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].

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].

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

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].

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

2234.64

C₁₀₃H₁₅₆N₂₈O₂₄S₂

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

Powder	-80deg;C	2 years
	-20deg;C	1 year

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

In Vitro:;

DMSO : 4 mg/mL (1.79 mM; Need ultrasonic)

*

请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。
储备液的保存方式和期限：-80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)。-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。

• [1]. Changhan Lee, et al. MOTS-c: A Novel Mitochondrial-Derived Peptide Regulating Muscle and Fat Metabolism. Free Radic Biol Med. 2016 Nov;100:182-187.