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Elampretide (SS-31)

Author: Dr. George Shanlikian, M.D.  |   Last Updated: November 26th, 2024

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Overall Health Benefits of Elampretide

Elamipretide benefits include improving cardiovascular health, boosting brain power, preventing cancer, and protecting against kidney and lung injuries.

  • Improves cardiovascular health [1-29]
  • Boosts brain power [30-42]
  • Prevents cancer [43-48]
  • Prevents kidney injury [49-63]
  • Treats lung injury [64-66]

Key Takeaways

  • Mitochondrial Protection: Elampretide binds to cardiolipin, a lipid crucial for maintaining the structural integrity of mitochondria, protecting it from oxidative damage.
  • Energy Production: By safeguarding cardiolipin and preventing mitochondrial dysfunction, Elampretide helps maintain the mitochondria’s role as the powerhouse of the cell, ensuring continued energy production for various cellular processes.
  • Disease Mitigation: Elampretide’s protective effects on mitochondria can help prevent or reduce the impact of inherited mitochondrial diseases and some age-related diseases, which are often linked to mitochondrial dysfunction.
  • Reduction of Oxidative Stress: By minimizing the production of harmful oxidative factors, Elampretide reduces oxidative stress, which is a significant contributor to cellular damage and aging.
  • Cellular Health Restoration: Through its action on mitochondria, Elampretide aids in restoring normal cellular functions and processes, potentially improving overall cellular health and longevity.

What is Elampretide?

Elampretide, also known as elamipretide or SS-31, is a synthetic tetrapeptide that reduces the production of harmful reactive oxygen species in the body. It works by targeting the cellā€™s powerhouse known as mitochondria which in turn restores various important cellular processes. Studies show that SS-31 has anti-aging effects that are beneficial for the treatment of age-related diseases, genetic disorders, impaired blood circulation, kidney injury, and heart disease.

How Elampretide Works


The mitochondria are known as the ā€œpowerhouse of the cellā€ as they produce the energy required for various cellular processes. Dysfunctional mitochondria can lead to a wide array of inherited mitochondrial diseases and some age-related diseases. In addition, dysfunctional mitochondria produce abnormally high levels of oxidative factors that can significantly damage cardiolipin, a lipid that plays an integral role in the maintenance of the structural integrity of the mitochondria. By binding to cardiolipin, elampretide protects it from the harmful effects of oxidative stress. This in turn prevents or reduces mitochondrial membrane dysfunction and cell death. In addition, the protective effects of elampretide on the mitochondria help restore various important cellular processes.

Chemical Structure of Elamipretide

Research on Elamipretide

A. Improves Cardiovascular Health

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Studies show that elampretide (SS-31) can help protect against heart disease via different mechanisms:

  1. In the failing human heart, SS-31 improved mitochondrial function. [1]
  2. In aged mouse hearts, SS-31 significantly improved mitochondrial function. [2]
  3. In patients with type 2 diabetes, SS-31 treatment protected against cardiovascular disease by reducing reactive oxygen species levels. [3]
  4. In patients with dilated cardiomyopathy, SS-31 reversed the mitochondrial fragmentation. [4]
  5. A study showed that SS-31 can help re-energize the mitochondria of heart cells. [5]
  6. In adult male mice, SS-31 therapy protected against heart damage caused by blood vessel constriction. [6]
  7. In mice exposed to systemic inflammation, SS-31 effectively protected the heart from infection-induced heart damage by inhibiting oxidative stress and inflammation. [7]
  8. In mice with heart failure, SS-31 ameliorated cardiomyopathy, a condition that affects the pumping ability of the heart. [8]
  9. In rats suffering from cardiac arrest, SS-31 treatment increased survival time. [9]
  10. A study showed that SS-31ā€™s effect on the cellā€™s mitochondria can be considered a therapeutic strategy for treating heart failure. [10]
  11. In healthy dogs and healthy donor human hearts, long-term SS-31 therapy normalized the critical abnormalities of the mitochondria. [11]
  12. In patients with heart enlargement and weakening, 12 weeks of SS-31 treatment improved heart function. [12]
  13. In patients with narrowing of the heart arteries, SS-31 treatment resulted in improvement of the symptoms. [13]
  14. In patients with heart disease, treatment with SS-31 increased exercise tolerance. [14]
  15. In rats, SS-31 administration for 6 weeks effectively treated heart disease caused by poor blood circulation. [15]
  16. In mouse hearts, SS-31 treatment for 8 weeks significantly reduced the levels of oxidative stress. [16]
  17. In cells derived from children with dilated cardiomyopathy with ataxia syndrome (DCMA), the abnormalities in the mitochondria were reversed by incubation with SS-31 for 24 hours. [17]
  18. In old mice that received SS-31 for 8 weeks, significant improvements in skeletal muscle function and endurance, cardiac function, and exercise endurance were observed. [18]
  19. In mice with cancer receiving SS-31 in both the heart and diaphragm muscle, a significant improvement in cardiorespiratory function and respiratory chain was seen. [19]
  20. In old mice and rats, SS-31 reversed cardiac dysfunction by reducing excessive proton leak. [20-21]
  21. In old mouse hearts, SS-31 was effective at restoring different aspects of mitochondrial and heart health via the reduction of oxidative stress. [22-24]
  22. In dogs with advanced heart failure, elamipretide improved left ventricular and mitochondrial function. [25-26]
  23. In rats with insufficient blood flow to the heart, elamipretide mitigated impairments in mitochondrial structure function. [27]
  24. In patients with Barth syndrome (characterized by an enlarged heart, muscle weakness, fatigue, and low blood cell count), elamipretide improved knee extensor strength, patient global impression of symptoms, and some cardiac parameters. [28]
  25. In aged mice, SS-31 reversed age-related redox stress and improved exercise tolerance. [29]

B. Boosts Brain Power

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SS-31 has also been found to improve cognitive function through its ability to protect the neurons (nerve cells) in the brain:

  1. In mice with cognitive deficits, SS-31 treatment rescued learning and memory deficits. [30]
  2. In developing rat brains, SS-31 protected against isoflurane-induced cognitive deficits through the reversal of mitochondrial dysfunction and regulation of BDNF (brain-derived neurotrophic factor) signaling. [31-32]
  3. In aged mice, treatment with SS-31 improved working memory, motor skill learning, and gait coordination. [33]
  4. A study showed that SS-31 has therapeutic potential in preventing damage from oxidative stress and brain cell inflammation. [34]
  5. In aged mice, treatment with elamipretide significantly enhanced working memory and motor skill learning by increasing the blood flow to the brain. [35]
  6. In aged mice, SS-31 treatment was associated with significant improvements in learning and spatial working memory and lower levels of inflammatory cytokines. [36]
  7. Treatment of aged mice with the mitochondrial-targeted peptide elamipretide protected against mitochondrial dysfunction and attenuated surgery-induced cognitive deficits. [37]
  8. In hypertensive rats with traumatic brain injury, SS-31 treatment reversed cerebrovascular oxidative stress which is linked to dysregulation of blood flow to the brain and cognitive dysfunction. [38]
  9. In animal models of Parkinsonā€™s disease (PD), SS-31 exerted neuroprotective effects on dopamine neurons (which play a role in memory, movement, motivation, mood, and attention) by targeting both mitochondrial dysfunction and oxidative damage. [39]
  10. In a model of Alzheimerā€™s disease, SS-31 protected the brain cells against programmed cell death (apoptosis) and significantly reduced mitochondrial dysfunction. [40]
  11. In murine cultured microglial cells (nervous system cells), SS-31 protected the cells against lipopolysaccharide (LPS)-induced inflammation and oxidative stress by stabilizing the mitochondrial structure. [41-42]

C. Prevents Cancer

Evidence also found that SS-31ā€™s antioxidant properties and ability to protect the mitochondria from damage may play a role in preventing cancer:

  1. In mice, SS-31 prevented mitochondrial dysfunction which in turn reduced cancer prevalence. [43]
  2. Studies also suggest that restoring the function of the cellā€™s mitochondria, which is the primary action of SS-31, can help prevent cancer. [44-46]
  3. In cancer patients, SS-31 prevented cancer cachexia (muscle wasting) and improved systemic energy homeostasis. [48]

D. Prevents Kidney Injury

Studies also show that SS-31 is essential for kidney health:

