≥99%HPLC Purity
COAIncluded
USAShipped
SS-31 (Elamipretide) Peptide
Mitochondria-targeted tetrapeptide. Studied for cardiolipin interaction and mitochondrial inner membrane stabilization research.
$89.00
This product may take an additional 5–7 days to arrive due to low stock.
Quick Facts
| SKU | ACR-SS31 |
|---|---|
| CAS Number | 736992-21-5 |
| Molecular Formula | C32H49N5O5 |
| Molecular Weight | 571.77 g/mol |
| Sequence | D-Arg-Dmt-Lys-Phe-NH2 |
| Purity | ≥99% |
| Physical Form | Lyophilized Powder |
| Storage | Store at -20°C |
What is SS-31?
SS-31 (Elamipretide/Bendavia) is a cell-permeable, mitochondria-targeted tetrapeptide with the sequence D-Arg-Dmt-Lys-Phe-NH2. Dmt (2,6-dimethyltyrosine) is a modified aromatic residue that enhances mitochondrial membrane interaction. The alternating aromatic-cationic motif allows the peptide to concentrate >1000-fold within mitochondria.
SS-31 selectively binds cardiolipin, a unique bis-phospholipid found exclusively on the inner mitochondrial membrane. Cardiolipin constitutes approximately 20% of inner membrane lipid content and is essential for cristae structure and electron transport chain complex organization.
For laboratory research use only.
Mechanism of Action: Cardiolipin Targeting
SS-31 (D-Arg-Dmt-Lys-Phe-NH₂) achieves mitochondrial targeting through its alternating aromatic-cationic motif. The mechanism involves multiple levels:
- Mitochondrial accumulation: The cationic charges (+3 at pH 7.4) drive >1,000-fold concentration within mitochondria via the large negative membrane potential (ΔΨm ≈ -180 mV) across the inner membrane
- Cardiolipin binding: Once in the inner membrane, SS-31 binds cardiolipin through electrostatic (Arg, Lys) and hydrophobic (Dmt, Phe) interactions. Cardiolipin is unique to mitochondria and essential for electron transport chain function
- Electron transport optimization: SS-31 binding prevents cytochrome c from converting to a peroxidase (a pathological conformational change), maintaining it as an efficient electron carrier between Complex III and IV
- ROS reduction: By optimizing electron flow, SS-31 reduces electron leakage at Complex I and III — the primary sites of mitochondrial superoxide generation. ROS production decreases without compromising ATP synthesis
This mechanism is fundamentally different from antioxidants (which scavenge ROS after production) — SS-31 prevents excessive ROS generation at the source while improving energy production.
Research & Clinical Studies
SS-31 and Heart Failure Research
Elamipretide advanced to Phase 2/3 clinical trials for heart failure with reduced ejection fraction (HFrEF) and Barth syndrome (genetic cardiomyopathy caused by cardiolipin remodeling defects). In Barth syndrome trials, SS-31 improved 6-minute walk distance and cardiac stroke volume. The mechanism — direct cardiolipin stabilization — addresses the root bioenergetic cause rather than symptoms.
In aged mice, SS-31 treatment restored cardiac diastolic function to young-adult levels, reversed age-related mitochondrial cristae disorganization, and improved cardiac reserve capacity. These findings position SS-31 as a lead compound in cardiac aging research.
[1] Szeto HH et al. Mitochondria-targeted peptide accelerates ATP recovery and reduces ischemic kidney injury. J Am Soc Nephrol. 2011;22(6):1041-1052. PubMed ↗
SS-31 and Aging/Longevity Research
SS-31 reverses multiple hallmarks of mitochondrial aging: restores cristae ultrastructure, normalizes Complex I-IV electron transport chain function, reduces mitochondrial ROS production, and improves ATP synthesis efficiency. In aged skeletal muscle, SS-31 restored exercise capacity and muscle strength to levels comparable to young animals within weeks of treatment. The rapidity of these effects suggests SS-31 optimizes existing mitochondria rather than requiring mitochondrial biogenesis.
SS-31 and Kidney Research
SS-31 demonstrated significant renoprotective effects in ischemia-reperfusion injury (the most common cause of acute kidney injury). In rat models, SS-31 administered before ischemia:
- Accelerated ATP recovery by 3-fold during reperfusion
- Reduced tubular cell necrosis and apoptosis by >50%
- Preserved mitochondrial cristae ultrastructure
- Reduced oxidative stress markers (F2-isoprostanes, protein carbonyls)
- Improved GFR recovery at 24 hours
The renoprotective effect was attributed to preservation of mitochondrial function during the ischemic period — maintaining enough ATP to prevent necrotic cell death while reducing reperfusion-induced ROS burst.
