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    MOTS-c
    Home / Buy Peptide Online UK / Buy Peptide Online EU

    MOTS-c

    €50.00

    Technical Specifications

    Specification Detail
    Product Name MOTS-c (Mitochondrial ORF of the Twelve S rRNA-c)
    Amino Acid Sequence Met-Arg-Trp-Gln-Glu-Met-Gly-Tyr-Ile-Phe-Tyr-Pro-Arg-Lys-Leu-Ser
    Molecular Formula C₈₉H₁₃₃N₂₅O₂₃
    Molecular Weight ~1953.2 Da
    Purity ≥99% (HPLC verified)
    Appearance White to off-white lyophilized powder
    Solubility Soluble in water, PBS, or appropriate buffer
    Biological Functions AMPK activation, insulin sensitivity enhancement, glucose uptake, fatty acid oxidation, mitochondrial biogenesis
    Key Target Tissues Skeletal muscle, adipose tissue, liver, heart, bone
    Regulated Pathways Folate cycle, purine biosynthesis, sphingolipid metabolism, monoacylglycerol metabolism, dicarboxylate metabolism
    Storage (Powder) -20°C; protect from light and moisture
    Storage (Reconstituted) 2-8°C (short-term); -20°C (long-term, aliquot)
    Shipping Ambient temperature with protective packaging
    Intended Use Research and laboratory use only
    Documentation Certificate of Analysis provided with each batch
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    • Description

    Research-Grade MOTS-c Peptide | ≥99% Purity | 48-Hour Delivery Across EU & UK

    MOTS-c: The Mitochondrial Signaling Peptide Redefining Metabolic Research

    Buy MOTS-c online EU, eupeptidelap.co.uk is proud to present MOTS-c (Mitochondrial ORF of the Twelve S rRNA-c), a premium research-grade mitochondrial-derived peptide manufactured to the highest analytical standards. As a trusted peptide vendor uk and leading EU peptide supplier, we provide researchers across Europe with MOTS-c for sale that delivers exceptional purity, consistency, and documented quality for advanced metabolic and aging studies.

    MOTS-c is a 16-amino acid bioactive peptide encoded by a short open reading frame (sORF) within the mitochondrial 12S rRNA region, representing a groundbreaking discovery in mitochondrial biology . Unlike most proteins encoded by nuclear genes, MOTS-c is produced within mitochondria and acts as a mitochondrial-derived signaling peptide (MDSP), establishing a direct communication link between mitochondrial function and systemic metabolic regulation . This peptide has been shown in extensive preclinical research to regulate metabolic homeostasis, stress responses, and cell survival—potentially influencing how cells age and adapt to metabolic stress .

    The molecular formula of MOTS-c is C₈₉H₁₃₃N₂₅O₂₃, with a molecular weight of approximately 1953.2 Da. Its amino acid sequence is Met-Arg-Trp-Gln-Glu-Met-Gly-Tyr-Ile-Phe-Tyr-Pro-Arg-Lys-Leu-Ser . MOTS-c translation obligatorily occurs in the cytoplasm using the standard genetic code, requiring export of its polyadenylated transcript from mitochondria—a mechanism that highlights the sophisticated communication between mitochondrial and nuclear genomes .

    MOTS-c has captured the attention of the scientific community for its remarkable effects on metabolic health. Treatment and overexpression of MOTS-c increase AMP-activated protein kinase (AMPK) activity, offering protection against insulin resistance . Its primary target organ appears to be skeletal muscle, where its cellular actions inhibit the folate cycle and its tethered de novo purine biosynthesis, leading to AMPK activation . MOTS-c treatment in mice prevents age-dependent and high-fat diet-induced insulin resistance, as well as diet-induced obesity .

    For researchers seeking to buy peptide online EU for investigations into metabolic disorders, insulin resistance, aging mechanisms, or mitochondrial function, eupeptidelap.co.uk offers this premium research compound with comprehensive documentation, including Certificates of Analysis and batch-specific purity data. Whether your laboratory is based in London, Berlin, Paris, or anywhere in the European Union, our guaranteed 48 hour delivery peptide service ensures your research continues without interruption.

    The Scientific Foundation of MOTS-c Research

    Discovery and Mitochondrial Origin

    The identification of MOTS-c emerged from an in silico search for potential short open reading frames (sORFs) within the human 12S rRNA region, revealing one consisting of 51 base pairs with a strong Kozak sequence that translates into a 16 amino acid peptide . Multiple peptide sequence alignment across 14 species demonstrates that MOTS-c is highly conserved, especially the first 11 residues, with four residues undergoing positive selection and two undergoing purifying selection, indicating evolutionary pressure to maintain its function .

