MOTS-c
Also known as: Mitochondrial ORF of the 12S rRNA type-c · MT-ORF peptide
MOTS-c is encoded by the mitochondrial genome and translocates to the nucleus in response to metabolic stress. In the nucleus, it regulates gene expression, particularly genes involved in the one-carbon folate cycle and purine biosynthesis. It activates AMPK (AMP-activated protein...
What It Is
MOTS-c is encoded by the mitochondrial genome and translocates to the nucleus in response to metabolic stress. In the nucleus, it regulates gene expression, particularly genes involved in the one-carbon folate cycle and purine biosynthesis. It activates AMPK (AMP-activated protein kinase), the master metabolic switch, improving insulin sensitivity, glucose uptake in skeletal muscle, and fatty acid oxidation. MOTS-c also reduces adipogenesis by suppressing de novo lipogenesis pathways. It improves exercise capacity, increases metabolic flexibility (ability to switch between fat and glucose oxidation), and levels decline significantly with aging.
Supplies Needed
Reconstitution
Subcutaneous injection
Sterilization
Storage
Store at -20°C; stable 2+ years
Refrigerate at 2–8°C; use within 30 days
This information is provided for educational and research purposes only. Not approved for human consumption by the FDA or any regulatory body. Always consult a qualified medical professional.
Dosing Protocols
Timing: Morning before exercise or fasted. Best taken before exercise to amplify AMPK activation and fat oxidation
↓ Apply these values to the reconstitution calculatorTiming: Pre-exercise or morning fasted. Stack with NAD+ for comprehensive mitochondrial support; combine with exercise for maximum metabolic benefit
↓ Apply these values to the reconstitution calculatorTiming: Morning fasted or pre-workout. Advanced metabolic optimization; stack with SS-31 and Humanin for full mitochondrial anti-aging protocol
↓ Apply these values to the reconstitution calculatorWeekly Timeline
| Week | Expected Effects |
|---|---|
| Week 1 | Improved energy during exercise; early improvements in insulin sensitivity; reduced post-meal blood glucose spikes |
| Week 2 | Enhanced fat oxidation; improved endurance; reduced fatigue during workouts |
| Week 4 | Measurable metabolic improvements; reduced visceral fat (with caloric deficit); improved body composition |
| Week 8 | Sustained AMPK activation; significant metabolic flexibility; improved fasting glucose and insulin markers |
Reconstitution Calculator
1 unit on U-100 syringe = 0.01 mL · Always label your vial after reconstitution
Injection Technique & Reconstitution
- Wipe vial stopper with alcohol swab and allow to dry
- Draw appropriate volume of bacteriostatic water into syringe
- Insert needle and inject BAC water slowly along the vial wall
- Gently swirl until fully dissolved u2014 do not vortex
- Refrigerate at 2u20138u00b0C
Use our free calculate your MOTS-c dose to get the exact syringe units for your vial size and dose.
Mechanism of Action
MOTS-c is encoded by the mitochondrial genome and translocates to the nucleus in response to metabolic stress. In the nucleus, it regulates gene expression, particularly genes involved in the one-carbon folate cycle and purine biosynthesis. It activates AMPK (AMP-activated protein kinase), the master metabolic switch, improving insulin sensitivity, glucose uptake in skeletal muscle, and fatty acid oxidation. MOTS-c also reduces adipogenesis by suppressing de novo lipogenesis pathways. It improves exercise capacity, increases metabolic flexibility (ability to switch between fat and glucose oxidation), and levels decline significantly with aging.
Key Research Papers
Demonstrated MOTS-c is released during exercise, increases with physical activity, and its exogenous administration improved exercise performance and muscle homeostasis in aged mice.
View on PubMed →Original discovery paper characterizing MOTS-c as a mitochondrial-encoded regulator of glucose and fatty acid metabolism.
View on PubMed →Stacks Well With
Humanin and MOTS-c are both mitochondrial-derived peptides that work synergistically u2014 MOTS-c optimizes metabolic function while Humanin provides cytoprotection and anti-apoptotic signaling
SS-31 protects IMM integrity while MOTS-c optimizes metabolic gene expression u2014 comprehensive mitochondrial restoration
NAD+ replenishes the electron carrier pool; MOTS-c optimizes the metabolic pathways that use NAD+ u2014 synergistic mitochondrial energy restoration
Frequently Asked Questions
MOTS-c activates AMPK in skeletal muscle, which increases GLUT4 translocation (more glucose uptake), enhances fatty acid oxidation, and improves mitochondrial efficiency u2014 all increasing exercise endurance and power output.
It's a metabolic regulator u2014 it improves the efficiency of fat metabolism and insulin sensitivity rather than acting as a stimulant-type fat burner. It works best combined with a caloric deficit and exercise.
Timing with exercise amplifies its effects significantly. AMPK activation from exercise and MOTS-c are synergistic u2014 take 30u201360 minutes pre-workout for best metabolic results.
Legal Status by Region
This information is provided for educational and research purposes only. Not approved for human consumption by the FDA or any regulatory body. Always consult a qualified medical professional.