This page is provided for research and educational purposes only and does not provide medical advice, diagnosis, treatment recommendations, dosing instructions, or instructions for human use. Research findings should be interpreted within the population, model, formulation, route, outcomes, and study design reported by each cited source.
SS-31 (50 mg Vial)
This information is for research and educational use only.
Quick Reference
What is SS-31?
Research overview based on the cited scientific literature.
Goal: Support mitochondrial function, enhance ATP production, and reduce oxidative stress in tissues with high metabolic demand[1][2].
Storage: Lyophilized frozen at −20 °C (−4 °F); reconstituted refrigerated at 2–8 °C (35.6–46.4 °F); use within 4 weeks.
Storage Instructions
Proper storage preserves peptide stability and potency.
Lyophilized: Store at −20 °C (−4 °F) in original sealed vial; keep dry and protected from light. Stable for months when frozen.
Reconstituted: Refrigerate at 2–8 °C (35.6–46.4 °F) immediately after mixing; use within 4 weeks for optimal stability.
Avoid freeze–thaw: Do not refreeze reconstituted solution; prepare aliquots if needed to minimize temperature fluctuations.
Allow refrigerated vials to reach room temperature before opening to reduce condensation inside the vial.
How is SS-31 studied?
SS31 (elamipretide) is a cellpermeable tetrapeptide with a unique mechanism of action targeting mitochondrial dysfunction[1]. The peptide selectively accumulates in the inner mitochondrial membrane where it binds to cardiolipin, a specialized phospholipid essential for organizing electron transport chain supercomplexes and maintaining cristae structure[2][7]. By stabilizing cardiolipinprotein interactions, SS31 optimizes electron transport efficiency, reduces pathological reactive oxygen species generation, and enhances ATP synthesis in metabolically active tissues[8].
Preclinical research demonstrated that SS31 protects against mitochondrial dysfunction across multiple disease models including heart failure, ischemiareperfusion injury, neurodegeneration, chronic kidney disease, and agerelated muscle atrophy[9]. In human clinical trials, SS31 showed favorable safety and tolerability profiles with no doselimiting toxicities[4][5]. While Phase II trials in heart failure and primary mitochondrial myopathy did not meet primary efficacy endpoints, the TAZPOWER trial in Barth syndrome demonstrated significant improvements in muscle strength and sixminute walk distance, leading to FDA accelerated approval in 2025[3][10].
What does the research report about SS-31?
Observations from preclinical models and human clinical trials.
Potential Benefits:
Stabilizes mitochondrial membranes and optimizes electron transport chain function[1][2].
Enhances ATP production and reduces pathological reactive oxygen species in metabolically active tissues[8].
Demonstrated functional improvements in Barth syndrome patients (increased muscle strength, improved exercise capacity)[3][10].
Shows protective effects in preclinical models of heart failure, neurodegenerative disease, and agerelated muscle atrophy[9].
Does not significantly alter blood pressure, heart rate, or standard laboratory parameters in clinical trials[4].
Common Side Effects:
Injectionsite reactions (most common): Mildtomoderate redness, itching, or transient discomfort at injection site; typically resolves within hours[4][6].
Approximately 80% of patients in clinical trials experienced mild injectionsite reactions[6].
No doselimiting toxicities or serious adverse events directly attributed to SS31 in published trials[4][5].
Longterm safety data beyond 12 weeks remains limited; extended use requires monitoring.
Important Note
This content is provided for scientific research and educational purposes only. It does not provide medical advice, diagnosis, treatment, dosing, or administration instructions. The compounds discussed may be investigational and are not presented as approved for human use.
What are the limitations of the research on SS-31?
Evidence should be interpreted within the population, experimental model, formulation, route, outcome measures, and study design used in each cited source. Preclinical or early-stage findings do not establish clinical efficacy, safety, or approved human use. Where human evidence is available, results should not be generalized beyond the populations and conditions actually studied.