    The mitochondrial origin of MOTS-c has been rigorously confirmed through multiple experimental approaches. Selective depletion of mitochondrial DNA in HeLa cells (HeLa-ρ0) eliminates both 12S rRNA and MOTS-c transcripts, while mitochondrial RNA depletion using actinonin results in time-dependent loss of MOTS-c expression . MOTS-c is detected in various tissues in mice and rats, as well as in circulation in human and rodent plasma . Notably, fasting lowers endogenous expression of MOTS-c in metabolically active and mitochondria-rich tissues (skeletal muscle and testes) while homeostatic tissues (such as brain and heart) show sustained levels .

    Mechanism of Action: AMPK Activation and Metabolic Regulation

    MOTS-c works by modulating several key pathways crucial for cellular energy balance and stress resilience :

    AMPK Pathway Activation: MOTS-c enhances AMP-activated protein kinase (AMPK) activity, which promotes glucose uptake, fatty acid oxidation, and mitochondrial biogenesis . Its cellular actions inhibit the folate cycle and its tethered de novo purine biosynthesis, leading to endogenous accumulation of 5-aminoimidazole-4-carboxamide ribonucleotide (AICAR)—a well-known AMPK activator . This mechanism positions MOTS-c as a central regulator of cellular energy homeostasis.

    Insulin Signaling Modulation: MOTS-c improves insulin sensitivity by increasing glucose uptake in skeletal muscle in response to insulin . This enhanced insulin sensitivity translates into better glucose control and energy utilization, making MOTS-c particularly relevant for metabolic research.

    Regulation of Oxidative Stress: MOTS-c helps buffer the intracellular environment against oxidative damage—a contributor to both aging and tissue degeneration . It interacts with pathways involving nuclear factor E2-related factor 2 (Nrf2) to defend antioxidant systems .

    Cellular Stress Adaptation: The peptide supports cellular adaptation during metabolic stress, such as fasting or intense exercise, by promoting mitochondrial function and metabolic flexibility .

    Effects on Plasma Metabolites

    Unbiased metabolomics studies have revealed that MOTS-c significantly alters plasma metabolites associated with insulin resistance . Three key pathways are reduced in MOTS-c-treated mice:

    • Sphingolipid Metabolism: Elevated ceramide and sphingosine 1-phosphate (S1P) levels in plasma contribute to insulin resistance and metabolic syndrome . MOTS-c reduces these sphingolipids, which directly inhibit mitochondrial electron transport and suppress beta-oxidation.

    • Monoacylglycerol Metabolism: MOTS-c modulates the activity of angiopoietin-like proteins (ANGPTLs) that regulate lipoprotein lipase activity, influencing fatty acid uptake by tissues .

    • Dicarboxylate Metabolism: Increases in dicarboxylates generally indicate dysfunction of normal mitochondrial and peroxisomal beta-oxidation. MOTS-c’s reduction of these metabolites suggests improved fatty acid oxidation capacity .

    These pathways are typically upregulated in obese and type 2 diabetes models, and their reduction by MOTS-c provides mechanistic insight into how the peptide improves insulin sensitivity, reduces body weight, and decreases fatty liver accumulation .

    MOTS-c in Metabolic Disease Research

    Insulin Resistance and Type 2 Diabetes: A systematic review and meta-analysis of 602 participants demonstrated that circulating MOTS-c levels are significantly reduced in diabetic individuals (SMD = -0.89; 95% CI -1.12 to -0.65; P < 0.05) . MOTS-c levels are correlated with markers of insulin resistance including fasting insulin level, HOMA-IR, and HbA1c . MOTS-c treatment in mice prevented age-dependent and high-fat diet-induced insulin resistance, as well as diet-induced obesity .

    Obesity Research: Interestingly, meta-analysis revealed opposite results for MOTS-c changes in obesity versus diabetes. In obese individuals (BMI > 28 kg/m²), MOTS-c levels were significantly increased (SMD = 0.51; 95% CI 0.21 to 0.81; P < 0.05) . This differential regulation suggests that MOTS-c may serve as a compensatory mechanism in obesity that becomes overwhelmed or dysregulated with progression to diabetes. MOTS-c levels are significantly positively correlated with total cholesterol (r = 0.29, 95% CI 0.20 to 0.38) and LDL-c (r = 0.30, 95% CI 0.22 to 0.39) .

    Age-Related Metabolic Decline: Observational studies have shown that circulating MOTS-c levels decline with age, which is associated with increased risk of age-related diseases, such as type 2 diabetes and frailty . MOTS-c treatment in mice prevented age-dependent insulin resistance, highlighting its potential for aging research .

