SS-31 (Elamipretide) 10mg Pre-Mixed Stabilized Pen

Description

SS-31 (Elamipretide, Bendavia, MTP-131) is a synthetic tetrapeptide that targets mitochondria. It enters cells and binds to cardiolipin on the inner mitochondrial membrane to keep its structure stable. Made from D-amino acids for better stability, this peptide has been tested on mammals, including humans. SS-31 strongly attaches to mitochondrial membranes and has several known benefits:

• It lowers oxidative stress and the production of reactive oxygen species (ROS).
• It protects mitochondria from damage and dysfunction.
• It helps cells use energy better.
• It reduces inflammation and apoptosis in tissues.
•  It protects the heart during ischemia, reperfusion, and heart failure.
• It protects the kidneys during acute kidney injury.
• It protects the brain from oxidative stress and neuroinflammation.
• It improves skeletal muscle function and reduces muscle atrophy.
• It changes the immune response from pro-inflammatory to anti-inflammatory pathways.
• It protects against fibrosis in various organs.
• It helps synchronize mitochondrial dynamics to control age-related changes.

SS-31 has gained interest from scientists due to these reasons. There’s a lot of research on this peptide, so covering everything is tough. Here’s a look at some main points, like how SS-31 stabilizes mitochondria, reduces inflammation and fibrosis in different organs, and changes oxidative stress.

SS-31 Peptide Structure

Amino acid sequence: H-D-Arg-Dmt-Lys-Phe-NH2 (Dmt is 2,6-dimethyltyrosine)
Molecular formula: C32H49N9O5
Human gene: No specific gene; synthetic peptide
Synonyms: SS-31, Elamipretide, Bendavia, MTP-131, Szeto-Schiller peptide 31

Intestinal Inflammation

One main way SS-31 works is by stabilizing mitochondria in the epithelial and immune cells of the gut. It lowers the production of ROS and pro-inflammatory cytokines, like TNF-α and IL-1β. SS-31 gets into cells and stops mitochondrial dysfunction, which helps develop anti-inflammatory responses, reduces inflammation, and fixes the barrier. SS-31 and similar compounds are being actively researched as potential modulators of inflammation in gut diseases like IBD [1], [2].

In inflammatory bowel diseases (IBD) like Crohn’s disease and ulcerative colitis, SS-31 improves the gut barrier and reduces inflammation caused by oxidative stress [3]. This action helps produce cells that create the anti-inflammatory factor interleukin-10 [4]. Mitochondrial dysfunction is critical in the development of IBD.

Improving the gut barrier is very important, as it is seen as contributing to IBD. When the barrier is damaged, more antigen material enters the space between cells, where it interacts with immune cells and causes an inflammatory response. By reducing oxidative stress, SS-31 lowers the presentation of antigens to immune cells, which interrupts the early steps leading to colitis and severe IBD [3].

SS-31 and Lung Function

SS-31 changes lung function in two ways. First, it adjusts mitochondrial function in alveolar cells, lowering ROS and suppressing pro-inflammatory cytokines like IL-6, which start fibrosis [5]. Like in other tissues, SS-31 controls inflammation in the lungs, which was hard to do in models before. Stopping fibrosis can prevent lung fibrosis, the end stage of many inflammatory conditions like COPD, idiopathic pulmonary fibrosis, and others [6]. SS-31 could help prevent the final stages of lung diseases that often need transplants and lead to high rates of illness and death.

Second, SS-31 stops the growth of fibroblasts and apoptosis in lung tissue. This growth is a long-term result of lung inflammation, especially bad in uncontrolled COPD [7]. SS-31 might help ease the effects of chronic inflammation caused by fibrosis.

Also, SS-31’s antioxidant effects, which affect cellular energy, can significantly impact the lung’s blood vessels. Early info shows that SS-31 improves gas exchange by reducing oxidative stress [8]. SS-31 looks like it could be a new treatment for improving lung function in primary inflammatory diseases, but more research is needed.

