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SS-31 (Elamipretide) — 10mg

$89.99Price
Pack Size
Single Vial
10-Pack (Ships in 2 Weeks)
Quantity

Research-grade SS-31 (Elamipretide), a synthetic mitochondria-targeting tetrapeptide (D-Arg-Dmt-Lys-Phe-NH₂) that selectively associates with cardiolipin on the inner mitochondrial membrane. Studied for its effects on mitochondrial bioenergetics, electron transport efficiency, and reactive oxygen species in cellular models. 10mg lyophilized powder, 99%+ purity verified by Janoshik Analytical via HPLC and mass spectrometry.


  • For laboratory research use only.

  • Not for human or veterinary use.

  • Not intended for diagnosis, treatment, cure, or prevention of any disease.

  • Use only in controlled laboratory settings by qualified personnel following appropriate safety procedures.

  • SS-31, also known as elamipretide (MTP-131), is a cell-permeable aromatic-cationic tetrapeptide that concentrates in the inner mitochondrial membrane, where it binds the phospholipid cardiolipin. By stabilizing cardiolipin and the cristae architecture it supports, SS-31 is widely used as a research tool for probing mitochondrial electron transport, ATP synthesis, and oxidative stress. Its D-amino acid and dimethyltyrosine (Dmt) residues confer resistance to peptidase degradation.


    BENEFITS


    • Mitochondrial bioenergetics — studied for effects on electron transport chain efficiency and ATP synthesis

    • Cardiolipin interaction — investigated for selective binding to inner-membrane cardiolipin and cristae stabilization

    • Oxidative stress research — explored for modulation of mitochondrial reactive oxygen species

    • Peptidase-resistant design — D-arginine and dimethyltyrosine residues confer metabolic stability

    • Cell-permeable — aromatic-cationic structure enables mitochondrial accumulation without a carrier


    WHAT RESEARCHERS LOOK AT


    • Cardiolipin binding and inner mitochondrial membrane cristae morphology

    • Electron transport chain coupling and ATP production efficiency

    • Mitochondrial reactive oxygen species generation under stress conditions

    • Ischemia–reperfusion and tissue-injury cellular models

    • Age-associated decline in mitochondrial function

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