Peptides > SS-31


SS-31 is known for its capacity to enhance mitochondrial function and boost ATP synthesis, leading to increased energy production. Scientific studies have demonstrated its effectiveness in reducing inflammatory cytokines, which are responsible for oxidative stress and inflammatory conditions like Alzheimer’s, Parkinson’s, heart disease, diabetes, kidney disease, and various other health issues.

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1. What is SS-31?


2. SS-31 Peptide Structure


3. SS-31 Research

What is SS-31?

SS-31, also known as elamipretide, is a compact aromatic peptide with a remarkable ability to penetrate cell and organelle membranes. Its primary function is believed to involve the regulation of reactive oxygen species (ROS or free radicals) production and the enhancement of cellular energy production. This is achieved by stabilizing the enzyme cardiolipin within the mitochondria, a critical component of the inner mitochondrial membrane that plays a fundamental role in the electron transport chain – the essential mechanism for generating the majority of cellular energy.

The malfunction of cardiolipin has been identified as a contributing factor in the development of several serious diseases, including Alzheimer’s disease, Parkinson’s disease, nonalcoholic fatty liver disease, diabetes, heart failure, HIV, cancer, chronic fatigue syndrome, and more. Furthermore, cardiolipin is believed to be a significant component in mitochondrial myopathy, a group of neuromuscular disorders resulting from mitochondrial damage rather than a single disease entity. Mitochondrial myopathy encompasses a range of symptoms, from muscle weakness and intolerance to exercise, to conditions such as heart failure, seizures, and dementia. Notably, SS-31 is a groundbreaking peptide as it has undergone clinical trials as a potential treatment for mitochondrial myopathy, marking a significant advancement in this field. 

SS-31 Peptide Structure

Sequence: D-Arg-Tyr(2,6-diMe)-Lys-Phe
Molecular Formula: C32H49N9O5
Molecular Weight: 639.8 g/mol
PubChem CID: 11764719
CAS Number: 736992-21-5
Synonyms: elamipretide, MTP-131, Bendavia

SS-31 Research

Enhancing Mitochondrial Function

Primary mitochondrial diseases (PMDs) are prevalent inherited conditions stemming from mitochondrial energy production dysfunction. Symptoms vary but frequently affect high-energy-demand organs like the nervous system, heart, and kidneys. Muscle issues and exercise intolerance are common, with symptoms including fatigue, exercise intolerance, and seizures.

Mitochondrial diseases, especially PMDs, are characterized by disruptions in ATP (adenosine triphosphate) production, which is vital for cellular functions. Efforts to stabilize ATP production in mitochondrial diseases have been ongoing. The development of SS-31 offers promising prospects for achieving this goal.

Initial animal studies demonstrated that SS-31 could restore ATP production in PMDs. Rats with kidney ischemia-perfusion injury, a non-genetic cause of mitochondrial disease, were administered SS-31, resulting in kidney protection, accelerated ATP recovery, and reduced cell damage. Subsequent mouse studies revealed that SS-31 interacted with cardiolipin in mitochondria’s inner membrane and mitigated mitochondrial disease symptoms, regardless of the cause. It also showed potential in addressing age-related mitochondrial dysfunction. These findings led to SS-31 receiving orphan drug status from the FDA and advancing to clinical trials.

In phase II human trials, SS-31 improved exercise performance within just five days of treatment, with no significant safety concerns or adverse effects. However, phase III trials did not provide strong evidence of SS-31’s clinical effectiveness. Some experts believe that the trial endpoints may have been inappropriate, and further research could lead to SS-31’s approval for specific mitochondrial conditions. Dr. Bruce Cohen, director of the Neurodevelopment Science Center at Akron Children’s Hospital, emphasized the encouraging results of prior phase II trials and the need for continued investigation. Other pharmaceutical companies are also showing interest in SS-31 research, planning trials for SS-31 derivatives and exploring alternative treatment endpoints.

Currently, SS-31 is undergoing testing for various human diseases and across different trial models. It is considered safe for human use and can be prescribed under compassionate care exceptions to patients with no other treatment options. While SS-31 is on its way to becoming a mainstream medical treatment for various conditions, it is already accessible to those in need during ongoing clinical trials.

Addressing Ischemia

SS-31 holds significant promise as a treatment for heart failure, a condition known to negatively impact mitochondrial function and exacerbate the disease’s progression. Research conducted on human heart tissue treated with SS-31 demonstrates marked improvements in mitochondrial oxygen flux and the activity of specific ATP production components. Interestingly, this study did not involve cardiolipin restructuring, suggesting that SS-31 might have an alternative mechanism of action on mitochondrial function that warrants further exploration. Several studies have replicated this finding, reinforcing the idea that SS-31’s benefits extend beyond ATP production via cardiolipin interaction. Researchers are actively investigating its ability to modulate the production of reactive oxygen species and enhance mitochondrial function in both acute and chronic scenarios.