  1. In mice with acute kidney injury, SS-31 treatment effectively suppressed mitochondrial reactive oxygen species which can contribute to further kidney damage. [49]
  2. In murine models of kidney injury, SS-31 was able to increase the production of angiotensin AT2 receptor (AT2R) which in turn reduced kidney damage. [50]
  3. In rats with unilateral ureteral obstruction, SS-31 significantly attenuated the effects of obstruction on all aspects of kidney damage. [51-52]
  4. In patients with severe atherosclerotic renal artery stenosis (narrowing of the kidney arteries due to blockage), intravenous infusion of elamipretide at 0.05 mg/kg per hour increased blood flow to the kidney and improved kidney function compared with placebo treatment. [53]
  5. In mice with diabetes, elamipretide protected against the progression of diabetic kidney disease. [54]
  6. In animal and cell models, SS-31 ameliorated kidney disease by preventing programmed cell death, inflammation, and scarring. [55]
  7. In pregnant mice, elamipretide was found to ameliorate the progression of kidney disease without any adverse effects. [56]
  8. In mice models of chronic kidney disease (CKD), SS-31 preserved mitochondrial integrity, ameliorated the increase in the levels of all inflammatory markers, restored glomerular filtration rate (filtering ability of the kidneys), and prevented kidney scarring. [57-58]
  9. In mice of advanced age, SS-31 improved glomerular filtration rate and mitochondrial structure. [59]
  10. In murine models of acute tubular injury and glomerular damage, SS-31 reduced damage to the kidneys by increasing the levels of the antibody known as AT2R. [60]
  11. In swine with atherosclerotic renal artery stenosis, treatment with subcutaneous elamipretide (5d/wk) for 4 weeks improved kidney function and alleviated fibrosis (scarring) and oxidative stress. [61]
  12. In mice fed with a high-fat diet, SS-31 prevented the loss of kidney cells and lipid accumulation. [62]
  13. In rats with insufficient blood flow to the kidneys (ischemia), SS-31 prevented mitochondrial swelling and protected against scarring and loss of blood vessels. [63]

E. Treats Lung Injury

SS-31 has also been found to treat various forms of lung injury:

  1. In a mouse model, SS-31 attenuated mitochondrial dysfunction, reduced inflammatory responses and alleviated the severity of lung damage. [64]
  2. In mice, SS-31 protected against spinal cord injury-induced lung injury. [65]
  3. In mice with acute liver injury due to blood infection (sepsis), the mitochondria-targeted antioxidant SS-31 reduced oxidative stress and inflammatory markers and alleviated sepsis-related acute liver injury. [66]

Elamipretide Mechanism of Action

Elamipretide, also known as SS-31 or Bendavia, exerts its therapeutic effects primarily through its unique mechanism of action targeting mitochondria. This mitochondria-targeted peptide is designed to interact with cardiolipin, a phospholipid found exclusively in the inner mitochondrial membrane. Cardiolipin plays a crucial role in maintaining mitochondrial structure and function, particularly in energy production and cellular signaling processes. In damaged or stressed mitochondria, such as those seen in various diseases and conditions, cardiolipin becomes oxidized and disrupts normal mitochondrial function. The primary outcome of many clinical trials involving Elamipretide is to assess its efficacy in restoring mitochondrial function and improving clinical symptoms.

Elamipretide binds selectively to cardiolipin and stabilizes its structure, thereby preserving mitochondrial integrity. By doing so, it helps maintain mitochondrial membrane potential and reduces the production of reactive oxygen species (ROS). ROS are byproducts of cellular respiration and can cause oxidative damage to mitochondria and other cellular components if not properly controlled. Elamipretide’s ability to reduce ROS production contributes to its antioxidant properties and helps protect mitochondria from further damage. In clinical studies, various treatment groups are established to compare the efficacy of Elamipretide against placebos or other treatments. These treatment groups allow researchers to observe the specific effects of elamipretide on mitochondrial function and overall cellular health, ensuring that any observed benefits can be attributed to the drug itself. This structured comparison is crucial for validating the therapeutic potential of Elamipretide across different patient populations and conditions.

Furthermore, elamipretide has been shown to inhibit the opening of the mitochondrial permeability transition pore (mPTP). The mPTP is a channel in the inner mitochondrial membrane whose opening can lead to mitochondrial swelling, disruption of membrane potential, and ultimately cell death. By preventing mPTP opening, elamipretide maintains mitochondrial function and promotes cell survival in conditions where mitochondrial integrity is compromised. Overall, elamipretide’s mechanism of action underscores its potential therapeutic value in various diseases characterized by mitochondrial dysfunction, including cardiovascular disorders, neurodegenerative diseases, and metabolic syndromes.

Elamipretide FDA Approval

The path to FDA approval involves rigorous phases of clinical testing. Elamipretide therapy has shown encouraging results in Phase I and II trials, demonstrating its ability to improve mitochondrial function and alleviate symptoms in patients with mitochondrial diseases. However, in Phase III trials, the outcomes have been mixed, with some studies meeting their primary endpoints and others not achieving statistically significant results. These mixed results have necessitated further investigation to better understand the drug’s efficacy across different patient populations and disease conditions. Elamipretide therapy has been particularly promising in improving energy production and reducing oxidative stress, offering hope for conditions that currently lack effective treatments.

To strengthen the case for FDA approval, researchers are focusing on refining the criteria for patient selection and optimizing dosing regimens. Additionally, long-term studies are being conducted to assess the safety and sustained efficacy of elamipretide therapy. These efforts aim to provide comprehensive data that can support the broader application of elamipretide therapy in treating a range of mitochondrial disorders, ultimately leading to its approval and widespread clinical use.

Stealth BioTherapeutics continues to work closely with the FDA, incorporating feedback and conducting additional studies to address the unmet needs in mitochondrial disease treatment. Stealth BioTherapeutics is also exploring potential biomarkers and patient-reported outcomes to strengthen its case for approval. The process underscores the complexities and challenges inherent in developing therapies for rare and multifaceted diseases. Despite the hurdles, the ongoing commitment to elamipretide research by Stealth BioTherapeutics reflects a broader hope within the scientific and medical communities that this innovative treatment will eventually gain FDA approval, providing new hope for patients suffering from debilitating mitochondrial disorders. Stealth BioTherapeutics’ dedication to advancing elamipretide therapy involves extensive collaboration with researchers and healthcare professionals. The company is focused on refining the criteria for patient selection and optimizing dosing regimens to enhance the efficacy of elamipretide therapy.

Additionally, Stealth BioTherapeutics is conducting long-term studies to assess the safety and sustained efficacy of the treatment, ensuring that it meets the highest standards for clinical application. The efforts of Stealth BioTherapeutics highlight the potential impact of elamipretide therapy on improving energy production and reducing oxidative stress in mitochondrial diseases. By addressing the specific needs of different patient populations, Stealth BioTherapeutics aims to provide comprehensive data that can support the broader application of elamipretide therapy. The ultimate goal of Stealth BioTherapeutics is to secure FDA approval and bring this promising therapy to market, offering new treatment options for patients with mitochondrial disorders. Through its ongoing research and development initiatives, Stealth BioTherapeutics is paving the way for significant advancements in mitochondrial medicine. The commitment of Stealth BioTherapeutics to addressing the challenges in this field demonstrates their dedication to improving patient outcomes and enhancing the quality of life for individuals affected by mitochondrial diseases.

SS-31 Dosage

SS-31, also known as Elamipretide, is a mitochondria-targeted peptide designed to treat mitochondrial dysfunction. Determining the appropriate dosage of SS-31 is crucial for its efficacy and safety. In preclinical studies and initial clinical trials, SS-31 has been administered in various dosages to evaluate its pharmacokinetics, therapeutic effects, and potential side effects. Typical dosages in animal studies range from 0.1 mg/kg to 10 mg/kg, tailored according to the specific model and the desired outcome. These studies have provided a foundational understanding of how SS-31 interacts with biological systems and its potential therapeutic window.

In human clinical trials, the dosage of SS-31 has been meticulously adjusted and monitored. Early phase studies often start with lower doses to ensure safety, gradually increasing to identify the maximum tolerated dose. For example, in trials involving patients with mitochondrial myopathies or heart failure, dosages have ranged from 0.25 mg/kg to 1.0 mg/kg per day, administered via daily subcutaneous injections or intravenous infusion. These trials aim to find the optimal balance between efficacy and minimizing adverse effects. The variations in dosage also help in understanding the pharmacodynamic responses in different patient populations, guiding the development of tailored treatment protocols.

