Studies suggest that the efficiency of mitochondria and the organism’s ability to produce energy via ATP synthesis may both be enhanced by SS-31. Scientific studies have suggested that it may decrease inflammatory cytokines, the messengers considered to be responsible for oxidative stress and inflammatory disorders like Alzheimer’s, Parkinson’s, cardiovascular disease, diabetes, renal illness, and many more.

SS-31 Peptide: What is it?

Research suggests the little aromatic peptide called SS-31 (elamipretide) may easily cross the membranes of both cells and organelles. Stabilizing the enzyme cardiolipin inside mitochondria is believed to enhance cellular energy production and inhibit the generation of reactive oxygen species (ROS or free radicals). Cardiolipin is an integral component of the electron transport chain, located within the mitochondria, and is considered to be responsible for producing most of the energy cells need to operate.

Diabetes, heart failure, Alzheimer’s disease, Parkinson’s disease, nonalcoholic fatty liver disease, cancer, chronic fatigue syndrome, HIV, and many other disorders have been linked to cardiolipin dysfunction. Mitochondrial myopathy is a collection of neuromuscular illnesses induced by mitochondrial damage; Cardiolipin is believed to be a key component of this group of diseases. Muscle atrophy, heart failure, seizures, and dementia are all considered to be symptoms of mitochondrial myopathy. Regarding peptides, SS-31 is theorized to be the pioneer in mitochondrial myopathy studies.

SS-31 Peptide and Mitochondria

One of the most prevalent types of hereditary disorders is primary mitochondrial disease (PMD). They develop when the energy-producing machinery of the mitochondria stops working properly. Different illnesses cause different symptoms, but the brain, heart, kidneys, and other systems that need a lot of energy are considered to be the most vulnerable. Nearly all mitochondrial diseases are characterized by muscle involvement and an aversion to physical activity.

Problems with ATP generation are the hallmark of PMDs and other mitochondrial illnesses. The cell’s energy currency, ATP, is considered to be essential for almost all cellular functions. Research has long focused on stabilizing ATP production in the context of mitochondrial illness. The creation of SS-31 brings researchers one step closer to that objective.

Research on animals provided the first speculation that SS-31 may revive PMDs’ energy output. In that study, SS-31 was given to rats that had experienced ischemia-perfusion damage, a non-genetic source of mitochondrial illness, in the kidneys. Reduced cell death and necrosis in the kidney, quicker recovery of ATP generation, and preserved kidney structure were all hypothesized effects of the peptide. Later, research in mice suggested SS-31 might alleviate symptoms of mitochondrial illness caused by any cause by interacting with Cardiolipin in the inner mitochondrial membrane. Additionally, it has been ascertained to alleviate age-related mitochondrial dysfunction.

After just 5 days of presentation, SS-31 appeared to improve exercise performance without unwanted effects in phase II studies. SS-31 is being tested in the context of illnesses and experimental models.

SS-31 Peptide and Ischemia

Researchers speculate the influence of SS-31 in the context of heart failure is one of its more interesting secondary research avenues for the peptide. For a long time, researchers have understood that cardiac failure negatively impacts mitochondrial function, which in turn makes heart failure worse. Studies on cardiac tissue presented with SS-31 suggest considerable enhancements in mitochondrial oxygen flow and activity of certain components relevant to ATP generation. While the design of this research did not allow for Cardiolipin rearrangement, it does raise the possibility that SS-31 may have an additional effect on mitochondrial function that should be investigated further. The fact that SS-31 could be helpful for more than just recovering ATP generation via Cardiolipin interaction has been suggested by many replications of this study. Acute and chronic effects on mitochondrial activity and changes in reactive oxygen species generation are the primary targets of the peptide’s current research.

For example, in the context of severe heart failure, studies in dogs indicate that prolonged presentation of SS-31 may enhance left ventricular function. This study purported a strong correlation between measures of mitochondrial respiration and maximum ATP synthesis and an overall improvement in left ventricular function.

The peptide SS-31 was speculated in the course of research studies to significantly lower HtrA2 levels in research models of ST-segment elevation myocardial infarction (heart attack). One way to quantify cardiomyocyte apoptosis is using HtrA2. In an acute heart attack, these findings point to SS-31’s potential in limiting damage and preserving cardiac tissue.

SS-31 peptide for sale is available on the Core Peptides website for scientists interested in further researching the compound. Please note that none of the substances mentioned in this paper have been approved for human consumption and should, therefore, not be used outside of laboratory settings and by unlicensed individuals.

References

[i] H. H. Szeto et al., “Mitochondria-Targeted Peptide Accelerates ATP Recovery and Reduces Ischemic Kidney Injury,” J. Am. Soc. Nephrol. JASN, vol. 22, no. 6, pp. 1041–1052, Jun. 2011, doi: 10.1681/ASN.2010080808.

[ii] M. P. Siegel et al., “Mitochondrial targeted peptide rapidly improves mitochondrial energetics and skeletal muscle performance in aged mice,” Aging Cell, vol. 12, no. 5, pp. 763–771, Oct. 2013, doi: 10.1111/acel.12102.

[iii] A. V. Birk et al., “The Mitochondrial-Targeted Compound SS-31 Re-Energizes Ischemic Mitochondria by Interacting with Cardiolipin,” J. Am. Soc. Nephrol. JASN, vol. 24, no. 8, pp. 1250–1261, Jul. 2013, doi: 10.1681/ASN.2012121216

[iv] K. C. Chatfield et al., “Elamipretide Improves Mitochondrial Function in the Failing Human Heart,” JACC Basic Transl. Sci., vol. 4, no. 2, pp. 147–157, Apr. 2019, doi: 10.1016/j.jacbts.2018.12.005.

[v] A. Karaa, R. Haas, A. Goldstein, J. Vockley, W. D. Weaver, and B. H. Cohen, “Randomized dose-escalation trial of elamipretide in adults with primary mitochondrial myopathy,” Neurology, vol. 90, no. 14, pp. e1212–e1221, Apr. 2018, doi: 10.1212/WNL.0000000000005255.

[vi] A. M. PhD, “Elamipretide Failed to Meet Promise of Earlier Trial Results for…,” Mitochondrial Disease News, Jan. 10, 2020. https://mitochondrialdiseasenews.com/2020/01/10/elamipretide-failed-to-meet-promise-of-earlier-trial-results-for-primary-mitochondrial-myopathy-data-show/ (accessed Jan. 06, 2024).

[vii] “Could Elamipretide Become the First Treatment Option for Primary Mitochondrial Myopathy?,” Neurology Live. https://www.neurologylive.com/view/could-elamipretide-treatment-option-primary-mitochondrial-myopathy (accessed Jan. 06, 2024).

[viii] H. N. Sabbah, R. C. Gupta, S. Kohli, M. Wang, S. Hachem, and K. Zhang, “Chronic Therapy With Elamipretide (MTP-131), a Novel Mitochondria-Targeting Peptide, Improves Left Ventricular and Mitochondrial Function in Dogs With Advanced Heart Failure,” Circ. Heart Fail., vol. 9, no. 2, p. e002206, Feb. 2016, doi: 10.1161/CIRCHEARTFAILURE.115.00220