SS-31 (also known as Elamipretide, MTP-131, Bendavia) is a synthetic cell-permeable tetrapeptide with the sequence D-Arg-Dmt-Lys-Phe-NH2 (where Dmt = 2′,6′-dimethyltyrosine). It selectively targets the inner mitochondrial membrane by binding to cardiolipin, a phospholipid critical for maintaining mitochondrial cristae structure, electron transport chain organization, and cytochrome c function. This cardiolipin interaction stabilizes membrane architecture and optimizes mitochondrial bioenergetics without acting as a conventional free-radical scavenger. Research compound — for laboratory use only.
Product Specifications
| Compound Name | SS-31 (Elamipretide / MTP-131) |
| CAS Registry Number | 736992-21-5 |
| Molecular Weight | 639.80 g/mol |
| Molecular Formula | C32H49N9O5 |
| Sequence | D-Arg-Dmt-Lys-Phe-NH2 |
| PubChem CID | 11764719 |
| Purity | ≥99% (HPLC) |
| Physical Form | Lyophilized powder |
| Solubility | Freely soluble in sterile water and bacteriostatic water |
| Storage | Store lyophilized at -20°C. Reconstituted solution stable at 2-8°C for up to 28 days. Avoid repeated freeze-thaw cycles. |
| Catalog Size | 10 mg |
Structural Overview
SS-31 belongs to the Szeto-Schiller (SS) family of mitochondria-targeting peptides, originally discovered during opioid receptor research. Its alternating aromatic-cationic motif (aromatic–basic–aromatic–basic) enables rapid, energy-independent cell penetration and selective accumulation at the inner mitochondrial membrane within minutes of exposure.
Key structural features:
- D-Arginine at position 1 — Provides cationic charge for membrane interaction and confers resistance to aminopeptidase degradation
- 2′,6′-Dimethyltyrosine (Dmt) at position 2 — Modified aromatic residue that enhances membrane partitioning and cardiolipin binding affinity
- Lysine at position 3 — Additional basic residue contributing to the cationic amphipathic character
- Phenylalanine-NH2 at position 4 — C-terminal amidation improves metabolic stability and membrane interaction
The net +3 charge at physiological pH drives electrostatic concentration at the highly negative inner mitochondrial membrane, achieving >1,000-fold accumulation relative to extracellular concentration.
Mechanism of Action
Unlike conventional antioxidants that scavenge reactive oxygen species after formation, SS-31 acts upstream at the site of ROS generation by stabilizing the electron transport chain itself:
- Cardiolipin binding: SS-31 interacts with cardiolipin through electrostatic and hydrophobic contacts, stabilizing the cristae architecture that houses respiratory chain supercomplexes
- Electron transport optimization: By preserving cardiolipin-dependent supercomplex assembly (Complexes I/III/IV), SS-31 facilitates efficient electron transfer and reduces electron leak that generates superoxide
- Cytochrome c modulation: SS-31 promotes the electron carrier function of cytochrome c while inhibiting its peroxidase activity — a key distinction from traditional antioxidant approaches
- Cristae remodeling: Research demonstrates that SS-31 promotes restoration of inner membrane cristae curvature, improving the structural basis for oxidative phosphorylation
- ADP sensitivity: SS-31 has been shown to improve mitochondrial ADP sensitivity through interactions with the adenine nucleotide translocator (ANT), enhancing the coupling between energy demand and ATP production
Research Context
SS-31 has been investigated across a broad range of research models examining mitochondrial dysfunction:
- Cardiac research models: Extensively studied in models examining ischemia-reperfusion, age-related cardiac dysfunction, and cardiomyopathy associated with cardiolipin remodeling defects
- Renal research: Investigated in models of acute kidney injury and chronic kidney disease, where mitochondrial dysfunction contributes to tubular cell damage
- Skeletal muscle research: Studied in aging models examining the relationship between mitochondrial ADP sensitivity, muscle fatigue resistance, and exercise capacity
- Neurodegenerative research: Examined in models investigating mitochondrial contributions to neuronal dysfunction, including oxidative phosphorylation deficits and synaptic energy failure
- Ophthalmic research: Investigated in retinal models where photoreceptor and retinal pigment epithelium cells have high mitochondrial density and energy demands
Handling & Reconstitution
SS-31 is a water-soluble tetrapeptide that reconstitutes readily:
- Recommended solvent: Sterile water or bacteriostatic water for injection
- Reconstitution: Add solvent slowly along the vial wall, then gently swirl — do not vortex aggressively
- Lyophilized storage: -20°C, protected from light and moisture
- Reconstituted storage: 2-8°C, use within 28 days
- Stability note: SS-31 is relatively stable in aqueous solution due to the D-amino acid and C-terminal amidation, but prolonged storage above 8°C may reduce activity
Quality Assurance
Every batch of SS-31 from Chameleon Peptides is independently tested for identity and purity:
- High-performance liquid chromatography (HPLC) — purity ≥99%
- Mass spectrometry (MS) — molecular weight confirmation
- Certificate of Analysis (COA) available on our Testing page
FOR RESEARCH USE ONLY — NOT FOR HUMAN CONSUMPTION
Limitations and Current Knowledge Gaps
The research summarized on this page reflects findings from preclinical models (primarily rodent and in vitro studies). Several important limitations should be acknowledged when evaluating this evidence:
- Lack of human clinical trials: No large-scale, randomized controlled trials in humans have been completed for most research peptides, including SS-31 — Published Research. Animal data does not directly translate to human outcomes.
- Dosing uncertainty: There are no standardized, clinically validated dosing protocols. Doses used in animal studies may not be relevant to human applications.
- Unknown long-term safety profile: Long-term toxicity, chronic administration effects, and potential off-target biological interactions remain unstudied.
- Regulatory status: SS-31 — Published Research is not approved by the FDA or other major regulatory agencies for human therapeutic use. Regulatory classification varies by jurisdiction.
- Publication bias: Positive results are more likely to be published than negative findings, which may inflate the apparent strength of evidence.
Researchers should evaluate these findings in context and avoid extrapolating preclinical results to clinical recommendations.