The dosage regimen of SS-31 is influenced by several factors, including the specific condition being treated, the severity of the disease, and individual patient responses. Ongoing and future studies continue to refine these dosages, focusing on long-term safety and effectiveness. The goal is to establish a standardized dosage that maximizes therapeutic benefits while minimizing risks, ultimately leading to potential approval and widespread use of SS-31 in clinical practice. As research progresses, the insights gained from these studies will be crucial in informing guidelines and recommendations for the clinical use of SS-31.

SS 31 Elamipretide

SS-31, also known as elamipretide, is a synthetic tetrapeptide designed to target and protect mitochondria from oxidative damage and dysfunction. Its sequence, D-Arg-Dmt-Lys-Phe-NH2, allows it to selectively bind to cardiolipin, a phospholipid located on the inner mitochondrial membrane. By stabilizing cardiolipin, Elamipretide helps maintain mitochondrial integrity and function, preventing the formation of reactive oxygen species (ROS) and mitigating mitochondrial depolarization. This mechanism is particularly important in conditions where mitochondrial dysfunction plays a critical role, such as cardiovascular diseases, neurodegenerative disorders, and certain metabolic syndromes.

Elamipretide’s potential therapeutic applications have been explored extensively in preclinical and clinical studies. In models of heart failure, elamipretide has demonstrated the ability to improve mitochondrial function, reduce ROS production, and enhance overall cardiac function. Similarly, in models of kidney disease, it has shown promise in reducing oxidative stress and preserving renal function. Clinical trials have further highlighted its benefits; for instance, in patients with primary mitochondrial myopathy, Elamipretide has been observed to improve muscle performance and reduce fatigue. These studies suggest that by protecting mitochondria, Elamipretide can address the underlying causes of various mitochondrial-related diseases and improve patient outcomes.

One of the most significant areas of research for elamipretide has been its impact on primary mitochondrial myopathy, a condition characterized by impaired mitochondrial function leading to muscle weakness and fatigue. In clinical settings, patients with primary mitochondrial myopathy treated with Elamipretide have shown marked improvements in muscle strength and endurance, suggesting that the drug can effectively target the mitochondrial deficiencies at the heart of the disease. These findings are particularly encouraging as they offer hope for a condition with limited treatment options.

Elamipretide Side Effects

Elamipretide, also known by its research name SS-31, is a mitochondria-targeted peptide with promising therapeutic potential for various conditions linked to mitochondrial dysfunction. However, like all medications, it can have side effects. Clinical trials have reported that Elamipretide is generally well-tolerated, but some patients have experienced adverse effects. Common side effects include injection site reactions such as pain, redness, and swelling, which are typical for medications administered via injection. Additionally, some patients have reported gastrointestinal issues, including nausea and vomiting, as well as headaches and dizziness.

In some studies, patients have also experienced changes in low-luminance visual acuity, necessitating careful monitoring of visual function during treatment. Further investigation into the long-term impact of elamipretide on low-luminance visual acuity is ongoing, as understanding these effects is crucial for ensuring the safety of patients. Despite these side effects, the potential benefits of elamipretide for improving mitochondrial function and addressing related conditions make it a promising therapeutic option, with its impact on low-luminance visual acuity being an important area of focus in ongoing clinical research. Monitoring low-luminance visual acuity is essential to ensure that the benefits of elamipretide outweigh any potential risks to visual health.

Beyond these relatively mild and transient side effects, there are concerns about the potential long-term impacts of elamipretide. Since the drug is designed to alter mitochondrial function, it is crucial to monitor any unintended consequences on cellular metabolism and overall energy production. In some clinical trials, patients have experienced fatigue and muscle pain, which might be related to the drug’s impact on mitochondrial activity. While these effects were generally not severe, they underscore the need for careful monitoring and more extensive research to fully understand the safety profile of elamipretide, especially over prolonged periods of use.

Elamipretide and Inner Mitochondrial Membrane

Elamipretide is a mitochondrial-targeted peptide that has shown promise in protecting and enhancing the function of the inner mitochondrial membrane. This membrane is crucial for the mitochondria’s ability to produce ATP, the primary energy currency of the cell. By binding to cardiolipin, a lipid unique to the inner mitochondrial membrane, Elamipretide helps stabilize and protect this vital component from oxidative damage. This action preserves the structural integrity and functionality of the mitochondria, ensuring efficient energy production and overall cellular health.

The inner mitochondrial membrane houses the electron transport chain (ETC), which is responsible for oxidative phosphorylation and ATP synthesis. When oxidative stress damages the membrane, the ETC’s efficiency is compromised, leading to reduced ATP production and increased production of reactive oxygen species (ROS). Elamipretide’s protective effect on cardiolipin helps maintain the proper functioning of the ETC, reducing the generation of ROS and preventing the cascade of cellular damage that can result from mitochondrial dysfunction. This protective mechanism is particularly beneficial in conditions characterized by high oxidative stress and mitochondrial impairment.

Elamipretide and Mitochondrial Dysfunction

Elamipretide is a peptide designed to combat mitochondrial dysfunction by targeting and protecting the mitochondria, the cell’s powerhouse. It binds to cardiolipin, a crucial lipid in the inner mitochondrial membrane, preserving its integrity and preventing oxidative damage. This action helps maintain the mitochondria’s structural and functional stability, which is essential for effective energy production.

Mitochondrial dysfunction is a hallmark of many degenerative diseases and aging, characterized by reduced ATP production and increased reactive oxygen species (ROS) generation. By protecting the mitochondria from oxidative stress, Elamipretide enhances ATP synthesis and reduces ROS levels. This mitigation of oxidative damage helps prevent the cascade of cellular dysfunction that can lead to various diseases.

Elamipretide and Reactive Oxygen Species

Elamipretide is a peptide that targets mitochondria and plays a crucial role in managing reactive oxygen species (ROS). ROS are byproducts of cellular metabolism that can cause significant oxidative damage to cellular structures, including the mitochondria. By binding to cardiolipin in the inner mitochondrial membrane, Elamipretide stabilizes and protects the mitochondria, reducing the excessive production of ROS.

One of the key benefits of elamipretide is its ability to maintain the efficiency of the electron transport chain (ETC) within the mitochondria. The ETC is a primary site for ROS generation, especially when it becomes dysfunctional due to oxidative stress. Elamipretide helps ensure that the ETC operates smoothly, thereby minimizing the leakage of electrons that lead to the formation of harmful ROS.

The reduction in ROS levels brought about by Elamipretide has broad therapeutic implications. Lower ROS levels mean less oxidative damage to cellular components, which helps prevent cell death and supports overall cellular health. This protective effect is particularly beneficial in conditions characterized by high oxidative stress, such as cardiovascular diseases, neurodegenerative disorders, and age-related conditions, making Elamipretide a promising therapeutic agent.

Elamipretide Purchase

Elamipretide, a mitochondrial-targeted peptide, is primarily available for purchase through clinical research channels rather than over-the-counter or standard pharmaceutical retailers. Given its investigational status, Elamipretide is typically supplied to institutions, laboratories, and researchers conducting studies on mitochondrial dysfunction and related conditions. One key area of focus in these studies is its role in preventing cardiolipin peroxidation, a process that can damage mitochondrial membranes and impair function. Accessing this peptide for clinical or experimental purposes generally requires adherence to specific regulatory and ethical guidelines, including obtaining appropriate approvals from relevant health authorities or institutional review boards. Preventing cardiolipin peroxidation is crucial because it helps maintain mitochondrial integrity and supports overall cellular health. Continued research on Elamipretide’s ability to inhibit cardiolipin peroxidation may provide further insights into its therapeutic potential for mitochondrial diseases.

For individuals or organizations interested in purchasing Elamipretide, the process often involves directly contacting the pharmaceutical company responsible for its development, Stealth BioTherapeutics. Potential buyers might need to provide detailed information regarding the intended use, study protocols, and any necessary compliance documentation. This is particularly crucial given the role of Elamipretide in enhancing mitochondrial energy generation, which is vital for research focused on mitochondrial dysfunction. Stealth BioTherapeutics may also require assurances that the peptide will be used solely for legitimate scientific research or therapeutic purposes, aligning with their mission to advance the understanding and treatment of mitochondrial diseases. Ensuring that Elamipretide is used appropriately helps maintain the integrity of studies investigating its effects on energy generation in various cellular processes. By adhering to these guidelines, researchers can contribute to significant advancements in mitochondrial medicine, potentially improving therapeutic options for conditions related to impaired energy generation.

