SS-31 10mg: Mitochondrial & Cellular Health

What is SS-31?

SS-31, also known as Elamipretide, Bendavia, or MTP-131, is a synthetic tetrapeptide developed by Hazel H. Szeto and Peter W. Schiller. It belongs to the Szeto-Schiller (SS) family of peptides and has the amino acid sequence D-Arg-Dmt-Lys-Phe-NH2 (D-Arginine, 2,6-Dimethyltyrosine, Lysine, Phenylalanine, amidated). With a molecular weight of approximately 639.8 g/mol, SS-31 is a water-soluble, cell-permeable peptide designed to target mitochondria. Its structure features alternating aromatic and basic amino acids, enabling it to cross cell membranes and concentrate in the inner mitochondrial membrane (IMM) at levels up to 1000-5000 times higher than in the cytosol. SS-31 is typically administered via subcutaneous injection (e.g., .05mg -40 mg/day) or intravenous infusion (e.g., 0.01-0.25 mg/kg/h) in research and clinical settings. It is currently under investigation for mitochondrial disorders and related conditions, available as a research chemical or through specialized medical protocols.

Mechanism of Action

SS-31’s primary mechanism involves targeting and stabilizing mitochondria, particularly under conditions of stress, through the following processes:

1. Cardiolipin Interaction:

   • SS-31 selectively binds to cardiolipin (CL), a key phospholipid in the IMM critical for cristae structure and respiratory chain function. This interaction prevents CL peroxidation by cytochrome c, maintaining mitochondrial membrane integrity.

2. Reactive Oxygen Species (ROS) Scavenging:

   • The dimethyltyrosine residue in SS-31 scavenges mitochondrial ROS (e.g., hydrogen peroxide, hydroxyl radicals), forming stable tyrosine radicals, thus reducing oxidative stress without affecting healthy mitochondria.

3. Mitochondrial Bioenergetics Enhancement:

   • By stabilizing CL, SS-31 optimizes the electron transport chain (ETC), promoting efficient ATP synthesis and reducing electron leakage that generates ROS.

4. Prevention of Mitochondrial Permeability Transition:

   • Inhibits the opening of the mitochondrial permeability transition pore (mPTP), preventing mitochondrial swelling, depolarization, and cytochrome c release, which lead to apoptosis.

5. Anti-Inflammatory Effects:

   • Reduces pro-inflammatory cytokine production (e.g., TNF-α, IL-6) by mitigating mitochondrial damage, which can trigger NLRP3 inflammasome activation.

6. Electrostatic Modulation:

   • Its cationic charge (3+ at physiological pH) allows SS-31 to alter IMM surface electrostatics, redistributing ions (e.g., calcium) and stabilizing membrane dynamics under stress.

SS-31’s specificity for distressed mitochondria and lack of effect on healthy ones make it a unique therapeutic candidate.

Benefits

SS-31’s benefits, supported by preclinical and early clinical studies, include:

1. Mitochondrial Protection:

   • Preserves mitochondrial structure and function, reducing damage from oxidative stress and ischemia.

2. Enhanced Energy Production:

   • Boosts ATP synthesis, improving cellular energy in tissues like skeletal muscle, heart, and brain.

3. Neuroprotection:

   • Mitigates cognitive decline and neuronal damage in models of Alzheimer’s, Parkinson’s, and traumatic brain injury by reducing hippocampal oxidative stress.

4. Cardioprotection:

   • Improves cardiac function, reduces ischemia-reperfusion injury, and reverses diastolic dysfunction in aging models.

5. Muscle Function:

   • Enhances skeletal muscle strength and endurance, particularly in aging or mitochondrial myopathy.

6. Renal Protection:

   • Ameliorates kidney injury by restoring mitochondrial function and reducing fibrosis in models of acute kidney injury (AKI) and diabetic nephropathy.

7. Anti-Aging Effects:

   • Counters age-related mitochondrial decline, improving vascular health, physical endurance, and glomerular architecture.

