SS-31
A mitochondria-targeted tetrapeptide studied for cardioprotection, bioenergetic rescue, and cellular oxidative-stress buffering in research models.
⏱ Half-Life
Short duration profile
SS-31 demonstrates a short half-life characteristic in research literature, shaping how observation windows and study timelines are typically structured.
⚡ Onset Characteristics
Moderate measurable response
Onset is observed as moderate — a property that influences how researchers structure comparative studies versus other compounds in the skin & regeneration category.
🧠 Key Notes
What makes it distinct
- 01Selectively concentrates in the inner mitochondrial membrane
- 02Studied for cellular bioenergetic rescue under stress
- 03Investigated across cardiac, neurodegenerative, and renal research models
🧬 Mechanism of Action
How it works
SS-31 (elamipretide) is a cell-permeable, mitochondria-targeted tetrapeptide that selectively accumulates in the inner mitochondrial membrane, where it binds cardiolipin — a phospholipid essential for mitochondrial cristae architecture and respiratory-complex assembly. By stabilising cardiolipin, SS-31 preserves the structural integrity of Complex I, Complex III, and Complex IV, maintaining electron-transport-chain efficiency and reducing reactive-oxygen-species leakage. It also suppresses mitochondrial permeability transition pore (mPTP) opening, preventing apoptosis and necrosis under ischaemic or oxidative stress. This targeted mitochondrial protection makes it a reference compound in bioenergetic-rescue research.
✨ Documented Benefits
What the research shows it supports
🔍 Research Insights
What the literature shows
Selectively binds cardiolipin in the inner mitochondrial membrane, preserving cristae architecture and respiratory-complex assembly.
Reduces ROS leakage by stabilising Complex I and Complex III supercomplexes — a distinct mechanism from generic antioxidants.
Studied across cardiac, neurodegenerative, and renal research models for bioenergetic rescue.
🧪 Typical Research Use Cases
Where it appears in study design
Cardiac ischaemia-reperfusion and cardioprotection research.
Mitochondrial-disease and bioenergetic-rescue models.
Comparative antioxidant research vs untargeted free-radical scavengers.
📚 References
Peer-reviewed literature
Primary research sources cited on this profile. All links resolve to PubMed or the publishing journal.
- [01]
Chu, S. G. et al. (2020). A mitochondria-targeted peptide ameliorates kidney fibrosis by restoring mitochondrial and metabolic homeostasis. Journal of the American Society of Nephrology, 31(12), 2713–2729.
Journal of the American Society of Nephrology ↗ - [02]
Szeto, H. H. (2014). First-in-class cardiolipin-protective compound as a therapeutic agent to restore mitochondrial bioenergetics. British Journal of Pharmacology, 171(8), 2029–2050.
British Journal of Pharmacology ↗ - [03]
Zhao, K. et al. (2004). Cell-permeable peptide antioxidants targeted to inner mitochondrial membrane inhibit mitochondrial swelling, oxidative cell death, and reperfusion injury. Journal of Biological Chemistry, 279(33), 34682–34690.
Journal of Biological Chemistry ↗ - [04]
Daiber, A. (2010). Redox signaling (cross-talk) from and to mitochondria involves mitochondrial pores and reactive oxygen species. Biochimica et Biophysica Acta (BBA) - Bioenergetics, 1797(6-7), 897–906.
Biochimica et Biophysica Acta ↗
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