1. Epigenetics
    PI3K/Akt/mTOR
    Membrane Transporter/Ion Channel
  2. AMPK
    GLUT
  3. MOTS-c(human) acetate

MOTS-c(human) acetate 

Cat. No.: HY-P2048A
Handling Instructions

MOTS-c(human) acetate is a mitochondrial-derived peptide. MOTS-c(human) acetate induces the accumulation of AMP analog AICAR, increases activation of AMPK and expression of its downstream GLUT4. MOTS-c(human) acetate induces glucose uptake and improves insulin sensitivity. MOTS-c(human) acetate has implications in the regulation of obesity, diabetes, exercise, and longevity.

For research use only. We do not sell to patients.

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MOTS-c(human) acetate Chemical Structure

MOTS-c(human) acetate Chemical Structure

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10 mg USD 300 In-stock
Estimated Time of Arrival: December 31
50 mg USD 750 In-stock
Estimated Time of Arrival: December 31
100 mg USD 1250 In-stock
Estimated Time of Arrival: December 31
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Description

MOTS-c(human) acetate is a mitochondrial-derived peptide. MOTS-c(human) acetate induces the accumulation of AMP analog AICAR, increases activation of AMPK and expression of its downstream GLUT4. MOTS-c(human) acetate induces glucose uptake and improves insulin sensitivity. MOTS-c(human) acetate has implications in the regulation of obesity, diabetes, exercise, and longevity[1].

IC50 & Target

AMPK

 

GLUT4

 

AICAR

 

In Vitro

MOTS-c inhibits the folate cycle at the level of 5Me-THF, resulting in an accumulation of AICAR [5-aminoimidazole-4-carboxamide ribonucleotide). MOTS-c also increases cellular NAD+ levels, which are also nucleotide precursors[1].
MOTS-c is a mitochondrial signal that stimulates cellular glucose uptake while suppressing respiration. The glucose taken up in response to MOTS-c is routed to the anabolic pentose phosphate pathway (PPP), which provides carbon sources for the synthesis of purines, rather than being metabolized through glycolysis. In addition, MOTS-c increases the levels of carnitine shuttles, which transport activated fatty acids into the mitochon-dria for β-oxidation, increases the level of a β-oxidation intermediate, and reduces intracellular levels of essential and non-essential fatty acids, suggesting enhanced lipid utilization; myocytes that stably overexpress MOTS-c also exhibits increased glucose uptake[1].

In Vivo

MOTS-c injections in mice show activation of skeletal muscle AMPK and increased the level of its downstream glucose transporter GLUT4. MOTS-c may also act as a potential mitochondrial signal that mediates an exercise-induced mitohormesis response, thereby stimulating physiological adaptation and increased tolerance to exercise[1].
The primary target organ of MOTS-c appears to be skeletal muscle and fat. MOTS-c levels in mice decline with age in skeletal muscle and in circulation concomitantly with the age-dependent development of insulin resistance. Restoring MOTS-c levels by systemic injections in older mice (12 mo.) successfully reverses age-dependent skeletal muscle insulin resistance[1].

Molecular Weight

2234.64

Formula

C₁₀₃H₁₅₆N₂₈O₂₄S₂

Sequence

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

Sequence Shortening

MRWQEMGYIFYPRKLR

Shipping

Room temperature in continental US; may vary elsewhere.

Storage

Please store the product under the recommended conditions in the Certificate of Analysis.

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Keywords:

MOTS-c(human)AMPKGLUTAMP-activated protein kinaseGlucose transporterMitochondriaobesitydiabetesexerciselongevityDNAskeletalmusclefatglucoseinsulinInhibitorinhibitorinhibit

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MOTS-c(human) acetate
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HY-P2048A
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