MOTS-c (Mitochondrial Open Reading Frame of the 12S rRNA-c) from Super Human Peptides UK is a highly unique, 16-amino acid mitochondrial-derived peptide (MDP). Unlike the vast majority of peptides that are encoded in the cell's nucleus, MOTS-c is encoded within the mitochondrial genome itself. In laboratory research, it is widely studied as an "exercise-mimetic" due to its profound ability to regulate metabolic homeostasis, enhance fatty acid oxidation, and promote glucose clearance.
Researchers utilize MOTS-c to investigate retrograde signalling—how mitochondria communicate with the nucleus under metabolic stress to alter gene expression. Produced under GMP-compliant conditions and verified for 99% purity or higher, MOTS-c is a cutting-edge model for studying systemic aging, obesity, and cellular energy optimization.
WarningFor laboratory research use only. Not for human consumption.
Key Features
- —Mitochondrial Origin: Exclusively encoded by the mitochondrial genome.
- —Exercise Mimetic: Studied for its ability to activate AMPK and replicate the cellular effects of physical exertion.
- —High Purity: 99% purity or higher (verified by HPLC and MS analysis).
- —Quality Standard: GMP / ISO certified manufacturing.
- —Documentation: Full Certificate of Analysis (COA) included with every batch.
Research Focus
- —Insulin Sensitivity: Modulation of systemic glucose uptake and lipid metabolism in diet-induced obesity models.
- —AMPK Activation: Research into the AMPK-SIRT1-PGC-1alpha signalling axis and cellular energy sensing.
- —Nuclear Translocation: Studying how the peptide travels from the mitochondria to the nucleus to regulate stress-response genes.
- —Mitochondrial Fitness: Investigating mitochondrial biogenesis and oxygen consumption rates in aging tissue.
- —Osteoblast Function: Preclinical models exploring the prevention of bone loss and promotion of bone marrow stem cell differentiation.
Published Research and Study Findings
MOTS-c was first identified in 2015 by researchers at the University of Southern California (USC). Laboratory studies demonstrated that administering MOTS-c to mice fed a high-fat diet prevented age-dependent and diet-induced insulin resistance, as well as diet-induced obesity. Further research has shown that MOTS-c operates primarily by targeting the folate cycle and activating AMPK (AMP-activated protein kinase), a master regulator of cellular energy that is typically activated during exercise.
In older animal models, MOTS-c administration significantly improved physical performance and skeletal muscle homeostasis, earning it significant attention in gerontology as a potential intervention for age-related physical decline and frailty.
NoteAll findings are derived from laboratory and non-clinical research settings.
Representative Scientific References
- 1.Lee, C. et al., "The mitochondrial-derived peptide MOTS-c promotes metabolic homeostasis and reduces obesity and insulin resistance," Cell Metabolism, 2015.
- 2.Reynolds, J.C. et al., "MOTS-c is an exercise-induced mitochondrial-encoded regulator of age-dependent physical decline and muscle homeostasis," Nature Communications, 2021.
- 3.Kim, S.J. et al., "The mitochondrial-derived peptide MOTS-c promotes osteogenic differentiation of bone marrow mesenchymal stem cells," Stem Cell Research & Therapy, 2018.
- 4.Zhai, D. et al., "MOTS-c peptide increases survival and decreases bacterial load in mice infected with MRSA," Molecular Immunology, 2017.
