SS-31

• Form: Lyophilized peptide
• Net per vial: 10 mg (filled to approximately 104% of label)
• Purity: ≥99% (HPLC-verified)
• Identity: MS-verified (per COA)
• Storage: 2–8 °C, protect from light
• Formula / M.W.: C₃₂H₄₉N₉O₅ / 639.8 Da
• CAS: 736992-21-5

SS-31 was developed in the early 2000s by Hazel Szeto and Peter Schiller as part of a research program at Cornell University and the Clinical Research Institute of Montreal aimed at producing cell-permeable peptide antioxidants. The Szeto-Schiller series introduced an alternating aromatic-cationic motif that allowed the peptides to cross plasma and mitochondrial membranes without requiring active transport — a defining property that distinguishes them from earlier mitochondrial-targeted compounds.

What sets SS-31 apart from other mitochondrial research tools is its mechanism of localization. Unlike triphenylphosphonium-based mitochondrial targeting strategies that rely on membrane potential, SS-31 binds cardiolipin directly and concentrates in the inner mitochondrial membrane independent of bioenergetic state. This makes it a reliable tool in research models where mitochondrial membrane potential is compromised — including ischemia-reperfusion, heart failure, and tafazzin-deficient cardiolipin-remodeling systems where conventional mitochondrial probes fail.

• Cardiolipin Stabilization & Cristae Structure — Published cell and animal studies have measured SS-31-driven preservation of cristae morphology and cardiolipin content in mitochondrial dysfunction models, with mechanistic work pointing to direct cardiolipin binding via the peptide's aromatic-cationic motif.
• Reactive Oxygen Species Reduction — SS-31 inhibits cardiolipin peroxidation and reduces mitochondrial ROS production in oxidative stress models, supporting its use as a reference tool in research designs probing redox-balance and antioxidant pathway biology.
• Cardiac Ischemia-Reperfusion — Preclinical work in rodent cardiac IR injury has reported reduced infarct size and preserved mitochondrial respiration in SS-31-treated cohorts, making the peptide a frequently cited tool in cardiac bioenergetics research.
• Skeletal Muscle Bioenergetics — Aged-rodent studies have measured improvements in skeletal muscle ATP production, exercise tolerance, and fatigue resistance following SS-31 exposure, generating sustained interest in the peptide for mitochondrial-myopathy and aging-muscle research.
• Renal & Neural Mitochondrial Research — Published animal models of renal ischemia, atherosclerotic renal artery stenosis, and neurodegeneration have characterized SS-31's effects on mitochondrial function in non-cardiac tissue, expanding its utility as a tool compound across multiple research domains.

Researchers working with SS-31 often investigate it alongside:

• Retatrutide (GLP-3) — SS-31's documented T2D research overlaps with the glycemic-endpoint literature for Retatrutide.
• MOTS-c — Mitochondria-derived signaling peptide that activates AMPK; complements SS-31's structural cardiolipin-stabilization mechanism with a signaling-pathway angle, and pairs with both compounds in our Mito Stack (see below). 
• NAD+ — Mitochondrial cofactor central to sirtuin signaling and redox balance; the third compound in the Mito Stack and a frequent companion in bioenergetics research designs.
• Mito Stack — Combined MOTS-c + SS-31 + NAD+ research blend for groups studying mitochondrial function across signaling, structural, and cofactor mechanisms in parallel.

Where can I buy SS-31 in Canada with verified purity?

Our SS-31 ships to Canadian research labs and independent investigators with a batch-specific certificate of analysis confirming ≥99% HPLC purity and mass-spec identity verification. Vials are filled to approximately 104% of the labeled 10 mg as a quality margin for residual losses during reconstitution work, and ship from within Canada to avoid border-related cold-chain interruptions.

How is SS-31 different from MOTS-c?

Both are mitochondria-focused peptides but engage entirely different mechanisms. SS-31 is a synthetic tetrapeptide that binds cardiolipin on the inner mitochondrial membrane to stabilize cristae structure and reduce ROS production — a structural mechanism. MOTS-c is a 16-amino-acid mitochondria-derived peptide that activates AMPK and acts as a mitochondrial-nuclear retrograde signal — a signaling mechanism. Many research designs use them together to address mitochondrial function from both structural and signaling angles.

Is SS-31 naturally occurring?

No. SS-31 is fully synthetic, designed by Szeto and Schiller as part of a structure-activity program targeting mitochondrial peptide antioxidants. The aromatic-cationic motif and the inclusion of D-arginine and 2',6'-dimethyltyrosine are deliberately non-natural, conferring both protease resistance and the cardiolipin-binding selectivity that defines the compound.

What is the evidence base for SS-31?

The published preclinical literature spans more than two decades and covers cardiac ischemia-reperfusion, heart failure, mitochondrial myopathy, renal ischemia, neurodegeneration, type 2 diabetes, and aging-related muscle dysfunction across cell, rodent, and large-animal models. Clinical trials have been conducted under the development codes elamipretide and MTP-131 in cardiomyopathy, mitochondrial myopathy, and Barth syndrome populations, providing a substantial human pharmacokinetic and safety dataset.