Product Usage: This PRODUCT IS INTENDED AS A RESEARCH CHEMICAL ONLY. This designation allows the use of research chemicals strictly for in vitro testing and laboratory experimentation only. All product information available on this website is for educational purposes only. Bodily introduction of any kind into humans or animals is strictly forbidden by law. This product should only be handled by licensed, qualified professionals. This product is not a drug, food, or cosmetic and may not be misbranded, misused or mislabeled as a drug, food or cosmetic.
MOTS-c 5mg

MOTS-c 5mg

MOTS-c is a mitochondria-derived peptide that has been studied for its role in cellular energy regulation, metabolic balance, and healthy aging pathways. Mitochondria are often referred to as the “powerhouse” of the cell because they help produce the energy cells need to function properly.

Research suggests that MOTS-c may help regulate how the body processes glucose and responds to insulin, making it an area of interest in metabolic health research. Under conditions of metabolic stress, MOTS-c can move into the cell nucleus, where it may influence gene activity related to energy production, cellular stress response, and metabolic adaptation.

Studies have explored MOTS-c for its potential role in supporting metabolic homeostasis, glucose regulation, insulin sensitivity, exercise capacity, obesity-related pathways, and age-associated conditions such as osteoporosis. Because of its connection to mitochondrial function and energy metabolism, MOTS-c remains an active area of research in longevity, metabolic health, and age-related disease processes.

$109.00

  • Peptides will arrive in a lyophilized (powder) form for maximum stability
Buy 3 and save 4%
$104.64 each
Buy 5 and save 5%
$103.55 each
Buy 18 and save 8%
$100.28 each

Popular Peptides

Peptide Blends

Cosmetic Peptides

Purchase Peptides

1. MOTS-c Overview

2. MOTS-c Structure

4. MOTS-c Research

5. Referenced Citations

What is MOTS-c

MOTS-c is a short peptide encoded by the mitochondrial genome and belongs to a broader group of compounds known as mitochondrial-derived peptides, or MDPs. These peptides have gained significant research interest for their role in mitochondrial signaling, cellular communication, and energy regulation.

Although MDPs were once believed to act only within the mitochondria, newer research suggests that many may also influence activity within the cell nucleus, while some appear to enter circulation and produce broader systemic effects. MOTS-c is one of the most studied MDPs and has been investigated for its potential role in metabolism, weight regulation, exercise performance, longevity, and age-related disease pathways, including osteoporosis.

Because MOTS-c has been detected both inside the nucleus and in general circulation, researchers consider it a naturally occurring hormone-like peptide with activity beyond the mitochondria. Its connection to metabolic health, mitochondrial function, and cellular stress response has made it an important area of investigation in recent years.

MOTS-c Structure

Sequence: Met-Arg-Trp-Gln-Glu-Met-Gly-Tyr-Ile-Phe-Tyr-Pro-Arg-Lys-Leu-Arg
Molecular Formula: C101H152N28O22S2
Molecular Weight: 2174.64 g/mol
PubChem SID: 255386757
CAS Number: 1627580-64-6
Synonyms: Mitochondrial open reading frame of the 12S rRNA-c, MT-RNR1

MOTS-c Research Overview

MOTS-c May Support Muscle Metabolism

Research in mice suggests that MOTS-c may help improve age-related insulin resistance in skeletal muscle, supporting better glucose uptake and energy use within muscle tissue. This effect appears to be linked to improved activation of AMPK, an important cellular energy regulator involved in metabolism, glucose transport, and mitochondrial function. [1]

By enhancing skeletal muscle response to AMPK activation, MOTS-c may increase the expression of glucose transporters, which help move glucose from the bloodstream into muscle cells. Importantly, this pathway appears to work independently of insulin signaling, suggesting that MOTS-c may offer an alternative mechanism for supporting glucose uptake when insulin response is reduced or impaired.

The overall result observed in research models is improved muscle glucose metabolism, better energy regulation, and reduced functional insulin resistance. These findings make MOTS-c an area of interest in studies related to muscle metabolism, aging, insulin sensitivity, and metabolic health.

How MOTS-c May Support Fat Metabolism

Research in mice suggests that low estrogen levels may contribute to increased fat mass and impaired adipose tissue function. This type of adipose dysfunction can increase the risk of insulin resistance and may contribute to the development of metabolic conditions such as diabetes.