The cost of Elamipretide can be substantial, reflecting its specialized nature and the extensive research and development investments behind its creation. Researchers and institutions must budget accordingly and may seek funding or grants to support their acquisition and use of the peptide. While Elamipretide shows promise in various therapeutic applications, its availability remains tightly controlled to ensure its use is consistent with ongoing scientific investigations and potential clinical development. This is particularly important for adults with primary mitochondrial diseases, where precise and regulated use of Elamipretide can contribute to better understanding and management of these conditions. Furthermore, ongoing studies specifically aim to assess the benefits of elamipretide for adults with primary mitochondrial disorders, potentially paving the way for targeted therapies that can significantly improve patient outcomes.

Elamipretide Dosage

Elamipretide, also known by its investigational names such as SS-31, MTP-131, and Bendavia, has been studied across a variety of clinical settings to determine the most effective and safe dosage for its potential therapeutic benefits. The peptide is primarily administered via intravenous infusion or daily subcutaneous injections, with the dosage and frequency tailored to the specific condition being treated. Clinical trials have investigated a range of dosages, often starting with a lower dose to monitor safety and gradually increasing to assess efficacy. For example, in studies involving patients with mitochondrial myopathy, dosages have typically ranged from 0.25 mg/kg to 0.75 mg/kg administered daily.

In cardiovascular and renal studies, the dosage regimen of Elamipretide has varied based on the acute or chronic nature of the condition being addressed. For instance, in acute settings like ischemia-reperfusion injury, higher doses administered over a shorter period may be required to mitigate immediate oxidative damage. Conversely, chronic conditions such as heart failure or chronic kidney disease might necessitate prolonged administration at lower doses to achieve sustained mitochondrial protection and functional improvement. The pharmacokinetics of Elamipretide support flexibility in dosing, as it is rapidly distributed to tissues and has a relatively short half-life, necessitating regular administration to maintain therapeutic levels. Placebo-controlled trials have been essential in determining these dosing strategies, ensuring that the benefits observed are attributable to the drug and not to placebo effects. Additionally, placebo-controlled trials are critical in validating the efficacy and safety of Elamipretide across various conditions. These trials help to fine-tune the dosing regimens by comparing different dosages and administration schedules against a placebo, providing a clear understanding of the drugā€™s impact. The data gathered from placebo-controlled trials thus play a pivotal role in guiding clinical decisions and optimizing treatment protocols for both acute and chronic conditions.

While the exact optimal dosage of elamipretide is still under investigation, ongoing and completed clinical trials have provided valuable insights into its safety and efficacy profile. These studies have demonstrated the beneficial effects of Elamipretide in improving mitochondrial function and reducing oxidative stress. Common side effects observed at varying doses include injection site reactions, gastrointestinal disturbances, and transient increases in blood pressure. These trials underscore the importance of balancing efficacy with tolerability, highlighting the beneficial effects of Elamipretide in various patient populations. As research progresses, more refined dosing strategies are likely to emerge, optimizing the therapeutic benefits of elamipretide while minimizing adverse effects. Understanding the beneficial effects of elamipretide on cellular energy production and overall health is crucial for developing effective treatment protocols.

Elamipretide Price

Elamipretide, known by various names including SS-31 and Bendavia, is a mitochondria-targeting peptide currently under investigation for its potential therapeutic benefits in various conditions, such as mitochondrial diseases, heart failure, and kidney diseases. The pricing of elamipretide is not straightforward to pinpoint due to its status as an investigational drug. As it is still in clinical trials and has not yet received full regulatory approval, its price is primarily speculative and dependent on the outcomes of these trials, the approval process, and subsequent market dynamics. Typically, the cost of developing and bringing such a drug to market is high, which can significantly influence its eventual pricing.

For patients and healthcare providers, the cost of elamipretide will ultimately be influenced by multiple factors, including the cost of production, the pricing strategies of the pharmaceutical company, Stealth BioTherapeutics, and the extent to which insurance companies or national health services will cover the medication. Given the complex manufacturing process of peptides and the specialized nature of mitochondrial-targeted therapies, the drug could be expected to have a high price point upon market release. Additionally, the rarity of the conditions it aims to treat could also lead to higher prices, as is often the case with orphan drugs designed for rare diseases.

Patients interested in accessing Elamipretide before its commercial release might explore options such as enrolling in clinical trials, which can provide the medication at no cost while also contributing to valuable research. Compassionate use programs, if available, might offer another route for patients with severe or life-threatening conditions to access the drug. As Elamipretide progresses through the clinical trial phases and moves closer to potential approval, clearer information about its pricing structure and accessibility will likely become available, enabling patients, healthcare providers, and payers to better plan for its integration into therapeutic regimens.

As Elamipretide progresses through the clinical trial phases and moves closer to potential approval, clearer information about its pricing structure and accessibility will likely become available, enabling patients, healthcare providers, and payers to better plan for its integration into therapeutic regimens. Clinical trials not only help in determining the optimal dosage and potential side effects but also play a crucial role in the regulatory approval process. By participating in these trials, patients can contribute to the scientific understanding of elamipretide and expedite its journey to market availability.

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FAQ

What is the function of elamipretide?Ā Ā Ā 

The protection of cell membranes ensures that the cells can effectively regulate the passage of ions, nutrients, and waste products, thus maintaining proper cellular homeostasis. Furthermore, Elamipretide’s ability to preserve mitochondrial function also indirectly supports the stability of cell membranes, as healthy mitochondria are essential for providing the energy required for various cellular processes, including those that reinforce the structure and function of cell membranes.

What are the other names for Elamipretide?Ā Ā Ā 

Other names for Elamipretide include MTP-131, SS-31, and Bendavia. This peptide is known for its ability to modulate cytochrome c peroxidase activity, which plays a crucial role in reducing oxidative stress within cells. By enhancing cytochrome c peroxidase activity, Elamipretide helps to protect cells from oxidative damage and improve overall mitochondrial function. Additionally, the increase in cytochrome c peroxidase activity facilitated by Elamipretide can lead to more efficient removal of reactive oxygen species (ROS), thus preserving cellular health and preventing apoptosis. This property makes Elamipretide a promising candidate for treating conditions associated with mitochondrial dysfunction and oxidative stress.

Who makes Elamipretide?Ā Ā Ā Ā Ā 

Elamipretide is developed and made by Stealth BioTherapeutics. This novel therapeutic agent targets the outer mitochondrial membrane, stabilizing its structure and improving mitochondrial bioenergetics. By doing so, Elamipretide enhances overall mitochondrial function and offers potential benefits for a range of mitochondria-related diseases.

What are the other names for SS-31?Ā Ā Ā Ā 

Other names for SS-31 include Elamipretide, MTP-131, and Bendavia. SS-31 works by targeting and stabilizing the inner mitochondrial membrane, which helps to protect and restore mitochondrial function. This stabilization is crucial for maintaining the production of adenosine triphosphate (ATP), the primary energy currency of cells. By preserving ATP levels, SS-31 helps to reduce oxidative stress and prevent cellular damage in various disease conditions. The peptideā€™s ability to support mitochondrial integrity and ensure efficient ATP production makes it a valuable therapeutic agent for diseases characterized by mitochondrial dysfunction, such as mitochondrial myopathies, neurodegenerative disorders, and heart failure. Additionally, the restoration of ATP levels by SS-31 can enhance overall cellular energy metabolism, leading to improved function and vitality of affected tissues. Maintaining adequate adenosine triphosphate levels is essential for the proper functioning of high-energy-demand organs such as the heart, brain, and muscles.

What is the use of Elamipretide?Ā Ā Ā Ā 

Elamipretide is used to protect and improve mitochondrial function, potentially benefiting conditions like heart failure, kidney diseases, and diabetic complications by reducing oxidative stress and cellular damage. One of its key properties is that it readily penetrates cell membranes, allowing it to reach the mitochondria efficiently and exert its protective effects. Moreover, the fact that Elamipretide readily penetrates cell membranes ensures that it can be utilized in a wide range of tissues and organs affected by mitochondrial dysfunction. This broad applicability makes it a versatile therapeutic agent for addressing multiple pathologies linked to impaired mitochondrial function.

