Buy SS-31 10mg

SS-31 (also known as Elamipretide, MTP-131, and Bendavia) is a synthetic mitochondria-targeted tetrapeptide with the sequence D-Arg-Dmt-Lys-Phe-NH2 (where Dmt is 2',6'-dimethyltyrosine). Its entry into the inner mitochondrial membrane (IMM) is driven by the alternating cationic (Arg, Lys) and aromatic (Dmt, Phe) residues that allow it to partition into lipid bilayers with a preference for highly curved membranes — precisely the property of the IMM cristae, whose extreme curvature is essential for ATP synthase assembly and function. This passive accumulation at the IMM is independent of the membrane potential, a critical advantage over older mitochondria-targeted antioxidants like MitoQ that require an intact membrane potential for accumulation and may therefore fail to reach the most severely damaged mitochondria. The primary molecular target of SS-31 is cardiolipin, a unique four-acyl-chain phospholipid found almost exclusively in the IMM where it is required for the function of virtually all ETC complexes and ATP synthase. Cardiolipin stabilizes the IMM cristae curvature, facilitates proton channeling within the cristae lumen to ATP synthase, and is essential for the formation of respiratory chain supercomplexes — highly organized assemblies of ETC Complexes I, III, and IV (and sometimes II) that dramatically increase electron transfer efficiency and minimize ROS generation. With aging and disease, cardiolipin undergoes peroxidative damage by mitochondria-generated ROS, driving cristae flattening, supercomplex disassembly, and impaired electron transport — a cycle of structural and functional deterioration that SS-31 interrupts. SS-31 binds directly to cardiolipin via electrostatic and hydrophobic interactions, reducing its susceptibility to peroxidation. This stabilization preserves cristae morphology, maintains supercomplex assembly, reduces electron "leakage" that generates superoxide at Complex I and III, and maintains the proton-motive force necessary for efficient ATP synthesis. The antioxidant mechanism is catalytic rather than stoichiometric: SS-31 does not permanently neutralize ROS but continuously protects the lipid environment from oxidative modification, meaning that nanomolar concentrations can produce sustained effects over extended time periods. This catalytic efficiency distinguishes SS-31 from consumable antioxidants like coenzyme Q10 or MitoQ. Beyond the direct cardiolipin effect, SS-31 has been shown to improve the assembly and stability of OPA1-mediated cristae junctions — the narrow connections between the cristae lumen and the intermembrane space that regulate cytochrome c retention. Maintaining cytochrome c in the cristae compartment is essential both for efficient electron transfer and for preventing inappropriate apoptosis signaling: once cytochrome c escapes to the cytoplasm, it triggers caspase activation and cell death. SS-31's preservation of cristae junction integrity may therefore contribute to both improved bioenergetics and reduced apoptotic sensitivity in aged or stressed tissues.

SS-31 contains 2',6'-dimethyltyrosine (Dmt), a non-standard amino acid that significantly complicates synthesis and is absent from most commercial peptide synthesis inventories. Suppliers without access to high-purity Dmt will either substitute standard tyrosine (producing an inactive or less active compound) or provide an impure product with Dmt-related synthesis byproducts. Request that certificates of analysis specifically confirm the incorporation of Dmt by mass spectrometry fragmentation, not just molecular weight confirmation, as some truncation fragments have molecular weights close to the intact peptide. Purity should be ≥95% by HPLC with a certificate of analysis specifying the column type and solvent gradient used for analysis. Endotoxin content should be <1 EU/mg for subcutaneous administration. SS-31 was dosed at 40 mg/day subcutaneously in the PROGRESS-HFpEF clinical trial — a substantially higher dose than typical research peptide protocols. Community research protocols for mitochondrial aging and performance applications frequently use 1–5 mg subcutaneously per day or on alternate days, for cycles of 4–12 weeks. This lower research dose is appropriate given the extrapolation from the therapeutic clinical dose and the absence of human dose-ranging data for non-cardiac indications. Storage at −20 °C for lyophilized powder is essential; Dmt-containing peptides can be more susceptible to oxidation at the phenolic ring, so minimize exposure to oxygen during reconstitution by using nitrogen-purged bacteriostatic water where possible. Pre-reconstituted solutions should be used within 2–3 weeks when refrigerated and protected from light. Given the synthesis complexity, SS-31 is one of the peptides where purchasing from established, well-reviewed suppliers with a track record of correct Dmt incorporation is most critical.

The mitochondria-targeted antioxidant field includes MitoQ (mitoquinone, coenzyme Q10 conjugated to a triphenylphosphonium cation), SkQ1 (a similar Russian compound), and various MitoVitE derivatives. These compounds accumulate in the IMM via the membrane potential-dependent electrophoretic force of their cationic carrier, reaching 100–1,000 fold higher concentrations than in the cytoplasm. MitoQ has the most human clinical trial data of any mitochondria-targeted antioxidant, with studies in fatty liver disease, Parkinson's disease, and exercise performance. However, because MitoQ requires an intact membrane potential for accumulation, it is expected to accumulate less efficiently in the most severely damaged mitochondria where potential is collapsed — precisely the pathological situation it is meant to address. SS-31's membrane potential-independent accumulation gives it a theoretical advantage in severe bioenergetic failure. Additionally, SS-31's cardiolipin-binding mechanism provides a structural stabilization effect that purely antioxidant molecules cannot replicate: protecting cristae morphology and supercomplex assembly goes beyond preventing oxidative damage to maintaining the architectural framework necessary for optimal ETC function. The two approaches are not mutually exclusive; combining SS-31's structural protection with the enzymatic antioxidant capacity of CoQ10 supplementation is mechanistically rational. SS-31 represents the most targeted and structurally sophisticated mitochondrial intervention currently available in peptide form.