About SS-31
Targets cardiolipin in inner mitochondrial membrane; stabilizes cristae structure; enhances electron transport chain efficiency; reduces mitochondrial ROS
SS-31 (elamipretide; Szeto-Schiller peptide 31; MTP-131; bendavia) is a synthetic cardiolipin-targeting tetrapeptide that selectively concentrates in the inner mitochondrial membrane through electrostatic interaction with cardiolipin, where it stabilizes cristae ultrastructure, preserves electron transport chain assembly, and reduces mitochondrial reactive oxygen species production to protect against ischemic and metabolic mitochondrial injury. By binding cardiolipin at the inner mitochondrial membrane, SS-31 maintains the protein-lipid interactions required for efficient electron transport chain supercomplex formation, preserving cytochrome c association with complexes I–IV, reducing electron leak, and sustaining the proton gradient required for ATP synthase activity — thereby protecting energy production in cardiomyocytes, neurons, and renal tubular cells under ischemic or oxidative stress. A randomized, placebo-controlled trial published in Circulation Heart Failure demonstrated that elamipretide improved cardiac function in patients with heart failure with reduced ejection fraction, and a Phase 2a trial published in Circulation Cardiovascular Interventions provided additional human evidence of mitochondrial protection in the context of renal artery stenosis revascularization. Elamipretide has not received FDA approval; it has received rare pediatric disease designation for Barth syndrome and has been studied in multiple Phase 2 trials including heart failure, primary mitochondrial myopathy, and geographic atrophy, with ongoing Phase 3 development programs as of 2025.
SS-31 Benefits & Research Areas
Research Signals
Population research notes
These signals reflect research interest areas, not treatment indications.
Regulatory & Evidence
Risk Profile
Generally considered lower risk in research contexts. Risk profile varies by individual — review contraindications before use.
Regulatory Status
- Availability Status
- Research Only
- FDA Status
- Investigational
Mitochondria-targeting tetrapeptide (elamipretide) by Stealth BioTherapeutics. FDA issued CRL for Barth syndrome NDA 2021 (additional data required). Continued by Mitobridge/AstraZeneca. Investigational.
Regulatory status reflects publicly available information and may change. This is not legal or medical advice.
Research Sources
7 sources cited · 7 moderate
2 RCTs · 3 Cohorts · 2 Reviews
Peroxiredoxin Ⅲ safeguards cardiac function against doxorubicin by regulating mitochondrial quality control via H(2)O(2) detoxification.
Redox Biol · 2026
# Summary Research found that peroxiredoxin III (PrxIII), a mitochondrial antioxidant enzyme, protects cardiac cells from doxorubicin-induced damage by regulating hydrogen peroxide levels and maintaining mitochondrial quality control processes. This study demonstrated that moderate mitochondrial hydrogen peroxide levels promote protective adaptations like enhanced mitophagy and mitochondrial fusion, whereas excessive accumulation impairs these protective mechanisms and triggers cell death.
Protective Effect of Mitochondria-Targeted Polydopamine Nanoparticles in Alleviating Hepatic Ischemia-Reperfusion Injury.
ACS Nano · 2026
# Summary Research found that mitochondria-targeted nanoparticles modified with the SS-31 peptide protected liver tissue from ischemia-reperfusion injury by restoring mitochondrial function, reducing reactive oxygen species accumulation, and suppressing inflammatory responses in animal models. This study demonstrated that SS-31 modification enabled efficient delivery of therapeutic nanoparticles to mitochondria, where they preserved cellular energy production and prevented cell death pathways associated with liver damage.
Mitochondrial dysfunction-driven inflammation and β-Cell apoptosis in type 2 diabetes mellitus: mechanistic insights and therapeutic implications.
Mol Biol Rep · 2026
# Summary Research found that mitochondrial dysfunction drives inflammation and β-cell death in type 2 diabetes through excessive reactive oxygen species production and impaired cellular energy metabolism. This review identified mitochondria-targeted antioxidants like SS-31 as a promising therapeutic approach to restore mitochondrial quality control and potentially address the disease's underlying mechanisms beyond glucose management alone.
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Effect of mitochondrial dysfunction on scar formation after spinal cord injury.
Front Neurol · 2026
# Summary Research found that mitochondrial dysfunction plays a central role in scar formation following spinal cord injury by triggering energy collapse, oxidative stress accumulation, and impaired cellular dynamics that promote glial and fibrotic scar development. This study demonstrated that mitochondrial-targeted therapies—including antioxidants like SS-31, metabolic modulators, and strategies enhancing mitochondrial repair processes—show promise in reducing scar formation and supporting neural regeneration.
