MOTS-C acronym stands for "mitochondrial-derived peptide" and it is also known by its CAS number, 1627580-64-6. MOTS-c is studied for the role it plays in regulating energy metabolism, stress, and aging. It is produced in response to exercise or stress and functions as a type of "mitochondrial hormone" or "mitokine".

What it is: A bioactive peptide encoded by the mitochondrial 12S rRNA gene.

Function: It promotes energy metabolism and stress homeostasis, with potential roles in improving insulin sensitivity, exercise capacity, and longevity.

MOTS-c – Research Overview
Full name: Mitochondrial Open Reading Frame of the 12S rRNA type-c
Class: Mitochondrial-derived peptide (MDP)
Sequence: 16–amino acid peptide
Primary target: AMPK activation + mitochondrial stress-response pathways
Molecular weight: ~2 kDa

MOTS-c is a peptide encoded within mitochondrial DNA (not nuclear DNA), making it part of a unique class of molecules known as mitochondrial-derived peptides (MDPs).

It has been investigated in preclinical studies for its effects on:

Metabolic regulation
Cellular energy production
Stress-response pathways
Insulin signaling
Mitochondrial function
All findings refer to animal and in-vitro research, not established human outcomes.

Molecular & Pharmacological Profile
In research models, MOTS-c functions as a mitochondrial stress signal that helps regulate:

Energy expenditure
Glucose use
Fat metabolism
Cellular homeostasis (cell balance and stability)

MOTS-c is known to:

Activate AMPK (energy sensor that increases fat burning + glucose uptake)
Improve mitochondrial efficiency (better use of fuel inside the cell)
Regulate nuclear gene expression (signals from mitochondria to nucleus)
Enhance cellular stress tolerance (more resilient cells during metabolic stress)
These features make it valuable in metabolic and aging-related research models.

Mechanism of Action (Preclinical)

Activation of AMPK (energy-sensing enzyme)
AMPK increases:
- Fatty-acid oxidation (burning fat for energy)
- Glucose uptake (cells use more sugar for fuel)
- Cellular resilience during stress
Regulation of Nuclear Genes
MOTS-c triggers a process called mitonuclear communication
(mitochondria sending signals to the nucleus to change gene expression).
This affects:
- Metabolism
- Stress response
- Repair pathways
Improved Mitochondrial Function
Preclinical models show:
- More efficient ATP production (cellular energy)
- Greater mitochondrial density in muscle tissue
- Enhanced resistance to metabolic damage
Increased Fat Burning
Via AMPK and mitochondrial pathways, MOTS-c enhances:
Fatty-acid oxidation (fat → energy)
Use of fat stores during activity
Enhanced Cellular Stress Tolerance
Research demonstrates improved survival and function in cells exposed to:
- Oxidative stress
- Metabolic stress
- High-fat diets
- Aging models

Preclinical Research: Potential Applications
MOTS-c has been studied extensively in rodent and cell-based models:

Metabolic Regulation Models
- Increased insulin sensitivity (cells respond better to insulin)
- Improved glucose utilization
- Reduced fat accumulation in high-fat diet rodents
- Enhanced AMPK-driven energy pathways
Obesity & Body-Weight Research
Rodent studies show:
- Reduced weight gain
- Increased energy expenditure
- Higher fat oxidation
- Improved metabolic flexibility (cells switching between fuels more easily)
Exercise & Muscle Performance Models
MOTS-c has been linked to:
- Increased muscle endurance
- Better glucose uptake in muscle cells
- Enhanced mitochondrial biogenesis (more / stronger mitochondria)
Cellular Stress & Longevity Pathways
- Greater resistance to oxidative damage
- Upregulation of protective genes
- Improved metabolic resilience in aging models
Inflammatory & Immune Pathways (Preclinical)
- Reduced inflammatory cytokines
- Mild immunomodulatory effects
  (shifts in immune markers in mice under metabolic stress)

Efficacy Observed in Preclinical Models
Rodent Metabolic Studies
-AMPK activation led to increased fat burning
-Improved insulin signaling
-Reduced adiposity (less stored fat)
-Enhanced physical endurance
-Protection against diet-induced obesity
Cellular Models
-Increased mitochondrial efficiency
-Greater energy availability (ATP)
-Reduced oxidative stress
-Better cell survival under stress conditions
Aging Models
-Improved metabolic biomarkers in older rodents
-Enhanced mitochondrial gene expression
-Greater exercise capacity
All findings are limited to preclinical research, not documented human effects.

Safety & Tolerability (Preclinical)

No major toxicity reported in rodent studies
Demonstrated good tolerability at research doses
Long-term safety, pharmacokinetics, and human interactions remain unestablished
MOTS-c is not FDA-approved

Regulatory Status & Disclaimer

MOTS-c is an investigational research peptide.
It is not approved for therapeutic, dietary, cosmetic, or medical use.
For Research Use Only.
Not for human consumption.
Not for veterinary use.
Not for diagnostic or therapeutic purposes.
No medical claims are made or implied.

Key References (Preclinical)
Lee C. et al. MOTS-c as a mitochondrial-derived peptide regulating metabolism. Cell Metabolism.
Reynolds J. et al. AMPK activation by MOTS-c in high-fat diet animals. Aging Cell.
Kim S.J. et al. Role of MOTS-c in exercise and mitochondrial biogenesis. Sci Rep.
Fuku N. et al. Mitochondrial peptides and metabolic stress response. J Physiol.
Yang C. et al. MOTS-c and mitonuclear communication pathways. PNAS.

Product Care:

Store in a cool, dry place away from light. If Constituted, Please Refrigerate. For longer term storage, freezing at -20°C is recommended to maintain integrity.

Product Note:

All products are shipped in lyphollized or powder form and must be reconstituted to a liquid for research and testing. We are unable to provide any dosing instructions, however all products should be considered pharmaceutical grade.

Mots-c 10MG

CAS Number: 1627580-64-6