Mitochondrial + redox research
SS-31 / Elamipretide
Lyophilized mitochondrial and cellular-signaling research material
SS-31 / Elamipretide is a mitochondria-targeting peptide studied around cardiolipin interaction, mitochondrial membrane function, and oxidative-stress models.
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Get catalog updatesFor laboratory research use only. Not for human or veterinary use. Not intended to diagnose, treat, cure, mitigate, or prevent disease.
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Research context
SS-31 / Elamipretide research profile
SS-31, also called elamipretide in pharmaceutical research, is a mitochondria-targeting tetrapeptide studied for interaction with cardiolipin in the inner mitochondrial membrane. Experimental work measures membrane structure, electron-transport function, reactive-oxygen-species markers, ATP-related endpoints, and tissue responses to mitochondrial stress. It differs from MOTS-c, which is approached as a mitochondrial-derived signaling peptide, and from NAD+, which is a redox coenzyme. SS-31 is most useful when membrane and cardiolipin biology are central to the study design. A substantial preclinical and clinical-development literature exists, but reported outcomes vary by model and do not validate a separate catalog material.
Proposed mechanism
A mitochondria-targeting tetrapeptide proposed to associate with cardiolipin in the inner mitochondrial membrane. This interaction may stabilize membrane curvature and respiratory-chain organization, reduce electron leak, and limit excess reactive-oxygen-species generation.
Effects reported in studies
- Cell and animal models report improved mitochondrial respiration, ATP-related measures, membrane potential, and resistance to oxidative injury.
- Preclinical studies report functional improvements in selected cardiac, skeletal-muscle, renal, neurologic, and ocular disease models.
- Human clinical-development studies have produced mixed results across indications and endpoints.
Common research endpoints
Cardiolipin interaction, oxygen consumption, electron transport, ATP, membrane potential, reactive oxygen species, mitochondrial morphology, tissue function, pharmacokinetics, and clinical endpoints.
Evidence and limitations
The mechanistic and preclinical literature is extensive, but human efficacy has not been consistent across clinical programs.
External reading
Literature for context—not product proof.
Third-party sources describe their own research materials and methods. They do not validate a specific Azure catalog batch.
Support and documentation
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