What is the mechanism of action of Elamipretide?Ā Ā Ā Ā Ā Ā Ā Ā 

Elamipretide works by selectively binding to cardiolipin on the inner mitochondrial membrane, stabilizing mitochondrial function, reducing reactive oxygen species production, and preventing mitochondrial depolarization and swelling. This mechanism of action makes Elamipretide particularly beneficial for a diverse patient population suffering from mitochondrial dysfunction. In clinical trials, Elamipretide has demonstrated the potential to improve outcomes in patient populations with various mitochondrial diseases, heart failure, and other conditions characterized by impaired mitochondrial function. Understanding the specific needs and responses of different patient populations will be essential in optimizing the therapeutic applications of elamipretide. Ongoing research aims to further elucidate how Elamipretide can be tailored to benefit specific patient populations, enhancing its efficacy and safety profiles across diverse medical conditions.

What class of drug is elamipretide?

Elamipretide is a mitochondria-targeted antioxidant peptide. It specifically interacts with the electron transport chain to enhance its efficiency and reduce the production of reactive oxygen species. By stabilizing the electron transport chain, Elamipretide helps maintain optimal mitochondrial function and bioenergetics. Additionally, the peptide’s interaction with the electron transport chain supports the prevention of mitochondrial dysfunction, which is crucial in the management of various mitochondria-related diseases.

What is the FDA-granted priority review?

FDA priority review is a designation given to drugs that, if approved, would offer significant improvements in the treatment, diagnosis, or prevention of serious conditions. This process ensures that promising therapies reach patients sooner, provided they demonstrate safety and efficacy with minimal adverse reactions. The FDA closely monitors clinical trials to assess any potential adverse reactions that could impact patient safety. Furthermore, during the post-marketing phase, the FDA continues to evaluate the drug to identify any long-term adverse reactions.

What are the side effects of SS-31 peptide?Ā 

FDA priority review is a designation that expedites the review process for drugs offering significant improvements in the treatment, diagnosis, or prevention of serious conditions. This designation is crucial for therapies designed to restore mitochondrial bioenergetics, as it can accelerate the availability of these treatments to patients in need. Drugs that restore mitochondrial bioenergetics can play a vital role in managing conditions associated with mitochondrial dysfunction.

What is the mechanism of action of SS-31?Ā Ā Ā 

The mechanism of action of SS-31 involves targeting and binding to cardiolipin in the inner mitochondrial membrane, thereby stabilizing mitochondrial function and reducing oxidative stress. This interaction is a significant aspect of mitochondrial biology, highlighting the peptide’s role in maintaining mitochondrial integrity. Understanding this process is crucial in the field of mitochondrial biology as it underscores how SS-31 can mitigate cellular damage. By stabilizing mitochondrial function, SS-31 helps to preserve cellular energy production and prevent mitochondrial damage, which is a key focus within mitochondrial biology research.

What are the 5 symptoms of mitochondrial disease?Ā Ā Ā Ā Ā 

Common symptoms of mitochondrial disease include muscle weakness, fatigue, neurological problems (such as seizures or strokes), gastrointestinal disorders, and cardiac abnormalities. Patients with mitochondrial disease may also experience serious adverse events, particularly when the condition progresses or is left untreated. Managing these serious adverse events is crucial in improving the quality of life for these patients. In addition, treatments need to be monitored closely for any potential serious adverse events to ensure patient safety and efficacy of the therapeutic approach.

How long can a person live with mitochondrial disease?Ā Ā Ā Ā Ā Ā Ā Ā Ā 

The life expectancy of a person with mitochondrial disease can vary widely depending on the severity and type of the disease, ranging from infancy to normal adulthood. This variability is similar to that observed in other neurodegenerative diseases, which also show a wide range of life expectancy based on disease progression and individual health factors. Understanding the overlap between mitochondrial disease and other neurodegenerative diseases can provide insights into potential treatment approaches. Research into mitochondrial disease can often inform studies on other neurodegenerative diseases, highlighting the interconnected nature of these conditions.

What is the life expectancy of someone with CPEO?Ā Ā Ā Ā Ā 

The life expectancy of someone with Chronic Progressive External Ophthalmoplegia (CPEO) is typically near normal, though it can vary based on the presence of other systemic complications. This condition primarily affects the eye muscles but can also involve other muscles and organs due to mitochondrial DNA mutations. These mutations often impact the mitochondrial matrix, where critical reactions for energy production occur. Consequently, while life expectancy remains generally stable, monitoring and managing systemic issues arising from mitochondrial dysfunction are crucial for maintaining overall health.

What are the symptoms of mitochondrial toxicity?Ā Ā Ā Ā 

Symptoms of mitochondrial toxicity include muscle weakness, fatigue, gastrointestinal issues, neuropathy, lactic acidosis, and organ dysfunction. These symptoms can significantly impact individuals with underlying conditions such as Duchenne muscular dystrophy, a severe form of muscular dystrophy characterized by progressive muscle degeneration. Patients with Duchenne muscular dystrophy are particularly vulnerable to mitochondrial toxicity, which can exacerbate their existing muscle weakness and fatigue. Effective management of mitochondrial toxicity is crucial in improving the quality of life for those affected by Duchenne muscular dystrophy. Therefore, understanding the interplay between mitochondrial toxicity and Duchenne muscular dystrophy is essential for developing targeted therapeutic strategies.

What does SS-31 do?Ā Ā Ā Ā 

Ā SS-31 is a mitochondria-targeted peptide that reduces oxidative stress, protects mitochondrial structure, and improves cellular function in various disease models. Studies using isolated mitochondria have shown that SS-31 can directly interact with cardiolipin, a crucial component of the inner mitochondrial membrane, thereby stabilizing mitochondrial function. In isolated mitochondria experiments, SS-31 has been observed to prevent the opening of the mitochondrial permeability transition pore, a key event leading to cell death. Furthermore, isolated mitochondria treated with SS-31 exhibit enhanced ATP production, which is vital for energy-demanding tissues such as the heart and brain. The protective effects of SS-31 on isolated mitochondria have been demonstrated in models of ischemia-reperfusion injury, where it mitigates damage and improves recovery. Additionally, SS-31’s ability to maintain the integrity of isolated mitochondria has shown promise in neurodegenerative diseases by preserving neuronal function. Research on isolated mitochondria continues to elucidate the broad therapeutic potential of SS-31 in various pathological conditions, highlighting its role as a versatile mitochondrial protectant.

What does Humanin do?Ā Ā Ā Ā Ā 

Humanin is a peptide that protects cells from stress and apoptosis, providing neuroprotective and cytoprotective effects in various disease models. One of the mechanisms by which Humanin exerts its protective effects is by modulating the immune response and reducing the production of proinflammatory cytokines. This reduction in proinflammatory cytokines helps to mitigate inflammation-related damage in tissues and supports cellular resilience against stressors. Additionally, Humanin’s ability to decrease the levels of proinflammatory cytokines has been shown to be beneficial in conditions such as neurodegenerative diseases and cardiovascular disorders, where inflammation plays a crucial role in disease progression. Overall, Humanin’s multifaceted protective actions make it a promising candidate for therapeutic development in a wide range of diseases.

What are the side effects of ss31 peptide?Ā Ā 

The side effects of SS-31 peptide, also known as elamipretide, may include mild to moderate injection site reactions, headache, and gastrointestinal symptoms such as nausea and vomiting. Despite these side effects, SS-31 shows promise in treating conditions associated with dysfunctional mitochondria. By targeting and stabilizing dysfunctional mitochondria, SS-31 helps improve cellular function and reduces oxidative stress. This effect is particularly beneficial in diseases where dysfunctional mitochondria play a key role, such as mitochondrial myopathies, heart failure, and neurodegenerative disorders. Ongoing clinical trials aim to further evaluate the efficacy and safety of SS-31 in various patient populations with mitochondrial diseases and other related disorders, emphasizing its potential to improve outcomes by addressing the root cause of these conditions: dysfunctional mitochondria.

What is the use of SS-31?

