SS-31 is a metabolic & longevity research compound currently in stock directly from a verified Chinese manufacturer. Every batch is HPLC-verified and shipped with a Certificate of Analysis (COA). Sourcing is direct — no intermediaries. Minimum order value is $600 USD. International shipping available.
SS-31 (also known as elamipretide or MTP-131) is a synthetic tetrapeptide belonging to the Szeto-Schiller (SS) peptide series, developed by Hazel Szeto and Peter Schiller at Weill Cornell Medical College. Its sequence — D-Arg-Dmt-Lys-Phe-NH₂ — incorporates two non-natural amino acids: D-arginine at position 1 (for metabolic stability) and 2',6'-dimethyltyrosine (Dmt) at position 2, which confers potent free radical scavenging activity and high affinity for cardiolipin. Cardiolipin is an anionic phospholipid unique to the inner mitochondrial membrane (IMM), where it plays structural roles in cristae architecture, electron transport chain (ETC) complex assembly, and mitochondria-associated membrane (MAM) organisation. SS-31's nanomolar affinity for cardiolipin allows it to concentrate approximately 1000-fold in mitochondria following systemic administration — its primary mechanism of action.
Research on SS-31 centres on mitochondrial dysfunction as a unifying pathological mechanism across ageing, cardiovascular disease, kidney injury, and neurodegenerative conditions. By stabilising cardiolipin in the IMM, SS-31 prevents cytochrome c dissociation from the membrane, maintains cristae morphology, reduces electron leak (and thus ROS production), and preserves ATP synthase activity. In cardiac ischaemia-reperfusion (I/R) injury models, SS-31 reduces infarct size by up to 40% when administered at reperfusion — one of the most reproduced findings in mitochondria-targeted cardioprotection research. The compound has been evaluated in Phase II and III clinical trials for heart failure with reduced ejection fraction (HFREF), Barth syndrome (a mitochondrial cardiomyopathy caused by tafazzin gene mutations), and acute kidney injury.
PeptidesFromChina.co supplies SS-31 (elamipretide) as lyophilized powder at ≥98% purity, verified by HPLC and confirmed by mass spectrometry. Certificates of Analysis available per batch. Wholesale quantities on request. For laboratory research use only.
| Chemical Class | Mitochondria-targeting Szeto-Schiller Tetrapeptide |
|---|---|
| INN | Elamipretide |
| CAS Number | 736992-21-5 |
| Molecular Weight | 663.8 Da |
| Sequence | D-Arg-Dmt-Lys-Phe-NH₂ (4 amino acids; Dmt = 2',6'-dimethyltyrosine) |
| Primary Target | Cardiolipin (inner mitochondrial membrane) |
| Synonyms | MTP-131, SS peptide-31, Elamipretide |
| Mitochondrial Accumulation | ~1000× concentration vs. cytoplasm |
| Storage | -20°C lyophilized; 4°C reconstituted (up to 14 days) |
| Molecular Formula | C₃₄H₄₉N₉O₅ |
| Name | Strength | Pack Size | Purity | Availability | Price (USD) |
|---|---|---|---|---|---|
| SS-31 | 10 mg | 10 vials | ≥98% | In Stock | $94.00 |
| SS-31 | 50 mg | 10 vials | ≥98% | In Stock | $325.00 |
Testing method: HPLC / LC-MS. Every batch is tested before shipment. Purity ≥99% confirmed per batch.
Certificate of Analysis (COA) is included with every order. Documentation covers purity, molecular weight, and batch identification.
Cardiac ischaemia-reperfusion (I/R) injury is characterised by a burst of ROS and mitochondrial membrane permeability transition pore (mPTP) opening at reperfusion, causing cardiomyocyte death. SS-31 administered at reperfusion (0.05–1 mg/kg i.v. in rodent models) reduces infarct size (TTC staining), preserves mitochondrial membrane potential (ΔΨm, measured by JC-1 or TMRE), and attenuates cytochrome c release — all consequences of cardiolipin stabilisation and reduced electron leak. Ex vivo Langendorff perfused heart preparations allow precise control of I/R timing and SS-31 concentration, making this one of the cleanest assay systems in mitochondria-targeted pharmacology.