Elamipretide (SS-31) promotes recovery by preserving mitochondrial bioenergetics and neural remodeling after spinal cord injury.
Neurochem Int · 2026
# Summary Research found that elamipretide (SS-31), a mitochondria-targeting peptide, significantly improved functional recovery and reduced tissue damage following spinal cord injury in mice by preserving mitochondrial function and reducing both early apoptotic cell death and chronic inflammatory responses. This study demonstrated that SS-31's neuroprotective mechanisms include maintaining mitochondrial energy production, decreasing oxidative stress, and supporting long-term neural repair processes including axonal and synaptic remodeling.
Elamipretide (MTP-131) Alters the Landscape of Myocardial Lipids and Reduces Oxidative Stress Following Cardiac Ischemia/Reperfusion Injury
Circulation: Heart Failure · 2017
In a double-blind randomized controlled trial of 36 patients, a single infusion of elamipretide (SS-31/MTP-131) was safe and well-tolerated, with the high dose significantly reducing left ventricular end-diastolic volume (-18 mL, p=0.009) and end-systolic volume, supporting its mitochondria-targeting mechanism for cardiac protection in heart failure.
Intrarenal Infusion of Elamipretide (MTP-131) During Stenting in Patients With Atherosclerotic Renovascular Disease
Circulation: Cardiovascular Interventions · 2017
In a phase 2a randomized trial of 14 patients undergoing percutaneous renal artery stenting, intrarenal elamipretide (SS-31) attenuated post-procedure renal hypoxia, increased stenotic kidney renal blood flow, and improved estimated glomerular filtration rate compared with placebo, establishing renal protective activity for this mitochondria-targeting peptide.
SS-31 Side Effects & Safety Considerations
Generally considered lower risk in research contexts. Individual response varies — review all considerations before use.
Reported contraindications & considerations
Consult a qualified healthcare professional before making any health decisions. This information is educational only and does not constitute medical advice.
Research Stacks
Browse all →Where to Buy SS-31 — Providers & Availability
42 providersClinics
10 providersHormone & Peptide Therapy Greenville SC
United StatesView →Montecito Concierge Medicine
Montecito, United StatesView →Optimize by JaeNix
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Chicago, United StatesView →Austin Regenerative Therapy
Austin, United StatesView →Pura Vida Body & Mind Spa
United StatesView →Pure Hydration
United StatesView →Better Med Spa
United StatesView →Meeting Point Health
United StatesView →The Hormone Zone
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Questions to Ask Your Provider
Frequently Asked Questions — SS-31
SS-31 (elamipretide; Szeto-Schiller peptide 31; MTP-131; bendavia) is a synthetic cardiolipin-targeting tetrapeptide that selectively concentrates in the inner mitochondrial membrane through electrostatic interaction with cardiolipin, where it stabilizes cristae ultrastructure, preserves electron transport chain assembly, and reduces mitochondrial reactive oxygen species production to protect against ischemic and metabolic mitochondrial injury. By binding cardiolipin at the inner mitochondrial membrane, SS-31 maintains the protein-lipid interactions required for efficient electron transport chain supercomplex formation, preserving cytochrome c association with complexes I–IV, reducing electron leak, and sustaining the proton gradient required for ATP synthase activity — thereby protecting energy production in cardiomyocytes, neurons, and renal tubular cells under ischemic or oxidative stress.
mitochondrial protection, cardioprotection, energy production, anti-aging.
Research on SS-31 primarily documents effects related to mitochondrial protection and cardioprotection and energy production and anti-aging. These are areas covered in preclinical and clinical literature — individual response varies and effects depend on context of use.
Reported contraindications and considerations for SS-31 include none well-established. This is educational information only — consult a qualified healthcare professional before use.
42 providers in the directory currently offer SS-31.
# Summary Research found that peroxiredoxin III (PrxIII), a mitochondrial antioxidant enzyme, protects cardiac cells from doxorubicin-induced damage by regulating hydrogen peroxide levels and maintaining mitochondrial quality control processes. This study demonstrated that moderate mitochondrial hydrogen peroxide levels promote protective adaptations like enhanced mitophagy and mitochondrial fusion, whereas excessive accumulation impairs these protective mechanisms and triggers cell death.
SS-31 is featured in the following research stacks on PeptideBase: MOTS-c + SS-31: Mitochondrial Optimization.