies and observational data involving naturally occurring MOTS-c in humans. A 2021 study published in Nature Communications investigated MOTS-c in relation to exercise and ageing, reporting changes in endogenous MOTS-c following exercise in human participants. The same programme examined administered MOTS-c in mice with changes in physical performance and age-associated muscle outcomes. The human observations primarily concern naturally occurring MOTS-c, while the intervention findings were obtained in animals. Consequently, the literature does not establish that MOTS-c administration improves exercise performance or longevity in humans.

• 5 mg per application (one metered dose)
• 8 doses per pen (40 mg total)
• Mitochondrial-derived peptide (16 amino acids): MRWQEMGYIFYPRKLR
• Pre-filled sterile solution — no reconstitution step required

Storage: Store refrigerated at 2–8 °C in the original sealed box. Do not freeze. Protect from light.

• For in-vitro laboratory and preclinical research only — not for human or animal administration
• Mechanism involves AMPK activation and the folate–methionine cycle — appropriate controls for these pathways required in metabolic studies
• Human data limited to observational studies of endogenous circulating MOTS-c levels; no approved human intervention application
• Nuclear translocation of MOTS-c under metabolic stress is described in some studies — relevant for nuclear signalling assay designs

• Very limited human intervention trial data — no established clinical adverse effect profile
• Animal model data (rodent studies): hypoglycaemia risk documented with high doses, consistent with AMPK activation and glucose uptake effects
• Generally well tolerated in published preclinical literature at studied doses
• Nature Communications 2021 human observational study: did not report adverse effects from administered MOTS-c — limited scope

Effects listed are observations from published research literature and are not predictions for any specific use. All FAB Research products are for in-vitro laboratory research — not for human or animal administration.