SS-31 is used to protect and restore mitochondrial function, thereby reducing oxidative stress and preventing cellular damage in various disease conditions. By specifically targeting the inner membrane of mitochondria, SS-31 helps to stabilize and preserve mitochondrial integrity. This stabilization is crucial for maintaining proper mitochondrial function and energy production. In addition, SS-31ā€™s ability to support the inner membrane structure makes it a valuable therapeutic agent for diseases characterized by mitochondrial dysfunction, such as mitochondrial myopathies, neurodegenerative disorders, and heart failure. The peptide’s effectiveness in reducing cellular damage and oxidative stress highlights its potential to improve patient outcomes across a range of mitochondrial-related conditions.

Reference

  1. Obi C, Smith AT, Hughes GJ, Adeboye AA. Targeting mitochondrial dysfunction with elamipretide. Heart Fail Rev. 2022 Sep;27(5):1925-1932. doi: 10.1007/s10741-021-10199-2. Epub 2022 Jan 17. PMID: 35037146.

  2. Nhu NT, Xiao SY, Liu Y, Kumar VB, Cui ZY, Lee SD. Neuroprotective Effects of a Small Mitochondrially-Targeted Tetrapeptide Elamipretide in Neurodegeneration. Front Integr Neurosci. 2022 Jan 17;15:747901. doi: 10.3389/fnint.2021.747901. PMID: 35111001; PMCID: PMC8801496.

  3. Jiang W, He F, Ding G, Wu J. Elamipretide reduces pyroptosis and improves functional recovery after spinal cord injury. CNS Neurosci Ther. 2023 Oct;29(10):2843-2856. doi: 10.1111/cns.14221. Epub 2023 Apr 20. PMID: 37081763; PMCID: PMC10493668.

  4. Pharaoh G, Kamat V, Kannan S, Stuppard RS, Whitson J, Martƭn-PƩrez M, Qian WJ, MacCoss MJ, VillƩn J, Rabinovitch P, Campbell MD, Sweet IR, Marcinek DJ. The mitochondrially targeted peptide elamipretide (SS-31) improves ADP sensitivity in aged mitochondria by increasing uptake through the adenine nucleotide translocator (ANT). Geroscience. 2023 Dec;45(6):3529-3548. doi: 10.1007/s11357-023-00861-y. Epub 2023 Jul 18. PMID: 37462785; PMCID: PMC10643647.

  5. Karanjia R, Sadun AA. Elamipretide Topical Ophthalmic Solution for the Treatment of Subjects with Leber Hereditary Optic Neuropathy: A Randomized Trial. Ophthalmology. 2024 Apr;131(4):422-433. doi: 10.1016/j.ophtha.2023.10.033. Epub 2023 Nov 3. PMID: 37923251.

  6. Grosser JA, Fehrman RL, Keefe D, Redmon M, Nickells RW. The effects of a mitochondrial targeted peptide (elamipretide/SS31) on BAX recruitment and activation during apoptosis. BMC Res Notes. 2021 May 22;14(1):198. doi: 10.1186/s13104-021-05613-9. PMID: 34022923; PMCID: PMC8141144.

  7. Chatfield KC, Sparagna GC, Chau S, et al. Elamipretide Improves Mitochondrial Function in the Failing Human Heart. JACC Basic Transl Sci. 2019;4(2):147-157. Published 2019 Apr 29. doi:10.1016/j.jacbts.2018.12.005.

  8. Available from https://www.pnas.org/content/117/26/15363.

  9. Escribano-Lopez, I., Diaz-Morales, N., Iannantuoni, F. et al. The mitochondrial antioxidant SS-31 increases SIRT1 levels and ameliorates inflammation, oxidative stress and leukocyte-endothelium interactions in type 2 diabetes. Sci Rep 8, 15862 (2018). https://doi.org/10.1038/s41598-018-34251-8.

  10. Machiraju P, Wang X, Sabouny R, Huang J, Zhao T, Iqbal F, King M, Prasher D, Lodha A, Jimenez-Tellez N, Ravandi A, Argiropoulos B, Sinasac D, Khan A, Shutt TE and Greenway SC (2019) SS-31 Peptide Reverses the Mitochondrial Fragmentation Present in Fibroblasts From Patients With DCMA, a Mitochondrial Cardiomyopathy. Front. Cardiovasc. Med. 6:167. doi: 10.3389/fcvm.2019.00167.

  11. Available from https://jasn.asnjournals.org/content/24/8/1250.

  12. Lu HI, Lee FY, Wallace CG, et al. SS31 therapy effectively protects the heart against transverse aortic constriction-induced hypertrophic cardiomyopathy damage. Am J Transl Res. 2017;9(12):5220-5237. Published 2017 Dec 15.

  13. Liu Y, Yang W, Sun X, Xie L, Yang Y, Sang M, Jiao R. SS31 Ameliorates Sepsis-Induced Heart Injury by Inhibiting Oxidative Stress and Inflammation. Inflammation. 2019 Dec;42(6):2170-2180. doi: 10.1007/s10753-019-01081-3. PMID: 31494795.

  14. Dai DF, Chen T, Szeto H, et al. Mitochondrial targeted antioxidant Peptide ameliorates hypertensive cardiomyopathy. J Am Coll Cardiol. 2011;58(1):73-82. doi:10.1016/j.jacc.2010.12.044.

  15. Zhang W, Tam J, Shinozaki K, Yin T, Lampe JW, Becker LB, Kim J. Increased Survival Time With SS-31 After Prolonged Cardiac Arrest in Rats. Heart Lung Circ. 2019 Mar;28(3):505-508. doi: 10.1016/j.hlc.2018.01.008. Epub 2018 Feb 7. PMID: 29503242; PMCID: PMC6081272.

  16. Chavez JD, Tang X, Campbell MD, Reyes G, Kramer PA, Stuppard R, Keller A, Zhang H, Rabinovitch PS, Marcinek DJ, Bruce JE. Mitochondrial protein interaction landscape of SS-31. Proc Natl Acad Sci U S A. 2020 Jun 30;117(26):15363-15373. doi: 10.1073/pnas.2002250117. Epub 2020 Jun 17. PMID: 32554501; PMCID: PMC7334473.

  17. Sabbah, H.N., Gupta, R.C., Singh-Gupta, V. et al. Abnormalities of Mitochondrial Dynamics in the Failing Heart: Normalization Following Long-Term Therapy with Elamipretide. Cardiovasc Drugs Ther 32, 319ā€“328 (2018). https://doi.org/10.1007/s10557-018-6805-y.

  18. Available from https://www.medrxiv.org/content/10.1101/2020.11.20.20235580v2.full.

  19. Available from https://www.ahajournals.org/doi/full/10.1161/circinterventions.117.005487.

  20. Available from https://europepmc.org/articles/pmc6588449/bin/nihms1005643-supplement-supplemental_material.pdf.

  21. Szeto HH, Liu S, Soong Y, et al. Mitochondria Protection after Acute Ischemia Prevents Prolonged Upregulation of IL-1Ī² and IL-18 and Arrests CKD. J Am Soc Nephrol. 2017;28(5):1437-1449. doi:10.1681/ASN.2016070761.

  22. Whitson, J. A., MartĆ­n-PĆ©rez, M., Zhang, T., Gaffrey, M. J., Merrihew, G. E., Huang, E., White, C. C., Kavanagh, T. J., Qian, W. J., Campbell, M. D., MacCoss, M. J., Marcinek, D. J., VillĆ©n, J., & Rabinovitch, P. S. (2021). Elamipretide (SS-31) treatment attenuates age-associated post-translational modifications of heart proteins. GeroScience, 43(5), 2395ā€“2412. https://doi.org/10.1007/s11357-021-00447-6.

  23. Rohani, L., Machiraju, P., Sabouny, R., Meng, G., Liu, S., Zhao, T., Iqbal, F., Wang, X., Ravandi, A., Wu, J. C., Khan, A., Shutt, T., Rancourt, D., & Greenway, S. C. (2020). Reversible Mitochondrial Fragmentation in iPSC-Derived Cardiomyocytes From Children With DCMA, a Mitochondrial Cardiomyopathy. The Canadian journal of cardiology, 36(4), 554ā€“563. https://doi.org/10.1016/j.cjca.2019.09.021.