In animal studies, MOTS-c supplementation has been shown to support brown fat activity while reducing excess adipose tissue accumulation. Brown fat is metabolically active and helps the body use energy more efficiently. MOTS-c also appears to help protect against adipose tissue dysfunction and inflammation, both of which are commonly associated with the progression toward insulin resistance. [2]

Part of MOTS-c’s effect on fat metabolism may be linked to activation of the AMPK pathway, a key cellular energy-sensing pathway. AMPK becomes active when cellular energy levels are low and helps increase the uptake and use of glucose and fatty acids for energy production. This pathway is also involved in metabolic adaptations seen during carbohydrate restriction and ketogenic-style diets, where the body shifts toward greater fat utilization while helping preserve lean tissue.

Research suggests that MOTS-c may influence this process by targeting the methionine-folate cycle, increasing AICAR levels, and activating AMPK. Together, these mechanisms may help support improved fat metabolism, glucose regulation, and overall metabolic flexibility.

Newer research also indicates that MOTS-c may move beyond the mitochondria and enter the cell nucleus, where it can influence nuclear gene expression. Under metabolic stress, MOTS-c has been shown to regulate genes involved in glucose restriction and antioxidant response pathways. This suggests that MOTS-c may play a broader role in helping cells adapt to metabolic stress and maintain energy balance. [3]

Evidence from mouse studies suggests that MOTS-c may play an important role in regulating fat metabolism, especially in the setting of obesity. Research indicates that MOTS-c may influence several lipid-related pathways, including sphingolipid, monoacylglycerol, and dicarboxylate metabolism. By downregulating these pathways while increasing beta-oxidation, the process by which fatty acids are broken down for energy, MOTS-c may help reduce excess fat accumulation. [4]

Some of these effects may be linked to MOTS-c activity within the cell nucleus, where it appears to influence gene expression related to metabolism and cellular stress response. This has led researchers to explore a newer theory about the relationship between mitochondrial fat metabolism, insulin resistance, obesity, and diabetes.

One hypothesis suggests that when mitochondrial fat metabolism becomes impaired, the body may oxidize fewer fatty acids for energy. As a result, circulating lipids may increase, forcing the body to produce more insulin in an effort to help clear excess fats from the bloodstream. Over time, chronically elevated insulin levels may contribute to increased fat storage and reduced insulin sensitivity.

This pattern may create a feedback loop where impaired fat oxidation leads to higher circulating fats, higher insulin demand, greater fat deposition, and eventually insulin resistance. Because MOTS-c appears to influence mitochondrial metabolism and fat oxidation pathways, it remains an important area of research for obesity, metabolic dysfunction, and diabetes-related processes. [5]

How MOTS-c May Support Insulin Sensitivity

Research comparing MOTS-c levels in insulin-sensitive and insulin-resistant individuals suggests that MOTS-c may be associated with insulin sensitivity, particularly in lean individuals. These findings indicate that MOTS-c may play a role in the early development of insulin resistance rather than simply maintaining the condition once it is already established. [6]

Because of this, researchers have proposed that MOTS-c levels may have potential value as an early biomarker for identifying lean individuals at risk of developing insulin insensitivity or prediabetic changes. Shifts in MOTS-c levels could potentially serve as an early warning sign before more advanced metabolic dysfunction develops.

In this setting, MOTS-c is being studied for its potential role in supporting healthier insulin regulation and helping delay or reduce the progression toward insulin resistance. Mouse studies have shown promising results, but additional research is still needed to better understand how MOTS-c influences insulin signaling, glucose regulation, and long-term metabolic health in humans.

How MOTS-c May Support Bone Health and Osteoporosis Research

MOTS-c has been studied for its potential role in bone health, particularly through its effects on osteoblasts, the cells responsible for building new bone. Research in osteoblast cell lines suggests that MOTS-c may help regulate the TGF-beta/SMAD pathway, a signaling pathway involved in osteoblast survival, function, and overall bone formation. [7]

By supporting osteoblast survival, MOTS-c may help improve the synthesis of type I collagen, a major structural protein that contributes to the strength, flexibility, and integrity of bone tissue. Because type I collagen forms an essential part of the bone matrix, this mechanism may be important in maintaining healthy bone structure.

Additional osteoporosis-related research suggests that MOTS-c may also promote the differentiation of bone marrow stem cells into bone-forming cells through the same TGF-beta/SMAD pathway. This process may support osteogenesis, or the formation of new bone. [8]

Together, these findings suggest that MOTS-c may influence bone health in two important ways: by helping protect existing osteoblasts and by supporting the development of new bone-forming cells. This makes MOTS-c an area of interest in osteoporosis, bone metabolism, and age-related bone health research.

