MOTS-c
Price range: $27.95 through $70.00
Description
MOTS-c is a single-component research material supplied for controlled research environments. Suitable for studies involving mitochondrial-derived peptide characterization and method development in model systems.
Composition
• MOTS-c
• Appearance:
Documentation & Quality Assurance
Each lot is sourced through our verified global supply chain with emphasis on traceability and quality control.These documents are reviewed internally and displayed as they become available. Independent third-party testing is also performed on select lots to confirm identity, purity, and alignment with our internal specifications.
Important Notice
This product is intended for laboratory research use only. It is not intended for human or veterinary use, and must not be used for diagnostic, therapeutic, or clinical purposes.
This material is not a drug, medical device, or dietary supplement, and has not been evaluated by the U.S. Food and Drug Administration.
Quality & Manufacturing
All materials are sourced from carefully vetted domestic and international manufacturing partners who follow quality systems consistent with ISO and cGMP principles. Each supplier is reviewed for reliability, documentation integrity, and transparency in testing.
We require a verified purity of 99% or higher and perform independent third-party spot testing to confirm that select lots meet our internal standards for identity, purity, and composition. Where available, endotoxin testing results are included on Certificates of Analysis to verify laboratory purity; their inclusion is for research quality assessment only and does not imply suitability for human or veterinary use.
All research materials are sealed for integrity and packaged for stability during storage and transport from manufacturing through final delivery.
Additional information
| Weight | 0.0625 lbs |
|---|---|
| Dosage | 10mg, 40mg |
Certificate of Analysis
Every batch undergoes independent third-party laboratory analysis to verify identity, potency, and safety. Testing includes quantitative assay verification, heavy metals screening, and comprehensive microbial analysis.
All Available COAs
Storage Instructions
All products from Research Vials are manufactured using a lyophilization (freeze-drying) process. This method is designed to maintain product integrity and allows vials to remain stable during shipping for approximately 3–4 months.
Once a vial is reconstituted with bacteriostatic water, it should be stored in the refrigerator to help maintain stability. Under these conditions, reconstituted material is generally considered stable for up to 30 days.
Lyophilization is a dehydration technique in which compounds are frozen and then exposed to low pressure. This causes the water in the vial to sublimate directly from solid to gas, leaving behind a stable, crystalline white structure. This powder can be kept at room temperature until reconstitution.
Upon receipt, products should be stored away from heat and light. For short-term use, refrigeration at approximately 4°C (39°F) is suitable. For long-term storage (several months to years), vials may be placed in a freezer at approximately -80°C (-112°F). Freezing is the preferred method for preserving product stability over extended periods.
⚠️ Important Notice:
These products are intended for research use only. Not for human consumption.
Research Use Only
These studies reference research-grade peptides for laboratory and scientific investigation only. Not for human consumption. Not intended to diagnose, treat, cure, or prevent any disease.
Published Scientific Research
Peer-reviewed laboratory research investigating research peptides from leading scientific databases
MOTS-c-modified functional self-assembly peptide hydrogels enhance the activity of nucleus pulposus-derived mesenchymal stem cells of intervertebral disc degeneration.
MECHANISTIC PROTECTION: MOTS-c significantly attenuated TBHP-induced NP-MSC apoptosis (Annexin V+/PI + cells reduced by 48 %, p < 0.001), senescence (SA-β-gal + cells decreased by 52 %, p < 0.005), and ROS overproduction (35 % reduction, p < 0.0001) via activation of the AMPK/SIRT1 pathway. Pharmacological inhibition of SIRT1 abolished these protective effects, confirming pathway specificity.
View Full StudyMitochondrial-Derived Peptides: Implication in the Therapy of Neurodegenerative Diseases.
This review systematically evaluates current literature retrieved from databases including PubMed, Scopus, and Web of Science using keywords such as "mitochondrial-derived peptides," "neurodegeneration," "humanin," "MOTS-c," and "SHLPs." Studies were included based on their relevance to mitochondrial function, oxidative stress, neuroprotection, and anti-inflammatory mechanisms in AD, PD, and HD models. Despite growing interest, current research remains limited in understanding the precise molecular pathways.
View Full StudyNovel function of MOTS-c in mitochondrial remodelling contributes to its antiviral role during HBV infection.
This study aims to explore the diagnostic and therapeutic potential of MOTS-c in HBV-related diseases and its molecular mechanism. MOTS-c was found to promote mitochondrial biogenesis and enhance the MAVS (mitochondrial antiviral signalling protein) signalling pathway.
View Full StudyMitochondrial-derived peptides in cardiovascular disease: Novel insights and therapeutic opportunities.
MDPs assume pivotal roles in the regulation of diverse cellular processes, encompassing apoptosis, inflammation, and oxidative stress, which are all essential for sustaining cellular viability and normal physiological functions. It seeks to elucidate the central roles and underlying mechanisms by which MDPs participate in the onset and development of cardiovascular diseases (CVDs), bridging the connections between cell apoptosis, inflammation, and oxidative stress.
View Full StudyThe DNA-dependent protein kinase catalytic subunit exacerbates endotoxemia-induced myocardial microvascular injury by disrupting the MOTS-c/JNK pathway and inducing profilin-mediated lamellipodia degradation.
We explored whether endotoxemia-induced myocardial microvascular injury involved DNA-PKcs and MOTS-c dysregulation. Lipopolysaccharide exposure increased DNA-PKcs activity in cardiac microvascular endothelial cells, while pharmacological inhibition or endothelial cell-specific genetic ablation of reduced lipopolysaccharide-induced myocardial microvascular dysfunction.
View Full StudyMOTS-c regulates pancreatic alpha and beta cell functions in vitro.
The results obtained from this study show that MOTS-c has a significant impact on the physiology of pancreatic cells.
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