Studies involving dogs with advanced heart failure have shown that chronic SS-31 treatment can enhance left ventricular function. Measures of mitochondrial respiration and maximum ATP synthesis correlated with overall improvement in left ventricular function, suggesting that SS-31 could be a valuable long-term treatment for enhancing energy dynamics and reducing cardiac remodeling in advanced heart failure.

Trials exploring SS-31’s use in ST-segment elevation myocardial infarction (heart attack) have found that it can significantly reduce levels of HtrA2, a marker of cardiomyocyte apoptosis. These results indicate that SS-31 may be beneficial in acute heart attacks by reducing injury extent and preserving cardiac tissue.



Diabetes, while seemingly caused by a simple inadequacy in insulin secretion or function, is a complex condition with multiple pathophysiologic manifestations. In recent years, there has been growing interest in the role of mitochondrial impairment in the pathogenesis of the disease, particularly in type 2 diabetes. Treating mitochondrial dysfunction would thus be a way to ameliorate some of the long-term consequences of diabetes such as oxidative damage to small vessels. In a study in humans given SS-31, a marked decrease in the production of reactive oxygen species was observed. This suggests that SS-31 can help to reduce the oxidative damage that usually accompanies mitochondrial dysfunction and may therefore slow or halt the progression of microvascular disease in type 2 diabetes. This hypothesis is further confirmed by the finding, in the same study, that SS-31 increased levels of SIRT1. SIRT1 levels have been associated with improved insulin sensitivity and reduced inflammation in type 2 diabetes[10].

Reduces Inflammation

A theme throughout the sections above is inflammation and the ability of SS-31 to reduce it. In particular, SS-31 appears to be a potent regulator of reactive oxygen species (free radicals) and thus helps to reduce the serious oxidative stress that arises from long-term illness such as diabetes, heart disease, and more.  Research in cell cultures suggests that SS-31 reduces inflammation and oxidative stress by reducing expression of FIS1[11]. FIS1 is a mitochondrial protein that is important for mitochondrial growth and division. Elevated levels of FIS1 have been observed in a number of neurodegenerative diseases as well as a variety of cancers and are thought to be evidence of dysfunctional mitochondrial division secondary to dysfunction and inflammation.

There is also good evidence from mouse models to show that SS-31 reduces levels of the inflammatory cytokine CD-36, reduces expression of activated MnSOD, suppresses NADPH oxidase function, and inhibits NF-kappaB p65[12]. All of these are markers of high oxidative stress, so reducing their levels is indicative of reduced free radical production and an improved inflammatory status in the cell. NF-kappaB expression, in particular, is heavily associated with cellular inflammation and is chronically active in a number of inflammatory diseases like rheumatoid arthritis and inflammatory bowel disease. With SS-31, mitochondria do not undergo inflammasome activation, which is to say they don’t convert from the primary production of ATP to primarily producing ROS.

SS-31 Summary

Though SS-31 was originally of interest because it is thought to regulate mitochondrial function in the setting of mitochondrial disease, there is also good evidence that the peptide can regulate mitochondria-induced inflammation. There is a lot of active interest in using SS-31 to improve mitochondrial function and thus overall production of energy via ATP synthesis. Though initial phase III trials were not successful, it is thought that this may be more a result of the endpoints measured as opposed to a true failure of the peptide to have any effect. Currently there are ongoing phase II trials and planned phase III trials to test SS-31 in a variety of different disease states and with a variety of different outcome measures. SS-31 may very well provide the key to understanding mitochondrial dysfunction in a variety of diseases and thus may prove useful in designing advanced treatments for Alzheimer’s disease, Parkinson’s disease, heart disease, diabetes, kidney disease, and more.

Article Author

The above literature was researched, edited and organized by Dr. Logan, M.D. Dr. Logan holds a doctorate degree from Case Western Reserve University School of Medicine and a B.S. in molecular biology.


The product information featured on this website pertains exclusively to in-vitro studies. In-vitro studies, also known as ‘in glass’ studies, are conducted outside of living organisms. It’s important to emphasize that these products do not constitute medicines or drugs and have not received FDA approval for the prevention, treatment, or cure of any medical conditions, ailments, or diseases. It is crucial to note that the introduction of these products into the bodies of humans or animals is strictly prohibited by law.