[1] Szeto HH et al. Mitochondria-targeted peptide accelerates ATP recovery and reduces ischemic kidney injury. J Am Soc Nephrol. 2011;22(6):1041-1052. PubMed ↗
SS-31 and Skeletal Muscle Aging
Muscle mitochondrial dysfunction is a primary driver of age-related sarcopenia. SS-31 research in aged mice demonstrates:
- Restored mitochondrial ATP production to young-adult levels within 1 hour of treatment
- Reversed age-related decline in exercise capacity (treadmill endurance +30%)
- Improved muscle force generation (specific force in isolated muscle +15-20%)
- Restored mitochondrial cristae density and organization (electron microscopy)
- Effects were apparent within days, not weeks — suggesting optimization of existing mitochondria rather than requiring new biogenesis
The rapid onset of SS-31 effects is particularly notable. Unlike interventions requiring mitochondrial biogenesis (exercise, PGC-1α activation), SS-31 immediately improves existing mitochondrial function by optimizing the cardiolipin-cytochrome c interaction.
Chemical Properties
| Sequence | D-Arg-Dmt-Lys-Phe-NH₂ (Dmt = 2'6'-dimethyltyrosine) |
|---|---|
| Formula | C₃₂H₄₉N₅O₅ |
| MW | 571.77 g/mol |
| CAS | 736992-21-5 |
| Target | Cardiolipin (inner mitochondrial membrane) |
| Amino Acids | 4 (tetrapeptide with non-natural residues) |
| Key Feature | Concentrates >1000-fold in mitochondria |
| Purity | ≥98% HPLC |
Handling & Reconstitution
Reconstitute with bacteriostatic water. SS-31 is a small tetrapeptide (571 Da) that dissolves readily. The D-Arg and Dmt (2,6-dimethyltyrosine) residues are non-natural amino acids — handle with standard peptide precautions.
Concentration: For a 5 mg vial, 1 mL BAC water = 5 mg/mL.
Note: SS-31 is light-sensitive due to the dimethyltyrosine (Dmt) residue. Protect from UV/visible light during reconstitution and storage. Use amber vials or wrap in foil.
Storage & Stability
Lyophilized: -20°C for 24 months (protect from light). Reconstituted: 2-8°C, use within 14 days, protected from light. SS-31 is moderately stable as a small tetrapeptide, but the Dmt residue is photosensitive. Always store in light-protected conditions.
Frequently Asked Questions
What is SS-31?
SS-31 (Elamipretide) is a mitochondria-targeted tetrapeptide that binds cardiolipin on the inner mitochondrial membrane. Its aromatic-cationic structure allows >1000-fold mitochondrial concentration. For research use only.
How does SS-31 target mitochondria?
SS-31 has an alternating aromatic-cationic motif (Arg-Dmt-Lys-Phe) that drives 1000x concentration in mitochondria via the large negative membrane potential (-180mV). Once there, it binds cardiolipin on the inner membrane, optimizing electron transport chain function.
What is cardiolipin and why does it matter?
Cardiolipin is a unique phospholipid found exclusively in the inner mitochondrial membrane. It is essential for Complex III and IV function, cristae formation, and ATP synthase assembly. Cardiolipin oxidation and depletion is a primary driver of mitochondrial dysfunction in aging.
Why not just take antioxidants instead of SS-31?
Fundamentally different approach. Antioxidants scavenge ROS after they are produced (damage already occurring). SS-31 prevents excessive ROS generation at the source by optimizing electron transport. Additionally, SS-31 concentrates 1000x in mitochondria; most oral antioxidants achieve minimal mitochondrial penetration.
What makes SS-31 different from CoQ10 or MitoQ?
CoQ10 is an electron carrier that requires reduction to ubiquinol for activity. MitoQ is a TPP+-conjugated CoQ analog. SS-31 works through a completely different mechanism — cardiolipin binding that optimizes cytochrome c electron transfer. SS-31 also has a different targeting mechanism (aromatic-cationic vs TPP+).
Is SS-31 in clinical trials?
Yes, elamipretide (SS-31) has been tested in Phase 2/3 trials for Barth syndrome (rare mitochondrial cardiomyopathy), heart failure with reduced ejection fraction (HFrEF), age-related macular degeneration, and primary mitochondrial myopathy. Mixed results — positive in Barth syndrome, inconclusive in broader HFrEF.
For laboratory and research use only. Not intended for human or animal consumption. All product information is derived from published preclinical research and does not constitute medical advice or claims.