  24. Rabinovitch P, Marcinek DJ. THE ROLE OF MITOCHONDRIAL ENERGETICS IN CARDIAC AND SKELETAL MUSCLE AGING. Innov Aging. 2018 Nov 11;2(Suppl 1):348. doi: 10.1093/geroni/igy023.1278. PMCID: PMC6227127

  25. Smuder AJ, Roberts BM, Wiggs MP, Kwon OS, Yoo JK, Christou DD, Fuller DD, Szeto HH, Judge AR. Pharmacological targeting of mitochondrial function and reactive oxygen species production prevents colon 26 cancer-induced cardiorespiratory muscle weakness. Oncotarget. 2020 Sep 22;11(38):3502-3514. doi: 10.18632/oncotarget.27748. PMID: 33014286; PMCID: PMC7517961.

  26. Zhang, H., Alder, N. N., Wang, W., Szeto, H., Marcinek, D. J., & Rabinovitch, P. S. (2020). Reduction of elevated proton leak rejuvenates mitochondria in the aged cardiomyocyte. eLife, 9, e60827. https://doi.org/10.7554/eLife.60827.

     

  27. Available from https://www.ahajournals.org/doi/abs/10.1161/res.125.suppl_1.287.

  28. Chiao, Y. A., Zhang, H., Sweetwyne, M., Whitson, J., Ting, Y. S., Basisty, N., Pino, L. K., Quarles, E., Nguyen, N. H., Campbell, M. D., Zhang, T., Gaffrey, M. J., Merrihew, G., Wang, L., Yue, Y., Duan, D., Granzier, H. L., Szeto, H. H., Qian, W. J., Marcinek, D., ā€¦ Rabinovitch, P. (2020). Late-life restoration of mitochondrial function reverses cardiac dysfunction in old mice. eLife, 9, e55513. https://doi.org/10.7554/eLife.55513.

  29. Whitson JA, Bitto A, Zhang H, Sweetwyne MT, Coig R, Bhayana S, Shankland EG, Wang L, Bammler TK, Mills KF, Imai SI, Conley KE, Marcinek DJ, Rabinovitch PS. SS-31 and NMN: Two paths to improve metabolism and function in aged hearts. Aging Cell. 2020 Oct;19(10):e13213. doi: 10.1111/acel.13213. Epub 2020 Aug 11. PMID: 32779818; PMCID: PMC7576234.

  30. Whitson, J. A., Johnson, R., Wang, L., Bammler, T. K., Imai, S. I., Zhang, H., Fredrickson, J., Latorre-Esteves, E., Bitto, A., MacCoss, M. J., & Rabinovitch, P. S. (2022). Age-related disruption of the proteome and acetylome in mouse hearts is associated with loss of function and attenuated by elamipretide (SS-31) and nicotinamide mononucleotide (NMN) treatment. GeroScience, 44(3), 1621ā€“1639. https://doi.org/10.1007/s11357-022-00564-w.

  31. Sabbah, H. N., Gupta, R. C., Kohli, S., Wang, M., Hachem, S., & Zhang, K. (2016). Chronic Therapy With Elamipretide (MTP-131), a Novel Mitochondria-Targeting Peptide, Improves Left Ventricular and Mitochondrial Function in Dogs With Advanced Heart Failure. Circulation. Heart failure, 9(2), e002206. https://doi.org/10.1161/CIRCHEARTFAILURE.115.002206.

  32. Sabbah HN, Gupta RC, Singh-Gupta V, Zhang K. Effects of elamipretide on skeletal muscle in dogs with experimentally induced heart failure. ESC Heart Fail. 2019 Apr;6(2):328-335. doi: 10.1002/ehf2.12408. Epub 2019 Jan 28. PMID: 30688415; PMCID: PMC6437430.

  33. Allen, M. E., Pennington, E. R., Perry, J. B., Dadoo, S., Makrecka-Kuka, M., Dambrova, M., Moukdar, F., Patel, H. D., Han, X., Kidd, G. K., Benson, E. K., Raisch, T. B., Poelzing, S., Brown, D. A., & Shaikh, S. R. (2020). The cardiolipin-binding peptide elamipretide mitigates fragmentation of cristae networks following cardiac ischemia reperfusion in rats. Communications biology, 3(1), 389. https://doi.org/10.1038/s42003-020-1101-3.

  34. Reid Thompson, W., Hornby, B., Manuel, R., Bradley, E., Laux, J., Carr, J., & Vernon, H. J. (2021). A phase 2/3 randomized clinical trial followed by an open-label extension to evaluate the effectiveness of elamipretide in Barth syndrome, a genetic disorder of mitochondrial cardiolipin metabolism. Genetics in medicine : official journal of the American College of Medical Genetics, 23(3), 471ā€“478. https://doi.org/10.1038/s41436-020-01006-8.

  35. Campbell, M. D., Duan, J., Samuelson, A. T., Gaffrey, M. J., Merrihew, G. E., Egertson, J. D., Wang, L., Bammler, T. K., Moore, R. J., White, C. C., Kavanagh, T. J., Voss, J. G., Szeto, H. H., Rabinovitch, P. S., MacCoss, M. J., Qian, W. J., & Marcinek, D. J. (2019). Improving mitochondrial function with SS-31 reverses age-related redox stress and improves exercise tolerance in aged mice. Free radical biology & medicine, 134, 268ā€“281. https://doi.org/10.1016/j.freeradbiomed.2018.12.031.

  36. Jia YL, Sun SJ, Chen JH, Jia Q, Huo TT, Chu LF, Bai JT, Yu YJ, Yan XX, Wang JH. SS31, a Small Molecule Antioxidant Peptide, Attenuates Ī²-Amyloid Elevation, Mitochondrial/Synaptic Deterioration and Cognitive Deficit in SAMP8 Mice. Curr Alzheimer Res. 2016;13(3):297-306. doi: 10.2174/1567205013666151218150004. PMID: 26679857.

  37. Wu J, Hao S, Sun XR, et al. Elamipretide (SS-31) Ameliorates Isoflurane-Induced Long-Term Impairments of Mitochondrial Morphogenesis and Cognition in Developing Rats. Front Cell Neurosci. 2017;11:119. Published 2017 Apr 25. doi:10.3389/fncel.2017.00119.

  38. Wu, J., Zhang, M., Li, H., Sun, X., Hao, S., Ji, M., Yang, J., & Li, K. (2016). BDNF pathway is involved in the protective effects of SS-31 on isoflurane-induced cognitive deficits in aging mice. Behavioural brain research, 305, 115ā€“121. https://doi.org/10.1016/j.bbr.2016.02.036.

  39. Tarantini, S, Valcarcelā€Ares, NM, Yabluchanskiy, A, et al. Treatment with the mitochondrialā€targeted antioxidant peptide SSā€31 rescues neurovascular coupling responses and cerebrovascular endothelial function and improves cognition in aged mice. Aging Cell. 2018; 17:e12731. https://doi.org/10.1111/acel.12731.

  40. Zhao, W., Xu, Z., Cao, J. et al. Elamipretide (SS-31) improves mitochondrial dysfunction, synaptic and memory impairment induced by lipopolysaccharide in mice. J Neuroinflammation 16, 230 (2019). https://doi.org/10.1186/s12974-019-1627-9.

  41. Tarantini, S., Valcarcel-Ares, N. M., Yabluchanskiy, A., Fulop, G. A., Hertelendy, P., Gautam, T., Farkas, E., Perz, A., Rabinovitch, P. S., Sonntag, W. E., Csiszar, A., & Ungvari, Z. (2018). Treatment with the mitochondrial-targeted antioxidant peptide SS-31 rescues neurovascular coupling responses and cerebrovascular endothelial function and improves cognition in aged mice. Aging cell, 17(2), e12731. https://doi.org/10.1111/acel.12731.

  42. Liu, Y., Fu, H., Wu, Y., Nie, B., Liu, F., Wang, T., Xiao, W., Yang, S., Kan, M., & Fan, L. (2021). Elamipretide (SS-31) Improves Functional Connectivity in Hippocampus and Other Related Regions Following Prolonged Neuroinflammation Induced by Lipopolysaccharide in Aged Rats. Frontiers in aging neuroscience, 13, 600484. https://doi.org/10.3389/fnagi.2021.600484.

  43. Zuo, Y., Yin, L., Cheng, X., Li, J., Wu, H., Liu, X., Gu, E., & Wu, J. (2020). Elamipretide Attenuates Pyroptosis and Perioperative Neurocognitive Disorders in Aged Mice. Frontiers in cellular neuroscience, 14, 251. https://doi.org/10.3389/fncel.2020.00251.