MOTS-C and Longevity

Research on MOTS-c has identified a specific genetic variation associated with longevity in certain human populations, including individuals of Japanese ancestry. This variation affects the MOTS-c peptide by replacing the lysine normally found at position 14 with glutamate. Because lysine and glutamate have very different chemical properties, researchers believe this substitution may alter the structure and function of the peptide, although the exact biological effects are still being studied. [9]

This MOTS-c variant has been found primarily in people with Northeast Asian ancestry and has been linked to exceptional longevity in that population. While more research is needed to understand the mechanism, the finding suggests that mitochondrial-derived peptides like MOTS-c may play an important role in aging, metabolic health, and lifespan-related biology.

According to Dr. Changhan David Lee of the USC Leonard Davis School of Gerontology, mitochondrial biology may be central to understanding both lifespan and healthspan. Mitochondria are deeply involved in metabolism, cellular energy production, and age-related disease processes, making them a major focus in longevity research.

Historically, dietary restriction has been one of the most reliable methods studied for influencing mitochondrial function and aging-related pathways. However, peptides such as MOTS-c may offer researchers a more direct way to study how mitochondrial signaling affects metabolism, cellular resilience, and healthy aging.

How MOTS-c May Support Heart Health

Research in humans undergoing coronary angiography suggests that lower circulating levels of MOTS-c may be associated with greater endothelial dysfunction. Endothelial cells line the inside of blood vessels and play an important role in regulating blood pressure, blood clotting, vascular tone, inflammation, and plaque formation. Because endothelial dysfunction is closely connected to cardiovascular risk, MOTS-c has become an area of interest in heart and vascular health research. [10]

Additional animal research suggests that MOTS-c may not directly change blood vessel responsiveness on its own, but may help endothelial cells respond more effectively to signaling molecules such as acetylcholine. In rat studies, MOTS-c supplementation was associated with improved endothelial function, along with better microvascular and epicardial blood vessel activity. [10]

MOTS-c is also part of a larger group of mitochondrial-derived peptides, or MDPs, that are being studied for their role in cardiovascular health. Research suggests that several MDPs may help protect cardiac cells against stress, inflammation, and metabolic injury. Scientists have also proposed that MDP dysregulation may contribute to cardiovascular disease, endothelial dysfunction, and reperfusion injury. [11]

MOTS-c has demonstrated minimal side effects in mouse studies, along with low oral bioavailability and strong subcutaneous bioavailability. However, dosing data from animal studies does not directly translate to humans.

MOTS-c sold by Quant Peptides is intended strictly for educational and scientific research purposes only. It is not for human consumption and should only be purchased by licensed researchers.

Article Author

The above literature was researched, edited and organized by Dr. Logan, M.D. Dr. Logan holds a doctorate degree from Case Western Reserve University School of Medicine and a B.S. in molecular biology.

Scientific Journal Author

Dr. Changhan David Lee, contributor to “MOTS-c: A novel mitochondrial-derived peptide regulating muscle and fat metabolism,” and “The Mitochondrial-Encoded Peptide MOTS-c Translocates to the Nucleus to Regulate Nuclear Gene Expression in Response to Metabolic Stress,” is a researcher at the School of Gerontology at USC Leonard Davis.

Pinchas Cohen, MD, is the dean of the USC Leonard Davis School of Gerontology, executive director of the Ethel Percy Andrus Gerontology Center, and holder of the William and Sylvia Kugel Dean’s Chair in Gerontology. He is an expert in the study of mitochondrial peptides and their possible therapeutic benefits for diabetes, Alzheimer’s, and other diseases related to aging. Cohen’s current research focus is on the emerging science of mitochondria-derived peptides, which he discovered. These peptides include humanin, a 24-amino acid peptide encoded from the mt-16S-rRNA. It is a novel, centrally acting insulin sensitizer and metaboloprotective factor representing a new therapeutic and diagnostic target in diabetes and related disease. Other mitochondrial peptides of interest include MOTS-c, a second peptide encoded from a small ORF in the 12S region of the mitochondrial chromosome that has potent anti-diabetes and anti-obesity effect and acts as an exercise-mimetic, and SHLP2, a peptide encoded from the light strand of the mt-16S-rRNA region whose levels correlate with prostate cancer.

Dr. Changhan David Lee and Dr. Pinchas Cohen are being referenced as leading scientists involved in the research and development of Humanin. In no way are these doctors/scientists endorsing or advocating the purchase, sale, or use of this product for any reason. There is no affiliation or relationship, implied or otherwise, between Quant Peptides and these doctors. The purpose of citing the doctors is to acknowledge, recognize, and credit the exhaustive research and development efforts conducted by the scientists studying this peptide. Dr. Changhan David Lee is listed in [1] [3] Dr. Pinchas Cohen is listed in [9] under the referenced citations.