    MOTS-c in Cardiovascular Research

    MOTS-c has emerged as a promising molecule for cardiovascular research, particularly in diabetic cardiomyopathy. In streptozotocin (STZ)-induced type 1 diabetic mouse models, MOTS-c administration for 3 months significantly improved cardiac function :

    • Improved Systolic Function: Left ventricular ejection fraction (LVEF) and left ventricular fractional shortening (LVFS) were significantly improved by MOTS-c administration .

    • Attenuated Cardiac Remodeling: Elevated cardiac chamber dimensions (left ventricular internal diameter at systole and diastole) were attenuated by MOTS-c .

    • Reduced Pathology: MOTS-c attenuated cardiac hypertrophy, fibrosis, and apoptosis in diabetic mouse hearts .

    • Molecular Effects: Significant activation of AMPK (phosphorylation at Thr172) and reduction in myocardial inflammation (tumor necrosis factor-α, Interleukin-1β) were observed .

    MOTS-c also regulates the ROS/TXNIP/NLRP3 pathway and repairs myocardial damage by inhibiting the CCN1/ERK1/2/EGR1 pathway in diabetic rats, demonstrating its multi-faceted cardioprotective effects .

    MOTS-c in Muscle and Aging Research

    Sarcopenia and Muscle Health: Mitochondrial dysfunction is well-established in sarcopenia—the progressive loss of skeletal muscle mass and function with advancing age . MOTS-c, as a mitochondria-derived peptide, targets several underlying causes of sarcopenia :

    • Impaired glucose uptake in muscle

    • Poor mitochondrial energy production

    • Deficient muscle regeneration

    • Increased oxidative stress

    In older adults, higher MOTS-c blood levels correlate with better muscle function, strength, and reduced frailty indices . MOTS-c reduces myostatin and muscle atrophy signaling, and some data suggest a link between MOTS-c and muscle adaptation to physical activity .

    Exercise Mimetic Properties: MOTS-c is an exercise-induced mitochondrial-encoded regulator of age-dependent physical decline and muscle homeostasis . It is induced in response to exercise and metabolic stress and travels to the nucleus in a retrograde fashion to control gene expression of many stress-responsive and antioxidant-responsive genes . The exercise benefits of MOTS-c have led to its inclusion in the World Anti-Doping Agency (WADA) list of prohibited substances .

    MOTS-c in Bone Health Research

    MOTS-c suppresses ovariectomy-induced osteoporosis via AMPK activation and improves osteoporosis through the TGF-β/Smad pathway . It suppresses ovariectomy-induced bone loss and regulates adipose homeostasis to prevent metabolic dysfunction . These findings highlight MOTS-c’s relevance for research into age-related bone loss and metabolic bone diseases.

    MOTS-c in Adrenal and Endocrine Research

    Recent studies have revealed that MOTS-c functions as a metabolic conductor that primes adrenocortical cells for enhanced steroidogenic responsiveness without stimulating basal hormone synthesis . Key findings include:

    • Novel Gene Targets: RNA-seq identified 39 differentially expressed genes, notably upregulation of purinergic receptor P2ry4 (4.3-fold, P < 0.05)—a novel MOTS-c target enhancing calcium signaling .

    • Pathway Modulation: Gene Set Enrichment Analysis revealed inhibition of cAMP response, mitophagy, and histone deacetylation pathways, alongside activation of cell proliferation, indicating metabolic reprogramming without steroidogenic activation .

    • Stress Marker Regulation: Downregulation of stress markers Bag3 and Smurf2, mitochondrial carrier Slc25a30, and peroxisomal factor Pex11a .

    These findings reveal a novel preparatory mechanism in adrenal physiology and identify MOTS-c as a potential therapeutic target for HPA axis disorders requiring enhanced adrenal reserve capacity without basal hypercortisolemia .

    Quality Assurance: Setting the Standard for Research Compounds

    Manufacturing Excellence

    eupeptidelap.co.uk sources MOTS-c from certified GMP facilities with rigorous quality control protocols:

    • HPLC Purity Analysis: ≥99% purity verified by high-performance liquid chromatography

    • Mass Spectrometry Verification: Molecular weight confirmation (1953.2 Da) via LC-HRMS

    • Batch-Specific Certificates of Analysis: Complete documentation for each production run