Mitochondrial dysfunction — reduced ATP production, elevated ROS, and fragmented cristae — is a hallmark of cellular ageing and senescence. SS-31 preserves ATP synthase activity by maintaining the cardiolipin-dependent supercomplex organisation of ETC complexes I, III, and IV (respirasome). In aged mouse models (24-month-old C57BL/6J), SS-31 treatment improves maximal oxygen consumption rate (OCR) in isolated mitochondria, increases muscle endurance on treadmill testing, and reduces 4-HNE adducts (a lipid peroxidation marker) in cardiac and skeletal muscle. These findings position SS-31 as a tool for studying whether mitochondrial cardiolipin remodelling is causal in age-related decline.
Renal tubular epithelial cells (RTECs) are highly mitochondria-dependent due to their reliance on oxidative phosphorylation. In cisplatin-induced nephrotoxicity, renal I/R, and contrast-induced AKI rodent models, SS-31 reduces serum creatinine, BUN, and histological tubular injury scores. Mitochondria isolated from treated kidneys show preserved morphology (electron microscopy), higher ΔΨm, and reduced cytochrome c release. The EMPOWER trial investigated SS-31 in primary mitochondrial myopathy — a condition with no approved therapy — using 6-minute walk distance and functional endpoints in patients with documented mitochondrial mutations.
Barth syndrome is caused by mutations in the tafazzin (TAZ) gene encoding a cardiolipin transacylase, leading to cardiolipin deficiency and abnormal monolysocardiolipin accumulation — making it the definitive genetic model for cardiolipin dysfunction. SS-31 in TAZ-knockdown cell lines and zebrafish models restores cristae morphology and mitochondrial ATP synthesis, providing direct functional validation of the cardiolipin-binding mechanism. The TAZPOWER Phase II trial evaluated SS-31 in Barth syndrome patients using cardiac MRI and exercise testing as endpoints. These studies remain the most mechanistically well-controlled clinical dataset for any cardiolipin-targeting compound.
SS-31's mitochondrial targeting does not rely on cationic charge (unlike typical mitochondria-targeting sequences or MitoQ-class compounds), making it unusual among mitochondria-targeting agents. Instead, Dmt's aromatic ring and the positively charged arginine and lysine residues enable high-affinity electrostatic interaction with the anionic phosphate head groups of cardiolipin, which is enriched ~1000-fold in the inner versus outer mitochondrial membrane. This cardiolipin affinity effectively concentrates the peptide in the IMM. The mechanism has been confirmed by radiolabelled (³H)-SS-31 subcellular fractionation studies.
Most antioxidant strategies scavenge free radicals after they are produced. SS-31 targets the upstream source of mitochondrial ROS — electron leak from the ETC resulting from destabilised cardiolipin-supercomplex organisation. By preserving the structural integrity of ETC supercomplexes, SS-31 reduces the probability of electron leak to oxygen, preventing ROS generation rather than quenching it. The Dmt residue also provides direct ROS scavenging activity, but the primary mechanism is structural stabilisation at the IMM level.
SS-31 is water-soluble and should be reconstituted in sterile PBS or distilled water to a stock concentration of 1–10 mM. For cell culture assays (Seahorse XF mitochondrial respiration, JC-1 membrane potential, cytochrome c release), working concentrations of 0.1–100 nM are typically used, added to culture medium 30–60 minutes before assay initiation or before an insult protocol. DMSO is not required. Store reconstituted aliquots at -20°C for long-term use.
Yes. SS-31 (elamipretide) is available through PeptidesFromChina.co on a B2B wholesale basis at ≥98% purity. Certificates of Analysis per batch. Contact us via the Request page for pricing and minimum order quantities.
For laboratory research use only. Not for human or veterinary use. PeptidesFromChina.co is a B2B wholesale supplier operating under strict research-use-only terms. All products are sold exclusively for in vitro and preclinical research purposes.