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MOTS-C 10MG

$85.00Price
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Mitochondrial‑encoded 16‑mer peptide involved in metabolic regulation. Preclinical studies suggest improved insulin sensitivity, AMPK activation, and exercise‑like adaptations, with possible roles in healthy aging. Early human data are limited; translational relevance and dosing are still being defined.
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  • MOTS‑c Research & Chemical Profile

    Description

    MOTS‑c (mitochondrial open reading frame of the 12S rRNA‑c) is a 16‑amino‑acid, mitochondrial‑derived peptide encoded within the 12S rRNA region of mitochondrial DNA. The peptide sequence is Met‑Arg‑Trp‑Gln‑Glu‑Met‑Gly‑Tyr‑Ile‑Phe‑Tyr‑Pro‑Arg‑Lys‑Leu‑Arg (MRWQEMGYIFYPRKLR). MOTS‑c functions as a metabolic regulator: it promotes insulin sensitivity and glucose uptake, activates AMPK signaling, and under metabolic stress can translocate to the nucleus to regulate gene expression.

     

    Chemical Structure / Identifiers

    Property

    Detail

    Sequence

    H‑Met‑Arg‑Trp‑Gln‑Glu‑Met‑Gly‑Tyr‑Ile‑Phe‑Tyr‑Pro‑Arg‑Lys‑Leu‑Arg‑OH (MRWQEMGYIFYPRKLR)

    Molecular Formula

    C101H152N28O22S2 (PubChem)

    Molecular Weight

    ≈ 2174.6 g/mol (PubChem/MedChemExpress)

    CAS Number

    1627580‑64‑6

    PubChem CID

    146675088 (also listed as 155885767 in alternate entry)

    Primary Pathways

    AMPK activation; AICAR biosynthesis; retrograde mito‑nuclear signaling

     

    Primary Research Focus

    • Metabolic homeostasis: improves insulin sensitivity and glucose handling; reduces diet‑induced obesity in mouse models.
    • Skeletal muscle metabolism: enhances glucose uptake and exercise‑like adaptations; targets skeletal muscle as a key effector tissue.
    • Stress response and gene regulation: translocates to the nucleus during metabolic stress to modulate nuclear genes linked to antioxidant and metabolic programs.
    • Aging and chronic disease research: explored for roles in healthy aging, cardiometabolic disease, and inflammatory/fibrotic conditions.

     

    Safety / Limitations

    • Predominantly preclinical evidence (cell and animal studies); limited human data available.
    • Not approved as a therapeutic; Research Use Only. Long‑term safety, dosing, and pharmacokinetics in humans remain under investigation.
    • Reported mechanisms and benefits may be context‑dependent (nutritional status, stress, tissue type).

     

    Key Publications / References

    Cell Metabolism (2015): The mitochondrial‑derived peptide MOTS‑c promotes metabolic homeostasis and reduces obesity and insulin resistance. PubMed: https://pubmed.ncbi.nlm.nih.gov/25738459/  Cell Metab full text: https://www.cell.com/cell-metabolism/fulltext/S1550-4131%2815%2900061-3

    Cell Metabolism (2018): The mitochondrial‑encoded peptide MOTS‑c translocates to the nucleus to regulate nuclear gene expression in response to metabolic stress. https://www.cell.com/cell-metabolism/fulltext/S1550-4131%2818%2930390-5

    Frontiers in Endocrinology (2023) review: MOTS‑c as a promising mitochondrial‑derived peptide for metabolic regulation and aging. PubMed: https://pubmed.ncbi.nlm.nih.gov/36761202/  Full text: https://www.frontiersin.org/journals/endocrinology/articles/10.3389/fendo.2023.1120533/full

    BMC Translational Medicine (2023) review: MOTS‑c effects and mechanisms in energy metabolism, stress homeostasis, and aging. https://translational-medicine.biomedcentral.com/articles/10.1186/s12967-023-03885-2

    UniProtKB entry (human MOTS‑c; MT‑RNR1‑encoded): https://www.uniprot.org/uniprotkb/A0A0C5B5G6/entry

    PubChem Compound Summary (MOTS‑c): https://pubchem.ncbi.nlm.nih.gov/compound/146675088  Alternate entry: https://pubchem.ncbi.nlm.nih.gov/compound/155885767

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