These benefits highlight SS-31’s potential across a range of mitochondrial dysfunction-related conditions.

Use Cases

SS-31 is primarily experimental or in clinical trials, with applications including:

1. Mitochondrial Disorders:

   • Investigated for primary mitochondrial myopathy, Barth syndrome, and Leigh syndrome (e.g., 40 mg/day SC), targeting bioenergetic failure.

2. Neurodegenerative Diseases:

   • Used in research for Alzheimer’s, Parkinson’s, and ALS (e.g., 5-10 mg/kg in animal models) to protect neurons and improve cognition.

3. Cardiovascular Conditions:

   • Explored for heart failure, myocardial infarction, and age-related diastolic dysfunction (e.g., 3 mg/kg/day in preclinical studies).

4. Renal Diseases:

   • Applied in models of AKI and chronic kidney disease (e.g., 1-3 mg/kg) to reduce oxidative stress and fibrosis.

5. Aging and Wellness:

   • Used off-label (e.g., 10-20 mg/day SC) to enhance energy, muscle function, and vascular health in aging populations.

6. Skeletal Muscle Recovery:

   • Investigated for exercise intolerance or injury recovery in preclinical and early human studies.

Administration varies from daily subcutaneous injections to IV infusions, with dosing tailored to condition severity and research protocols.

Research Studies

Below is a summary of key studies on SS-31, focusing on its mechanisms and benefits:

1. Zhao et al. (2004) - Biochemical Pharmacology

   • Demonstrated SS-31 prevents mitochondrial depolarization and apoptosis in neuronal cell lines exposed to oxidative stress, establishing its ROS-scavenging role.

2. Birk et al. (2013) - Journal of the American Society of Nephrology

   • Showed SS-31 accelerates ATP recovery and reduces AKI in rats post-ischemia by binding cardiolipin and inhibiting CL peroxidation.

3. Szeto et al. (2014) - British Journal of Pharmacology

   • Reviewed SS-31’s ability to rejuvenate mitochondrial function and promote tissue regeneration in aging models via CL stabilization.

4. Campbell et al. (2019) - Circulation Research

   • Found SS-31 (8 weeks, 3 mg/kg/day) reverses age-related diastolic dysfunction in mice by reducing mitochondrial ROS and proton leak.

5. Liu et al. (2021) - Frontiers in Aging Neuroscience

   • Reported SS-31 (5 mg/kg) improves memory and hippocampal connectivity in aged rats with LPS-induced neuroinflammation.

6. Sweetwyne et al. (2017) - Kidney International

   • Showed SS-31 (3 mg/kg) improves glomerular architecture and reduces senescence in 26-month-old mice after 8 weeks.

7. Chavez et al. (2022) - Scientific Reports

   • Demonstrated SS-31 (3 mg/kg/day, 10 weeks) enhances mitochondrial respiration and supercomplex formation in TazKD mice (Barth syndrome model).

8. TAZPOWER Trial (2019-2020) - Phase 2/3 Clinical Trial

   • In Barth syndrome patients, SS-31 (40 mg/day SC) improved exercise capacity and cardiac function over 36 weeks, though results were modest.

These studies highlight SS-31’s promise, with ongoing trials refining its therapeutic scope.

Considerations

• Safety: Well-tolerated in trials, with mild side effects like injection-site reactions or transient nausea. Long-term effects beyond 24 weeks are unstudied.

• Regulation: Available as a research chemical or via clinical trials; not widely accessible outside specialized settings.

• Evidence: Strong preclinical support; human data are promising but limited to small trials, requiring larger studies for broader validation.

In conclusion, SS-31 is a mitochondria-targeted peptide with significant potential to improve bioenergetics, protect against oxidative stress, and treat conditions linked to mitochondrial dysfunction. Its specificity and efficacy in preclinical and early clinical studies make it a compelling candidate, though further research is needed to solidify its therapeutic role.

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