    • Third-Party Lab Testing: Independent verification of purity and potency

    Chemical and Product Specifications

    Specification Detail
    Product Name MOTS-c (Mitochondrial ORF of the Twelve S rRNA-c)
    Amino Acid Sequence Met-Arg-Trp-Gln-Glu-Met-Gly-Tyr-Ile-Phe-Tyr-Pro-Arg-Lys-Leu-Ser
    Molecular Formula C₈₉H₁₃₃N₂₅O₂₃
    Molecular Weight ~1953.2 Da
    Purity ≥99% (HPLC verified)
    Appearance White to off-white lyophilized powder
    Form Lyophilized powder
    Solubility Soluble in water, PBS, or appropriate buffer
    Biological Role Mitochondrial-derived signaling peptide, AMPK activator, insulin sensitivity regulator
    Key Pathways AMPK, folate cycle, purine biosynthesis, sphingolipid metabolism
    Storage (Powder) -20°C; protect from light and moisture
    Storage (Reconstituted) 2-8°C for short-term; aliquot and freeze at -20°C for longer storage
    Shipping Ambient temperature with protective packaging
    Intended Use Research and laboratory use only
    Documentation Certificate of Analysis provided with each batch

    Stability and Handling Guidelines

    Lyophilized Powder Storage: MOTS-c powder should be stored at -20°C in a dry, dark environment, protected from light and moisture. Use manual-defrost freezers and store vials in the back (not doors) to avoid temperature fluctuations.

    Reconstitution Protocol:

    1. Allow vial and solvent to reach ambient temperature before opening to prevent condensation

    2. Reconstitute using sterile water, PBS, or appropriate buffer according to research protocol

    3. Gently swirl until powder is completely dissolved—do not shake vigorously

    4. Use fresh sterile needles for each vial access

    5. Clean rubber stoppers with alcohol swabs before each puncture

    Reconstituted Solution Storage: Once reconstituted, MOTS-c solutions should be stored at 2-8°C for short-term use. For longer-term storage, aliquot into single-use portions and freeze at -20°C. Avoid repeated freeze-thaw cycles as this can degrade the peptide.

    Protection from Light and Moisture:

    • Store in amber vials or protect from light

    • Keep vials tightly sealed when not in use

    • Allow frozen vials to reach room temperature before opening to prevent condensation

    Key Benefits

    • Premium Quality Manufacturing: GMP-certified production, ≥99% HPLC-verified purity

    • Mitochondrial-Derived Signaling Peptide: Direct link between mitochondrial function and systemic metabolic regulation

    • AMPK Activation: Enhances AMPK activity, promoting glucose uptake, fatty acid oxidation, and mitochondrial biogenesis

    • Insulin Sensitivity Research: Improves insulin sensitivity and prevents age-dependent and diet-induced insulin resistance

    • Metabolic Regulation: Modulates sphingolipid, monoacylglycerol, and dicarboxylate metabolism—pathways dysregulated in obesity and diabetes

    • Obesity Research: Prevents diet-induced obesity and reduces fat accumulation in liver

    • Cardiovascular Research: Protects against diabetic cardiomyopathy, improves cardiac function, reduces hypertrophy and fibrosis

    • Muscle Health Research: Correlates with better muscle function, strength, and reduced frailty in older adults

    • Sarcopenia Studies: Targets underlying causes including impaired glucose uptake, poor mitochondrial function, and deficient muscle regeneration

    • Exercise Mimetic Properties: Induced by exercise; regulates age-dependent physical decline

    • Bone Health Research: Suppresses ovariectomy-induced osteoporosis via AMPK activation

    • Adrenal Research: Primes adrenocortical cells for enhanced steroidogenic responsiveness

    • Aging Research: Circulating levels decline with age, correlating with increased disease risk

    • Anti-Inflammatory Effects: Reduces myocardial inflammation and oxidative stress

    • Metabolite Profiling: Well-characterized effects on plasma metabolites

    • Well-Conserved Peptide: Highly conserved across species, indicating essential biological function

    • Comprehensive Documentation: Certificates of Analysis with batch-specific purity data

    • 48-Hour EU & UK Delivery: Rapid shipping to research facilities across Europe

    • Batch Consistency: Rigorous quality control ensures lot-to-lot reproducibility

    • EU Sourced: Available from within the European Union

    Frequently Asked Questions

    Q: What is MOTS-c and where does it come from?

    A: MOTS-c (Mitochondrial ORF of the Twelve S rRNA-c) is a 16-amino acid bioactive peptide encoded by a short open reading frame (sORF) within the mitochondrial 12S rRNA region . It is produced within mitochondria and acts as a mitochondrial-derived signaling peptide (MDSP), establishing direct communication between mitochondrial function and systemic metabolic regulation .

    Q: What purity level can I expect when I buy MOTS-c from eupeptidelap.co.uk?

