Source comparison
Best SS-31 Dosage for Mitochondrial Function: Research Comparison
Cardiac ischemia-reperfusion (animal) 0.5–1mg/kg Intravenous bolus Single dose or 3–7 days Infarct size, ejection fraction Lowest effective dose due to high cardiac cardiolipin density. IV ensures rapid tissue penetration during acute injury window Heart failu
This comparison does not assign a generated winner or score.
- Cardiac ischemia-reperfusion (animal)
- 0.5–1mg/kg
- Intravenous bolus
- Single dose or 3–7 days
- Infarct size, ejection fraction
- Lowest effective dose due to high cardiac cardiolipin density. IV ensures rapid tissue penetration during acute injury window
- Heart failure (human)
- 40mg (fixed dose)
- Subcutaneous daily
- 28 weeks
- Left ventricular end-diastolic volume, ejection fraction
- Fixed dosing reflects weight-independent mitochondrial dysfunction burden. Chronic administration required for remodelling benefit
- Chronic kidney disease (animal)
- 2–3mg/kg
- 8–12 weeks
- Glomerular filtration rate, tubular injury markers
- Higher dose compensates for lower renal cardiolipin density and slower tissue turnover. Sustained dosing prevents progressive damage
- Acute kidney injury (animal)
- 1–2mg/kg
- Intravenous or subcutaneous
- 3–7 days
- Serum creatinine, tubular necrosis
- Moderate dose for acute injury. Early initiation critical as delayed dosing beyond 24 hours loses efficacy
- Skeletal muscle atrophy (animal)
- 1.5–3mg/kg
- 4–8 weeks
- Muscle mass, mitochondrial respiration, fatigue resistance
- Mid-range dosing for tissue with moderate cardiolipin. Prolonged duration needed to support mitochondrial biogenesis alongside stabilisation
- Neurological models (Parkinson's, TBI)
- 2–4mg/kg
- Subcutaneous daily or intravenous
- 4–12 weeks
- Motor function, neuronal survival, ROS markers
- Higher dose reflects blood-brain barrier considerations and neuronal mitochondrial heterogeneity. Longer duration for chronic degeneration vs acute TBI