MOTS-c vs SLU-PP-332
Side-by-side comparison of key properties, dosing, and research.
Anti-Aging & Longevity
MOTS-cRecovery & RepairFat Loss & Metabolic
SLU-PP-332- Summary
- MOTS-c is a mitochondria-derived peptide (MDP) encoded within the mitochondrial genome. It acts as a metabolic regulator, improving insulin sensitivity, enhancing exercise capacity, and counteracting age-related metabolic decline. It is often called a 'mitochondrial hormone.'
- SLU-PP-332 is a small molecule exercise mimetic that activates estrogen-related receptors ERRalpha and ERRdelta (ERRa/d), transcription factors that drive oxidative metabolism programs. In animal studies it significantly enhanced endurance capacity and metabolic fitness without exercise, mimicking many of the cardiovascular and metabolic adaptations of aerobic training.
- Half-Life
- Estimated 1–2 hours
- Not established in humans; rodent pharmacokinetics suggest hours
- Admin Route
- SubQ
- Oral (research), Subcutaneous (research)
- Research
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- Typical Dose
- 5–15 mg
- Not established for humans; rodent studies used ~100 mg/kg/day
- Frequency
- 3–5 times per week
- Once daily in rodent studies
- Key Benefits
- Improves insulin sensitivity and glucose metabolism
- Enhances exercise capacity and endurance
- Reduces age-related metabolic decline
- Activates AMPK — the master metabolic regulator
- Promotes fat oxidation
- Anti-inflammatory effects
- May extend healthspan via mitochondrial optimization
- Increases energy and reduces fatigue
- Significant enhancement of aerobic endurance capacity
- Increases mitochondrial density and oxidative metabolism in muscle
- Promotes beneficial shift toward oxidative muscle fiber phenotype
- Improves cardiac efficiency and cardiovascular fitness markers
- Potential for obesity, metabolic syndrome, and heart failure treatment
- Exercise mimetic for populations unable to exercise (disability, frailty, disease)
- Side Effects
- Injection site irritation
- Fatigue during initial adaptation
- Unknown long-term profile (limited human data)
- Limited human data; all studies are preclinical (rodent)
- Unknown cardiovascular effects with long-term or high-dose use in humans
- Potential hormonal interactions via ERR pathway (ERRs modulate estrogen-related signaling)
- Off-target effects not fully characterized
- Stacks With
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