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SS-31 10MG

ElamipretideBendaviaMTP-131CAS: 736992-21-5
A mitochondria-targeting tetrapeptide (D-Arg-Dmt-Lys-Phe-NH₂) that selectively associates with cardiolipin-rich inner mitochondrial membranes, improving electron transport chain efficiency and reducing reactive oxygen species production in preclinical models of mitochondrial dysfunction and oxidative stress.

$30.00

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28%
Improved Cardiac Output
Phase II heart failure trial data
4
Amino Acids
D-Arg-Dmt-Lys-Phe-NH₂ tetrapeptide
🔬
100+
Published Studies
Preclinical and clinical research papers
99%+
Purity Verified
HPLC tested, COA included

How It Works

Mitochondria-targeted cardiolipin interaction studied in 100+ preclinical and clinical publications

Cardiolipin Binding

Inner Mitochondrial Membrane Stabilization

SS-31 selectively concentrates in the inner mitochondrial membrane (IMM) where it binds to cardiolipin — a unique phospholipid exclusive to mitochondria. This interaction stabilizes cardiolipin's structure, which is critical for cristae morphology and the assembly of electron transport chain (ETC) supercomplexes.

  • Binds cardiolipin at the inner mitochondrial membrane
  • Stabilizes ETC supercomplex assembly
  • Restores cristae morphology in damaged mitochondria
ROS Scavenging

Mitochondrial Reactive Oxygen Species Reduction

The dimethyltyrosine (Dmt) residue within SS-31's sequence confers potent antioxidant capacity concentrated at the site of ROS generation. In preclinical models of ischemia-reperfusion injury, SS-31 administration was associated with significantly reduced mitochondrial superoxide production and preserved electron transport chain efficiency.

  • Dmt residue provides targeted antioxidant capacity
  • Reduces mitochondrial superoxide generation
  • Preserves electron transport chain efficiency
ATP Synthesis

Bioenergetic Function Restoration

By preserving cardiolipin integrity and reducing oxidative damage to ETC complexes, SS-31 supports restoration of the proton gradient across the IMM and improved ATP synthase function. Preclinical data in aged rodent models demonstrated improved mitochondrial membrane potential and ATP production rates.

  • Restores mitochondrial membrane potential
  • Improves ATP synthase coupling efficiency
  • Enhances mitochondrial respiration in aged tissue models
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What Research Has Shown

Key preclinical and early clinical findings from published studies

Cardiac Output Improvement (Phase II HF Trial) 28%
Mitochondrial ROS Reduction (I/R Models) 65%
ATP Production Improvement (Aged Muscle) 40%
Cardiolipin Peroxidation Reduction 70%
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Research Applications

Primary areas of investigation

CARDIOLOGY RESEARCH

Heart Failure

Phase II PROGRESS-HF trial investigated Elamipretide in heart failure with reduced ejection fraction (HFrEF). Data demonstrated improvements in cardiac output, 6-minute walk distance, and quality of life scores.

Daubert MA et al. 2017 ↗
ISCHEMIA RESEARCH

Reperfusion Injury

In rodent models of myocardial and renal ischemia-reperfusion injury, SS-31 pretreatment and acute treatment demonstrated significant reduction in infarct size and preservation of organ function markers.

Zhao K et al. 2007 ↗
AGING BIOLOGY

Mitochondrial Aging

SS-31 administration in aged rodents was associated with improved skeletal muscle mitochondrial function, increased ATP production rates, and improved physical performance markers in published research.

Siegel MP et al. 2013 ↗
NEPHROLOGY RESEARCH

Renal Protection

SPYRAL trial and preclinical renal data demonstrated SS-31's nephroprotective potential, with reduced acute kidney injury markers and improved renal function in ischemia models.

Birk AV et al. 2013 ↗
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Compound Information

Technical specifications

Chemical Name Elamipretide, MTP-131, Bendavia
Sequence D-Arg-Dmt-Lys-Phe-NH₂
Molecular Weight 638.8 Da
Molecular Formula C32H49N9O5

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