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MOTS-C
MOTS-C
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A mitochondrial-derived peptide investigated for its role in modulating metabolic processes. In preclinical research—most notably rodent studies—this compound has demonstrated significant implications for exercise metabolism, including effects on energy utilization, metabolic flexibility, and adaptive cellular responses to physical stress.
Its function as a mitochondrial signaling molecule makes it a key subject in research exploring mitochondrial communication, metabolic regulation, and exercise-related bioenergetics.
For Research Use Only.
Current Batch:
10MG : IF-8561878

Understanding the Science
Excercise - At the Molecular level
MOTS-c is a 16–amino acid peptide encoded by the mitochondrial genome and studied for its involvement in mitochondria-to-cellular metabolic signaling. Research has explored its interaction with energy-regulating pathways in skeletal muscle commonly examined in exercise metabolism models.
Preclinical Studies + Phase 1 Analog Trial
Physical Performance Outcomes in Aged Murine Models
In controlled preclinical studies involving aged mice (22–23.5 months), MOTS-c–treated groups demonstrated significant improvements in physical performance metrics compared to untreated controls.
Observed Research Outcomes:
- Running time increased ~2.0×
- Running distance increased ~2.16×
These findings highlight MOTS-c’s role as a research model for exercise-mimetic signaling, offering insight into peptide-mediated pathways associated with endurance and cellular energy regulation in aging models.
Preclinical Findings - Key Research Outcomes
Data derived from multiple preclinical murine studies
Observed Research Outcomes:
High-fat diet mouse models
- 100% of subjects — Prevention of diet-induced obesity
Middle-aged mouse models
- 100% of subjects — Prevention of age-related insulin resistance
Compared to 20% survival in untreated controls
- 79% of subjects — Survival following MRSA infection
MOTS-C Effects on Metabolic Signaling - A Comparison
Preclinical Murine Models
Observed Research Outcomes:
(Aged mice)
- Insulin sensitivity
100% restored relative to baseline reference models
(High-fat diet models)
- Body weight
85% of control body weight observed
Fat oxidation
140% increase compared to control groups
*Preclinical murine data. Human safety data limited to analog studies.*