MOTS-c (human) 

MOTS-c (human) is a blood-brain barrier-penetrating, mitochondrial-derived peptide that modulates the AMPK/PGC-1α pathway to enhance insulin sensitivity. MOTS-c (human) inhibits the folate cycle and de novo purine synthesis, increases AICAR levels to activate AMPK, and then regulates the Nrf2/Keap1 antioxidant pathway and inhibits the NF-κB inflammatory pathway, while promoting mitochondrial biogenesis and energy metabolism. MOTS-c (human) has the effects of improving glucose and lipid metabolism, anti-oxidative stress, anti-inflammatory and neuroprotection, and can be used in the study of type 2 diabetes, traumatic brain injury, inflammatory diseases and aging-related metabolic disorders^[1][2][3][4].

Recent advances in high-resolution sequencing have led to the discovery of unique peptides derived from the mitochondrial genome. Eight peptides have been identified: humanin, the mitochondrial open reading frame of 12S tRNA-c (MOTS-c), and six small peptides (humanin-like peptides (SHLP1-6)). All of these peptides are released from mitochondria into the cytoplasm and are associated with extended lifespan and cell viability, reduced apoptosis, and other beneficial functions^[1].
MOTS-c (human) (10 μM; 24-72 h) activates AMPK (Thr172 phosphorylation) and the expression of downstream antioxidant proteins Nrf2 and Keap1, and inhibits the phosphorylation of MAPKs (ERK, JNK, P38) in HEK293 cells^[2].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

MOTS-c (human) (25-50 mg/kg; ip; once daily; 21 days) can reduce neurological deficits and inhibit the HMGB1/TLR4/NF-κB inflammatory pathway in brain tissue in a traumatic brain injury model in male C57BL/6 mice^[2].
MOTS-c (human) (5 mg/kg; ip; twice daily; 4 days) can reduce inflammation associated with obesity and insulin resistance by recruiting IL-6 and TNF-α in an acute treatment model in male CD-1 mice^[2].
MOTS-c (human) (50 mg/kg; ip; once a day; single dose) can reduce paw licking time and inhibit the expression of spinal p-ERK/p-JNK/p-P38 and c-fos in the formalin inflammation model of male ICR mice, exerting anti-nociceptive and anti-inflammatory effects^[3].
MOTS-c (human) (0.5 mg/kg; ip; once a day; 8 weeks) can reduce fasting blood glucose, glycosylated serum protein and blood lipid levels, improve myocardial ultrastructural damage and activate myocardial AMPK/Nrf2 antioxidant pathway^[4] in the male Sprague-Dawley rat type 2 diabetes model^[4].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

2174.59

C₁₀₁H₁₅₂N₂₈O₂₂S₂

1627580-64-6

Solid

White to off-white

Met-Arg-Trp-Gln-Glu-Met-Gly-Tyr-Ile-Phe-Tyr-Pro-Arg-Lys-Leu-Arg

MRWQEMGYIFYPRKLR

Room temperature in continental US; may vary elsewhere.

Sealed storage, away from moisture

*In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)

• [1]. Mohtashami Z, et al. MOTS-c, the Most Recent Mitochondrial Derived Peptide in Human Aging and Age-Related Diseases. Int J Mol Sci. 2022 Oct 9;23(19):11991.  [Content Brief]

  [2]. Lee C, et al. The mitochondrial-derived peptide MOTS-c promotes metabolic homeostasis and reduces obesity and insulin resistance. Cell Metab. 2015 Mar 3;21(3):443-54.  [Content Brief]

  [3]. Yin X, et al. The intraperitoneal administration of MOTS-c produces antinociceptive and anti-inflammatory effects through the activation of AMPK pathway in the mouse formalin test. Eur J Pharmacol. 2020 Mar 5;870:172909.  [Content Brief]

  [4]. Tang M, et al. The role of MOTS-c-mediated antioxidant defense in aerobic exercise alleviating diabetic myocardial injury. Sci Rep. 2023 Nov 13;13(1):19781.  [Content Brief]