SS-31 in Transplants

A major problem in organ transplants is immune rejection. Even when the donor and recipient are well-matched, the body reacts against the transplant, which destroys it. Widespread immunosuppressants are used to solve this, but they raise the risk of infections and cause side effects, like scarring and organ fibrosis.

SS-31 research shows it affects mitochondria in immune cells, lowering the activation of pro-inflammatory pathways and helping with regeneration. By lowering oxidative stress, SS-31 prevents early immune reactions. Importantly, it mainly affects cells linked to tolerogenic signals, selectively stopping those that might cause rejection [9]. This area is being actively studied. SS-31 could lower rejection with fewer side effects and infection risks and might become key in future anti-rejection treatments.

SS-31 as a Neuroprotector

SS-31’s role in the CNS is threefold: it is an antioxidant, anti-inflammatory, and mitochondrial stabilizer. Like in other tissues, SS-31 supports the blood-brain barrier (BBB) in the CNS by lowering ROS [10]. The BBB controls what enters the brain, regulating nutrition, oxygenation, and immune functions. Its disruption is seen in the development of multiple sclerosis, Alzheimer’s disease, and stroke.

SS-31 also adjusts the buildup of beta-amyloid in mouse models of Alzheimer’s disease and has neuroprotective effects in Parkinson’s disease [11], [12]. It protects the developing brain, preventing oxidative damage and improving myelination [13]. In Parkinson’s disease, SS-31 shifts the immune balance from pro-inflammatory to anti-inflammatory pathways, reducing inflammation [14].

SS-31’s role in Alzheimer’s disease is less clear. Mitochondrial dysfunction is higher in patients with AD, and stabilization reduces beta-amyloid [15], [16]. Giving SS-31 to mice reduces beta-amyloid, supporting its importance in development.

SS-31 protects neurons by binding to cardiolipin, boosting energy use and the secretion of neurotrophic factors, which protect synapses and neurons.

Cardiac Fibrosis

Fibrosis is the last stage of many heart diseases, causing valve dysfunction, reduced contraction, filling problems, and electrical issues. As with the lungs, transplants are often needed to prevent death.

Most research focuses on preventing scarring. Some drugs slow remodeling, but they rarely completely stop fibrosis. Recent model data, though, shows that SS-31 not only slows but also reverses fibrosis, partly by lowering ROS and pro-inflammatory factors [17]. This makes sense, as mitochondrial antioxidants are the first line in preventing fibrosis.

SS-31 and COVID-19

Recent info suggests that SS-31 may ease lung problems in bad cases of COVID-19. SS-31 stops ROS production in mitochondria, protecting type 2 alveolar cells, which are responsible for gas exchange. SS-31 can prevent excessive inflammation and fibrosis caused by SARS-CoV-2 [18].

SS-31 quickly reduces inflammation in models of acute lung injury, even with other conditions present. The peptide has been studied in viral infections, showing suppression of oxidative stress.

SS-31 belongs to a group of mitochondria-targeted peptides, affecting the CNS, GI tract, lungs, and immune system. It helps with cell regeneration.

Research confirms SS-31’s ability to lower systemic inflammation, especially in neurodegenerative diseases, lung fibrosis, IBD, and cardiac fibrosis. The peptide is effective in fibrotic processes, suggesting benefits against fibrosis, which causes much illness and death.

Besides its anti-fibrotic effects (from antioxidant action), SS-31 is a strong mitochondrial protector and anti-inflammatory. It protects the CNS from damage and is useful for preserving cognitive functions during neurodegeneration.

SS-31 has shown results in clinical trials and has been quickly studied for applications. This could help develop other treatments, giving data for future trials and encouraging drug companies to create drugs with a high chance of approval.

SS-31 has minimal side effects, low oral availability, and good injectable availability in models. Model doses don’t equal human doses.

*For laboratory purposes and personal observations only.
The information is collected from numerous studies and analyses conducted over the years and is not intended to diagnose, treat, or prevent any diseases.