  44. Czigler, A., Toth, L., Szarka, N., Berta, G., Amrein, K., Czeiter, E., Lendvai-Emmert, D., Bodo, K., Tarantini, S., Koller, A., Ungvari, Z., Buki, A., & Toth, P. (2019). Hypertension Exacerbates Cerebrovascular Oxidative Stress Induced by Mild Traumatic Brain Injury: Protective Effects of the Mitochondria-Targeted Antioxidative Peptide SS-31. Journal of neurotrauma, 36(23), 3309ā€“3315. https://doi.org/10.1089/neu.2019.6439.

  45. Yang, L., Zhao, K., Calingasan, N. Y., Luo, G., Szeto, H. H., & Beal, M. F. (2009). Mitochondria targeted peptides protect against 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine neurotoxicity. Antioxidants & redox signaling, 11(9), 2095ā€“2104. https://doi.org/10.1089/ars.2009.2445.

  46. Reddy, P. H., Manczak, M., Yin, X., & Reddy, A. P. (2018). Synergistic Protective Effects of Mitochondrial Division Inhibitor 1 and Mitochondria-Targeted Small Peptide SS31 in Alzheimer’s Disease. Journal of Alzheimer’s disease : JAD, 62(4), 1549ā€“1565. https://doi.org/10.3233/JAD-170988.

  47. Mo, Y., Deng, S., Zhang, L., Huang, Y., Li, W., Peng, Q., Liu, Z., & Ai, Y. (2019). SS-31 reduces inflammation and oxidative stress through the inhibition of Fis1 expression in lipopolysaccharide-stimulated microglia. Biochemical and biophysical research communications, 520(1), 171ā€“178. https://doi.org/10.1016/j.bbrc.2019.09.077.

  48. Nhu NT, Xiao SY, Liu Y, Kumar VB, Cui ZY, Lee SD. Neuroprotective Effects of a Small Mitochondrially-Targeted Tetrapeptide Elamipretide in Neurodegeneration. Front Integr Neurosci. 2022 Jan 17;15:747901. doi: 10.3389/fnint.2021.747901. PMID: 35111001; PMCID: PMC8801496.

  49. Smuder AJ, Roberts BM, Wiggs MP, Kwon OS, Yoo JK, Christou DD, Fuller DD, Szeto HH, Judge AR. Pharmacological targeting of mitochondrial function and reactive oxygen species production prevents colon 26 cancer-induced cardiorespiratory muscle weakness. Oncotarget. 2020 Sep 22;11(38):3502-3514. doi: 10.18632/oncotarget.27748. PMID: 33014286; PMCID: PMC7517961.

  50. Ā Wang B, Fu J, Yu T, Xu A, Qin W, Yang Z, Chen Y, Wang H. Contradictory effects of mitochondria- and non-mitochondria-targeted antioxidants on hepatocarcinogenesis by altering DNA repair in mice. Hepatology. 2018 Feb;67(2):623-635. doi: 10.1002/hep.29518. Epub 2018 Jan 7. PMID: 28898446.

  51. Chavez JD, Tang X, Campbell MD, Reyes G, Kramer PA, Stuppard R, Keller A, Zhang H, Rabinovitch PS, Marcinek DJ, Bruce JE. Mitochondrial protein interaction landscape of SS-31. Proc Natl Acad Sci U S A. 2020 Jun 30;117(26):15363-15373. doi: 10.1073/pnas.2002250117. Epub 2020 Jun 17. PMID: 32554501; PMCID: PMC7334473.

  52. Ma W, Zhu X, Ding X, et al. Protective effects of SS31 on tā€‘BHP induced oxidative damage in 661W cells. Mol Med Rep. 2015;12(4):5026-5034. doi:10.3892/mmr.2015.4055.

  53. BallarĆ², R., Lopalco, P., Audrito, V., BeltrĆ , M., Pin, F., Angelini, R., Costelli, P., Corcelli, A., Bonetto, A., Szeto, H. H., O’Connell, T. M., & Penna, F. (2021). Targeting Mitochondria by SS-31 Ameliorates the Whole Body Energy Status in Cancer- and Chemotherapy-Induced Cachexia. Cancers, 13(4), 850. https://doi.org/10.3390/cancers13040850.

  54. BeltrĆ , M., Pin, F., BallarĆ², R., Costelli, P., & Penna, F. (2021). Mitochondrial Dysfunction in Cancer Cachexia: Impact on Muscle Health and Regeneration. Cells, 10(11), 3150. https://doi.org/10.3390/cells10113150.

  55. Available from https://www.sciencedirect.com/science/article/pii/S0753332220307149.

  56. Wyss J-C, Kumar R, Mikulic J, Schneider M, Mary J-L, Aebi JD, Juillerat-Jeanneret L and Golshayan D (2019) Differential Effects of the Mitochondria-Active Tetrapeptide SS-31 (D-Arg-dimethylTyr-Lys-Phe-NH2) and Its Peptidase-Targeted Prodrugs in Experimental Acute Kidney Injury. Front. Pharmacol. 10:1209. doi: 10.3389/fphar.2019.01209.

  57. Available from https://journals.physiology.org/doi/full/10.1152/ajprenal.00395.2007.

  58. Mizuguchi, Y., Chen, J., Seshan, S. V., Poppas, D. P., Szeto, H. H., & Felsen, D. (2008). A novel cell-permeable antioxidant peptide decreases renal tubular apoptosis and damage in unilateral ureteral obstruction. American journal of physiology. Renal physiology, 295(5), F1545ā€“F1553. https://doi.org/10.1152/ajprenal.00395.2007.

  59. Saad, A., Herrmann, S., Eirin, A., Ferguson, C. M., Glockner, J. F., Bjarnason, H., McKusick, M. A., Misra, S., Lerman, L. O., & Textor, S. C. (2017). Phase 2a Clinical Trial of Mitochondrial Protection (Elamipretide) During Stent Revascularization in Patients With Atherosclerotic Renal Artery Stenosis. Circulation. Cardiovascular interventions, 10(9), e005487. https://doi.org/10.1161/CIRCINTERVENTIONS.117.005487.

  60. Miyamoto, S., Zhang, G., Hall, D., Oates, P. J., Maity, S., Madesh, M., Han, X., & Sharma, K. (2020). Restoring mitochondrial superoxide levels with elamipretide (MTP-131) protects db/db mice against progression of diabetic kidney disease. The Journal of biological chemistry, 295(21), 7249ā€“7260. https://doi.org/10.1074/jbc.RA119.011110.

  61. Zhu, Y., Luo, M., Bai, X., Li, J., Nie, P., Li, B., & Luo, P. (2022). SS-31, a Mitochondria-Targeting Peptide, Ameliorates Kidney Disease. Oxidative medicine and cellular longevity, 2022, 1295509. https://doi.org/10.1155/2022/1295509.

     

  62. Daneshgar, N., Liang, P. I., Lan, R. S., Horstmann, M. M., Pack, L., Bhardwaj, G., Penniman, C. M., O’Neill, B. T., & Dai, D. F. (2022). Elamipretide treatment during pregnancy ameliorates the progression of polycystic kidney disease in maternal and neonatal mice with PKD1 mutations. Kidney international, 101(5), 906ā€“911. https://doi.org/10.1016/j.kint.2021.12.006.

  63. Szeto HH, Liu S, Soong Y, Seshan SV, Cohen-Gould L, Manichev V, Feldman LC, Gustafsson T. Mitochondria Protection after Acute Ischemia Prevents Prolonged Upregulation of IL-1Ī² and IL-18 and Arrests CKD. J Am Soc Nephrol. 2017 May;28(5):1437-1449. doi: 10.1681/ASN.2016070761. Epub 2016 Nov 23. PMID: 27881606; PMCID: PMC5407729.

     

  64. Available from https://www.karger.com/Article/FullText/484919.

  65. Zhu LL, Li MQ, He F, Zhou SB, Jiang W. Mitochondria Targeted Peptide Attenuates Mitochondrial Dysfunction, Controls Inflammation and Protects Against Spinal Cord Injury-Induced Lung Injury. Cell Physiol Biochem. 2017;44(1):388-400. doi: 10.1159/000484919. Epub 2017 Nov 13. PMID: 29132140.

     

  66. Available from http://www.lcgdbzz.org/en/article/doi/10.3969/j.issn.1001-5256.2022.02.025.

Other Peptides

Thymosin Alpha 1

KPV

Dihexa

Nicotinamide Riboside

5-amino-1MQ

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