SS-31

Lyophilized (Dry Powder) — Unopened Vials
Unopened lyophilized vials should be stored away from direct light, heat, and moisture. For use within a few weeks, room temperature storage is acceptable. For storage over several months, refrigeration at 2–8°C (36–46°F) is recommended. For long-term storage, freezing best preserves peptide integrity.

When removing a vial from frozen storage, allow it to reach room temperature before opening to prevent condensation from introducing moisture into the vial.

Reconstitution
Reconstitute using bacteriostatic water (BAC). Inject the solution slowly down the inside wall of the vial rather than directly onto the peptide cake. Gently swirl until fully dissolved; do not shake. Vigorous shaking may cause foaming and mechanical stress to the peptide structure.

Reconstituted Vials
After reconstitution, store vials refrigerated at 2–8°C (36–46°F) and protected from light. Always use clean, sterile technique when accessing the vial to minimize contamination.

Solution stability may vary with concentration, diluent, temperature, and formulation. Extended storage after reconstitution should be avoided unless supported by product-specific stability data.

General Guidelines

• Keep vials away from excessive heat and prolonged light exposure.
• Do not freeze after reconstitution.
• Avoid repeated warming and cooling cycles.
• Discard any solution showing cloudiness, discoloration, or visible particulate matter.
• Label vials with the reconstitution date for tracking purposes.

Study 1: Targeting Mitochondrial Cardiolipin to Promote Electron Transport and Optimize ATP Synthesis

Authors: A.V. Birk et al.
Source: British Journal of Pharmacology

Scientific Findings
This mechanistic research examined how SS-31 interacts with cardiolipin in the inner mitochondrial membrane. The peptide selectively bound to cardiolipin and inhibited the peroxidase activity of the cytochrome c-cardiolipin complex while preserving cytochrome c activity within the electron transport chain.

The findings suggested that SS-31 may protect cardiolipin from oxidative damage while supporting electron transfer and mitochondrial ATP synthesis.

Plain English Interpretation
Researchers found that SS-31 attaches to a specialized fat called cardiolipin that helps organize the machinery mitochondria use to produce energy. This interaction appeared to protect the membrane while allowing energy-producing processes to continue more efficiently.

Study 2: SS-31 Re-Energizes Ischemic Mitochondria Through Interaction with Cardiolipin

Authors: A.V. Birk et al.
Source: Journal of the American Society of Nephrology

Scientific Findings
This study investigated SS-31 in experimental models of mitochondrial dysfunction associated with ischemia. Researchers demonstrated high-affinity binding between SS-31 and cardiolipin and observed protection against cardiolipin oxidation, improved mitochondrial respiration, and restoration of ATP production.

The results provided direct evidence linking cardiolipin binding with improved mitochondrial bioenergetics during cellular stress.

Plain English Interpretation
Scientists studied mitochondria exposed to reduced blood flow and found that SS-31 helped restore their ability to produce energy. The effect appeared to come from protecting cardiolipin and preserving the structure of the inner mitochondrial membrane.

Study 3: SS-31 Reverses Age-Related Redox Stress and Improves Exercise Tolerance in Aged Mice

Authors: M.D. Campbell et al.
Source: Free Radical Biology and Medicine

Scientific Findings
This preclinical study examined SS-31 in aged mice with impaired skeletal muscle mitochondrial function. Treatment restored redox balance, improved mitochondrial quality, and increased treadmill endurance without increasing mitochondrial content.

The findings suggested that improving the performance of existing mitochondria may influence age-related energetic deficits even without producing additional mitochondria.

Plain English Interpretation
Researchers found that SS-31 improved how existing mitochondria functioned in the muscles of older mice. The animals showed better exercise endurance even though they did not develop more mitochondria.

Study 4: Elamipretide Improves Mitochondrial ATP Production in Older Adult Skeletal Muscle

Authors: B. Roshanravan et al.
Source: PLOS ONE

Scientific Findings
This randomized, double-blind, placebo-controlled human study examined mitochondrial ATP production in older adults following a single dose of elamipretide. Researchers observed a transient improvement in skeletal muscle mitochondrial energy production shortly after treatment, while volitional fatigue resistance was not significantly changed.

The study provided human evidence that cardiolipin-directed mitochondrial targeting can influence bioenergetic function, although the effect was short-lived and long-term physiological outcomes were not established.

Plain English Interpretation
Researchers measured energy production in the muscles of older adults and found that a single dose of elamipretide produced a short-term improvement in mitochondrial ATP production. The effect did not persist, and measures of fatigue resistance did not improve, so the study showed a brief biological effect rather than a lasting functional benefit.

Study 5: Elamipretide in Primary Mitochondrial Myopathy

Authors: A. Karaa et al.
Source: Neurology

Scientific Findings
The MMPOWER-3 randomized clinical trial evaluated elamipretide over 24 weeks in participants with primary mitochondrial myopathy. The study did not find a significant improvement over placebo in either the six-minute walk test or the primary fatigue measure.

Later analyses suggested that responses may differ among particular genetic subgroups, but those findings were exploratory and require prospective confirmation.

Plain English Interpretation
In this larger clinical trial, elamipretide did not improve walking distance or fatigue for the overall study population. Follow-up analysis raised the possibility that certain genetic forms of mitochondrial disease may respond differently, but that has not yet been conclusively established.

Study 6: Elamipretide in Barth Syndrome and Mitochondrial Cardiolipin Dysfunction

Authors: W.R. Thompson et al.
Source: Genetics in Medicine

Scientific Findings
This Phase 2/3 study evaluated elamipretide in participants with Barth syndrome, a genetic disorder affecting mitochondrial cardiolipin metabolism. The randomized crossover portion did not meet its primary endpoints. During the subsequent open-label extension, researchers reported improvements in walking distance, symptom scores, muscle strength, and selected cardiac measures.

These results contributed to continued clinical investigation and the later accelerated approval of elamipretide for a limited Barth syndrome indication.

Plain English Interpretation
The controlled portion of the study did not show a clear advantage over placebo, but improvements emerged during longer open-label treatment. Because the disease directly affects cardiolipin, the findings supported further study of SS-31 in this specific mitochondrial disorder.