Mitochondrial Repairing Peptide SS-31

Mitochondrial Repairing Peptide SS-31

Mitochondrial Repairing Peptide SS-31

There is more to mitochondria than merely being “the powerhouse of the cell,” as has long been believed. New research indicates that their performance is an important indicator of age:

The mitochondria have lately come to the forefront as a key regulator of cellular life and death. Oxidative damage to mitochondria may trigger apoptosis by releasing cytochrome c into the cytoplasm and activating the caspase cascade.

Many illnesses and conditions, such as ischemia-reperfusion injury, neurological diseases, diabetes, inflammatory diseases, medication toxicity, and age-related degenerative diseases, involve cell death driven by mitochondrial oxidative damage. This post will explain why SS-31 is an intriguing bio-regulator of aging. For more information, go to Biotech Peptides. Visit website now.

To begin with, what is SS-31?

SS-31, also known as Elampretide, Bendavia, and MPT-141, is a synthetic tetrapeptide (i.e., 4 amino acids long) developed in the early 2000s by scientists Hazel H. Szeto and Peter W. Schiller.

This fortunate turn of events occurred when Schiller and Szeto developed novel compounds to specifically target the opioid receptor in the brain and relieve extreme pain.

The first breakthrough was the discovery that compounds based on peptides could traverse the blood-brain barrier; the second, possibly more important, was the discovery that the peptides could target the mitochondria with exquisite specificity.

As the first compound to selectively target the IMM, where the ETC is located, SS-02 was discovered through mitochondria fractionation studies to be present at concentrations of >85% in the fraction containing inner mitochondrial membrane (IMM) [without being distributed in the mitochondrial matrix]. The concentration of SS-02 in the IMM is predicted to be more than 1,000-fold higher than its concentration outside of cells.

Schiller and Szeto aimed to improve upon SS-02, the initial iteration in which the mitochondria-targeted antioxidant capabilities were identified, by retaining these novel features while reducing SS-02’s affinity for the opioid receptor. SS-31 is the end consequence of a series of amino acid changes.

To bridge the gap between SS-02 and SS-31, an intermediary called SS-20 was developed. Affinity for the receptor was reduced 450-fold by SS-20 and 2,000-fold by SS-31. Extraordinarily high dosages in mice showed almost NO opioid action.

But getting back to mitochondria, what makes SS-31 such a groundbreaking finding in the field of mitochondrial disease? This is because no effective treatment for mitochondrial dysfunction has been available until recently.

The medicine elamipretide can cross the outer mitochondrial membrane and bind to a specific protein that is essential for maintaining mitochondrial function. This is a significant challenge since it is difficult to create medications that can traverse both the cell and the outside mitochondrial membranes.

Studies suggest that elamipretide may enhance mitochondrial function by normalizing the shape of the inner mitochondrial membrane. Some examples of this include enhanced energy production and reduced free radical creation.

Mitochondrial Repairing Peptide SS-31

Action Principle Of The SS-31

Cardiolipin, a lipid molecule found in the inner mitochondrial member (IMM), is the “secret sauce” driving SS-31’s action in the body. It stabilizes the inner membrane proteins, which is necessary for developing mitochondrial cristae and the effective oligomeric assembly of electron transport chain complexes.

Acting as a proton trap for ATP synthase and facilitating electron transport through electrostatic contact with cytochrome c allows maximum ATP generation. There is more oxidized cardiolipin because cardiolipin increases the peroxidase activity of cytochrome c. Mitochondrial fission and fusion also depend on cardiolipin.

Thus, cardiolipin is essential for proper mitochondrial function. Its absence causes respiratory complex disruption, increased proton leak, ROS generation, decreased ATP synthesis, altered mitochondrial shape, and ultimately compromised mitochondrial dynamics and stability.

I’m still confused about SS-31’s role.

In a nutshell, it binds to Cardiolipin, enhancing the good effects while blocking the bad ones (mitochondrial dysfunction due to a lack of reactive oxygen species (ROS) buildup and consequent oxidative damage) (antioxidant properties, ATP production, etc.). SS-31’s health effects, according to brilliant scientist Nick Andrews, are principally driven by its ability to increase ATP levels.

Best SS-31 Health Advantages

A cursory search via PubMed reveals an overwhelming amount of papers demonstrating the health advantages of SS-31, with over 135 studies published on the topic since 2005. This is hardly unexpected considering the mitochondria’s essential role in maintaining human health. Now, let’s go right into it!

The SS-31 Has the Potential to Treat Cognitive Impairment.

The potential use of SS-31 in treating chronic fatigue syndrome is an intriguing prospect (CFS). This is predicated on Dr. Ron Davis’s theory that cells in CFS don’t “behave” normally:

ME [Myalgic encephalomyelitis]/CFS is driven by an unidentified substance in the blood that may make healthy cells behave like ME/CFS cells. Nanoneedle salt stress testing was illuminating in chronic fatigue syndrome. Sodium chloride (common table salt) does the trick by making cells use up their energy (sodium enters the cell and is a little toxic to them, so they must use energy to pump it out again).

When salt is introduced, there is little electrical activity in a control sample of healthy cells. A decrease in electrical impedance is seen when salt is introduced to a ME/CFS sample. This is done for every patient tested (26 after the first 20), but not for any control subjects.

Therefore, something in the plasma (or its absence) appears to be impacting cells and causing them to behave improperly in patients with ME/CFS. Identifying the underlying cause of this phenomenon would be a significant step in elucidating the nature of ME/CFS. His preliminary research suggests that SS-31 is certainly doing something to normalize damaged cells, but this in no way guarantees a cure. Behavioral assessments assessing learning and memory were dramatically improved after treatment with elamipretide.

In particular, elamipretide acted as a protective factor against mitochondrial dysfunction and oxidative stress, and it facilitated the regulation of brain-derived neurotrophic factor (BDNF) signaling, which included the reversal of key synaptic-signaling proteins and an increase in synaptic structural complexity.

Another research in mice observed the same thing with SS-31 therapy, this time utilizing the “poison” of isoflurane to induce cognitive impairments, and also noted how it was protective against mitochondrial damage. This is crucial since it has recently been shown that stress-induced oxidative damage to mitochondria may reduce blood supply to the brain.

By enhancing NO-mediated cerebromicrovascular dilatation, SS-31 treatment [in old mice] markedly enhanced neurovascular coupling responses, which were then linked to considerable enhancements in spatial working memory, motor skill acquisition, and gait coordination.

Similar protective effects of SS-31 were seen on the mitochondrial generation of reactive oxygen species and mitochondrial respiration in cultured cerebromicrovascular endothelial cells taken from old animals, supporting our results.