    A: All MOTS-c from eupeptidelap.co.uk is tested to ≥99% purity by HPLC. Each batch is individually analyzed, and Certificates of Analysis are provided with every order, ensuring you receive material suitable for rigorous research applications.

    Q: What is the mechanism of action of MOTS-c?

    A: MOTS-c enhances AMP-activated protein kinase (AMPK) activity, which promotes glucose uptake, fatty acid oxidation, and mitochondrial biogenesis . Its cellular actions inhibit the folate cycle and its tethered de novo purine biosynthesis, leading to endogenous accumulation of AICAR—a well-known AMPK activator . MOTS-c also modulates sphingolipid metabolism, reduces oxidative stress, and supports cellular stress adaptation .

    Q: What research areas commonly use MOTS-c?

    A: MOTS-c is widely used in insulin resistance and type 2 diabetes research , obesity research , cardiovascular research (particularly diabetic cardiomyopathy) , muscle health and sarcopenia studies , aging research , bone health research , and adrenal and endocrine research .

    Q: How should I store MOTS-c for long-term stability?

    A: Store lyophilized MOTS-c powder at -20°C, protected from light and moisture. After reconstitution, store at 2-8°C for short-term use. For longer-term storage, aliquot into single-use portions and freeze at -20°C. Avoid repeated freeze-thaw cycles as this can degrade the peptide.

    Q: Does MOTS-c have applications in cardiovascular research?

    A: Yes. MOTS-c has demonstrated significant cardioprotective effects in diabetic cardiomyopathy models, improving left ventricular function, attenuating cardiac hypertrophy and fibrosis, and reducing myocardial inflammation . It regulates the ROS/TXNIP/NLRP3 pathway and repairs myocardial damage by inhibiting the CCN1/ERK1/2/EGR1 pathway .

    Q: How is MOTS-c regulated in metabolic diseases?

    A: A systematic review and meta-analysis revealed that circulating MOTS-c levels are significantly reduced in diabetic individuals (SMD = -0.89) but significantly increased in obese individuals (SMD = 0.51) . This differential regulation suggests MOTS-c may serve as a compensatory mechanism in obesity that becomes overwhelmed with progression to diabetes. MOTS-c levels are positively correlated with total cholesterol and LDL-c .

    Q: Do you ship MOTS-c to EU countries?

    A: Yes. As a dedicated EU peptide supplier, we ship MOTS-c to all European Union member states with our guaranteed 48 hour delivery peptide service. Our EU fulfilment centre ensures rapid delivery without customs delays.

    Q: What documentation do you provide with MOTS-c orders?

    A: Every order includes a Certificate of Analysis with batch-specific purity data. Additional documentation, including HPLC chromatograms and mass spectrometry data, is available upon request for researchers requiring comprehensive analytical verification.

    Q: What is the relationship between MOTS-c and exercise?

    A: MOTS-c is an exercise-induced mitochondrial-encoded regulator of age-dependent physical decline and muscle homeostasis . It is induced in response to exercise and metabolic stress, and its exercise benefits have led to its inclusion in the World Anti-Doping Agency (WADA) list of prohibited substances .

    Q: Does MOTS-c have effects on muscle health?

    A: Yes. In older adults, higher MOTS-c blood levels correlate with better muscle function, strength, and reduced frailty indices . MOTS-c reduces myostatin and muscle atrophy signaling, and experimental evidence suggests it may enhance muscle fiber regeneration and improve mitochondrial function in aged muscle .

    Q: Do you offer bulk quantities of MOTS-c for institutional research?

    A: Yes. We accommodate bulk orders for research institutions. Contact our team at sales@eupeptidelap.co.uk for volume pricing, custom requirements, and supply agreements for ongoing research programs. ...........................................

    Advance Your Research with MOTS-c

    eupeptidelap.co.uk is your trusted source for MOTS-c, the premium choice for researchers investigating mitochondrial signaling, metabolic regulation, insulin resistance, and aging mechanisms. As a mitochondrial-derived peptide that directly links mitochondrial function to systemic metabolic homeostasis, MOTS-c represents a revolutionary tool for exploring the complex interplay between cellular energetics and whole-body metabolism .

    Whether you are exploring insulin sensitivity pathways, designing obesity studies, investigating cardiovascular protection, or researching age-related muscle decline, our rigorously tested compound provides the quality and consistency your work demands. .  .  .  .  . .   .  .  . . . . . . . . . . . . . . . . . . . . . . . .  . . . . . . . . . 

    Order today and experience the eupeptidelap.co.uk difference – premium quality, rapid 48-hour delivery across the EU and UK, and expert support for the European research community.

    ........ .. ..  google

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