Compound reference
SS-31 (Elamipretide)
Cellular & Longevity Research · vial. For laboratory research use only. Not for human or veterinary consumption, diagnostic use, therapeutic use, or clinical use.
Chemistry identity
Reference identifiers
COA documentation
Lot record status
COA on file - lab confirmation pendingView Lab ReportsPublished literature
Research context
Peer-reviewed literature referencing this compound, provided for research context.
Targeting Mitochondrial Dysfunction With Elamipretide (SS-31) Improves Skeletal Muscle Performance in a HFpEF Rat Model2026
Vahle B, Weidner S, Tomalka A, Schauer A, Augstein A, Männel A, et al.
Circulation. Heart failure
In a rat model of heart failure with preserved ejection fraction, skeletal muscle showed reduced cardiolipin content and tafazzin expression versus lean controls; twelve weeks of elamipretide administration increased whole-muscle and single-fiber contractile force and reduced fiber atrophy, effects the authors attributed to cardiolipin-mediated stabilization of mitochondrial oxidative phosphorylation.
Mitochondria-Targeted Peptides and Bilayer Composition Modulate Membrane Electroporation under Elevated Electrochemical Stress2025
Tamucci JD, Zweifach A, Alder NN, May ER
Langmuir : the ACS journal of surfaces and colloids
Using all-atom molecular dynamics simulations of lipid bilayers with explicit transmembrane potentials, cardiolipin and elamipretide were shown to increase membrane capacitance and protect against electroporation under elevated electrochemical stress, characterizing a biophysical mechanism by which the peptide modulates inner-membrane electrostatics.
The mitochondria-targeted peptide SS-31 binds lipid bilayers and modulates surface electrostatics as a key component of its mechanism of action2020
Mitchell W, Ng EA, Tamucci JD, Boyd KJ, Sathappa M, Coscia A, et al.
The Journal of Biological Chemistry
Using biophysical and computational approaches, this study showed that the tetrapeptide SS-31 (elamipretide) partitions into the interfacial region of model and mitochondrial membranes in proportion to surface charge, altering lipid packing and modulating membrane surface electrostatics — including divalent-cation (calcium) distribution at the interface — characterizing a cardiolipin-dependent, membrane-biophysical mechanism of action.
Cell-permeable peptide antioxidants targeted to inner mitochondrial membrane inhibit mitochondrial swelling, oxidative cell death, and reperfusion injury2004
Zhao K, Zhao GM, Wu D, Soong Y, Birk AV, Schiller PW, et al.
The Journal of biological chemistry
In neuronal cell culture and isolated liver mitochondria, this foundational study characterized a class of aromatic-cationic tetrapeptides -- including the compound now known as SS-31 -- that concentrate in the inner mitochondrial membrane, reduce reactive-oxygen-species production, inhibit calcium-induced mitochondrial permeability transition and swelling, and preserve contractile force in an ex vivo ischemia-reperfusion heart model; a dimethyltyrosine-lacking analog lost this activity, identifying that residue as mechanistically essential.
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