Referenced Citations

1

C. Lee, K. H. Kim, and P. Cohen, “MOTS-c: A novel mitochondrial-derived peptide regulating muscle and fat metabolism,” Free Radic. Biol. Med., vol. 100, pp. 182–187, Nov. 2016. [PMC]

2

H. Lu et al., “MOTS-c peptide regulates adipose homeostasis to prevent ovariectomy-induced metabolic dysfunction,” J. Mol. Med. Berl. Ger., vol. 97, no. 4, pp. 473–485, Apr. 2019. [PubMed]

3

K. H. Kim, J. M. Son, B. A. Benayoun, and C. Lee, “The Mitochondrial-Encoded Peptide MOTS-c Translocates to the Nucleus to Regulate Nuclear Gene Expression in Response to Metabolic Stress,” Cell Metab., vol. 28, no. 3, pp. 516-524.e7, Sep. 2018. [PMC]

4

S.-J. Kim et al., “The mitochondrial-derived peptide MOTS-c is a regulator of plasma metabolites and enhances insulin sensitivity,” Physiol. Rep., vol. 7, no. 13, p. e14171, Jul. 2019. [PubMed]

5

R. Crescenzo, F. Bianco, A. Mazzoli, A. Giacco, G. Liverini, and S. Iossa, “A possible link between hepatic mitochondrial dysfunction and diet-induced insulin resistance,” Eur. J. Nutr., vol. 55, no. 1, pp. 1–6, Feb. 2016. [BMJ]

6

L. R. Cataldo, R. Fernández-Verdejo, J. L. Santos, and J. E. Galgani, “Plasma MOTS-c levels are associated with insulin sensitivity in lean but not in obese individuals,” J. Investig. Med., vol. 66, no. 6, pp. 1019–1022, Aug. 2018. [PubMed]

7

N. Che et al., “MOTS-c improves osteoporosis by promoting the synthesis of type I collagen in osteoblasts via TGF-β/SMAD signaling pathway,” Eur. Rev. Med. Pharmacol. Sci., vol. 23, no. 8, pp. 3183–3189, Apr. 2019. [PubMed]

8

B.-T. Hu and W.-Z. Chen, “MOTS-c improves osteoporosis by promoting osteogenic differentiation of bone marrow mesenchymal stem cells via TGF-β/Smad pathway,” Eur. Rev. Med. Pharmacol. Sci., vol. 22, no. 21, pp. 7156–7163, Nov. 2018. [PubMed]

9

N. Fuku et al., “The mitochondrial-derived peptide MOTS-c: A player in exceptional longevity?,” Aging Cell, vol. 14, Aug. 2015. [Research Gate]

10

Q. Qin et al., “Downregulation of circulating MOTS-c levels in patients with coronary endothelial dysfunction,” Int. J. Cardiol., vol. 254, pp. 23–27, 01 2018. [PubMed]

11

Y. Yang et al., “The role of mitochondria-derived peptides in cardiovascular disease: Recent updates,” Biomed. Pharmacother. Biomedecine Pharmacother., vol. 117, p. 109075, Jun. 2019. [PubMed]

ALL ARTICLES AND PRODUCT INFORMATION PROVIDED ON THIS WEBSITE ARE FOR INFORMATONAL AND EDUCATIONAL PURPOSES ONLY.

The products offered on this website are furnished for in-vitro studies only. In-vitro studies (Latin: in glass) are performed outside of the body. These products are not medicines or drugs and have not been approved by the FDA to prevent, treat or cure any medical condition, ailment or disease. Bodily introduction of any kind into humans or animals is strictly forbidden by law.

Storage Instructions:

Storage & Stability

Our peptides are produced using a specialized freeze-drying process known as lyophilization. This process removes moisture from the peptide while preserving its structure, helping maintain stability during storage and shipping.

Before reconstitution, lyophilized peptides are typically presented as a dry, white powder or cake inside the vial. In this form, they are generally more stable than liquid peptides and can better tolerate short-term temperature changes that may occur during transit.

Once received, peptides should be stored in a cool, dry place away from direct light. For short-term storage, refrigeration at approximately 4°C / 39°F is commonly recommended. For longer-term storage, keeping lyophilized peptides frozen may help preserve their stability over time.

After the peptide is reconstituted with bacteriostatic water, it should be stored in the refrigerator and protected from light. Reconstituted peptides are generally recommended for use within 30 days to help maintain quality and stability.

In simple terms:
Lyophilized peptides are designed to remain stable while dry, but once mixed, they should be kept cold and handled with care.

View Cart Checkout Continue Shopping