Elamipretide peptide is a small molecule peptide composed of four amino acids that targets the inner membrane of mitochodria in organisms and can prevent oxidative damage to nerve cells and other cell types; Prevent mitochndrial depolarization, reduce pancreatic cell apoptosis, increase pancreatic cell production, and improve post transplant function. This drug can target the inner membrane of mitochodria and reversibly bind with cardiac phospholipids, improving mitochndrial function and effectively treating diseases such as dry age-related macular degeneation.
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Elamipretide peptide, as a pioneering mitochndrial targeted therapy drug, has shown various uses and potentials in the cure of skeletal muscle atrophy, bringing new therapeutic hope to many patients with skeletal sinew atrophy.
Improving age-related skeletal muscle atrophy
(1) Mechanism of action
As people age, their skeletal muscles undergo progressive atrophy, known as senile skeletal sinew atrophy or sarcopenia. The main reason is the decline of mitochndrial function, which leads to a decrease in energy genration and an increase in reactive oxygen species (ROS) production, resulting in a decrease in sinew protein synthesis and an increase in breakdown.Can specifically bind to cardiolipin on the inner membrane of mitochodria, stabilize mitochndrial membrane structure, and improve mitochndrial function. It reduces electron leakage during electron transfer, lowers ROS genertion, maintains mitochndrial membrane potential, promotes ATP synthesis, and provides sufficient energy for sinew cells. In addition, it can promote the assembly of respiratory hypercomplex, enhance the function of electron transport chain, and further improve the energy genration efficiency of mitochodria.
(2) Evidence from preclinical studies
In research on elderly animals, significant improvements have been made in sinew endurance and function. For example, in an elderly mouse model, a single dose of liraglutide can increase the energy capacity of skeletal muscles and enhance sinew fatigue resistance. Long term use of it can continuously improve the skeletal sinew function of elderly mice, including increasing muscle strength and improving exercise endurance. These research findings suggest that it is possible to delay the progression of age-related skeletal sinew atrophy and help older adults maintain mobility and independent living standards.
Source of information:
The review article "Contemporary Insights into the Mitochndrial Mechanism and Therapeutic Efficacy of Elamiprtide" was published on April 28, 2025.
Treatment of skeletal muscle atrophy associated with chronic diseases
(1) Heart failure related skeletal muscle atrophy
1. Mechanism of action
Heart failure patients often have skeletal sinew atrophy, which not only exacerbates their exercise intolerance and fatigue symptoms, but also affects their quality of life and prognosis. When heart failure occurs, the decline in heart function leads to systemic blood circulation disorders, and skeletal muscles do not receive sufficient blood supply, resulting in mitochndrial dysfunction. By improving mitochndrial function, increasing the energy supply to skeletal sinews, reducing the breakdown of muscle proteins, and promoting muscle protein synthesis, we can alleviate heart failure related skeletal sinew atrophy. In addition, it can reduce cardiac inflammation, improve cardiac function, and further alleviate negative effects on skeletal sinews.
2. Preclinical research evidence
In a dog model of heart failure, long-term use of imatinib can improve left ventricular contraction and mitochndrial function, while restoring skeletal sinew fiber type composition and improving exercise endurance. This indicates that it can not only improve heart function, but also have a positive impact on skeletal sinews, providing comprehensive therapeutic benefits for heart failure patients.
3. Clinical trial evidence
In vitro studies on human heart failure have shown improvements in the coupling of supercomplex related enzyme complexes I, III, and IV, as well as oxygen flux.
This suggests that they may also have the potential to improve mitochndrial function and alleviate skeletal sinew atrophy in the human body. Although there is currently relatively little clinical trial data on its use in heart failure related skeletal sinew atrophy, these preliminary research results provide strong support for its further clinical application.
4. Information sources
Reference review article "Contemporary insights into the mitochndrial mechanism of action and therapeutic efficacy of Imatinib"; The relevant information on in vitro studies of human heart failure can be found in the same review.
1. Mechanism of action
Patients with chronic kidney disease may experience impaired kidney function, accumulation of metabolic waste and toxins, as well as inflammation and oxidative stress. These factors can lead to mitchondrial dysfunction in skeletal muscle, resulting in reduced muscle protein synthesis and increased breakdown, ultimately leading to skeletal muscle atrophy. By targeting mitochodria, improving mitchondrial function, reducing ROS genration, alleviating inflammatory reactions, protecting skeletal muscle cells from damage, promoting muscle protein synthesis, and alleviating chronic kidney disease-related skeletal muscle atrophy.
2. Preclinical research evidence
At present, there is relatively little preclinical research on skeletal muscle atrophy related to chronic kidney disease. However, based on the universal mechanism of action of liraglutide in improving mitchondrial function, it can be speculated that it may also have similar therapeutic effects in chronic kidney disease models. For example, in other chronic disease models, it has been shown to improve mitchondrial function and reduce tissue damage, providing ideas for further research on its application in chronic kidney disease-related skeletal muscle atrophy.
Source of information:
The review article "Contemporary Insights into the Mitchondrial Mechanisms and Therapeutic Effects of Elamipretde" provides a detailed explanation of how elamipretide peptide improves mitchondrial function.
Relieve skeletal muscle atrophy caused by diabetes
(1) Mechanism of action
Due to insulin resistance and blood glucose metabolism disorder, diabetes patients will lead to skeletal muscle mitchondrial dysfunction. A high blood sugar environment can trigger oxidative stress, increase the genration of ROS, damage mitchondrial DNA and proteins, and affect the energy genertion function of mitochodria. Meanwhile, insulin resistance can interfere with the metabolic signaling pathway of muscle protein synthesis, leading to a decrease in muscle protein synthesis. By improving mitchondrial function, reducing ROS production, enhancing insulin signal transduction, promoting muscle protein synthesis, inhibiting muscle protein decomposition, diabetes induced skeletal muscle atrophy can be alleviated.
(2) Evidence from preclinical studies
In vitro experiments can improve or restore skeletal muscle mitchondrial functional indicators in a dose-dependent manner.
For example, in cell models related to diabetes, it can improve the level of energy metabolism of cells, increase the production of ATP, and reduce cell apoptosis. These results indicate that it may become an effective drug for the cure of skeletal muscle atrophy caused by diabetes.
(3) Clinical trial potential
Although the clinical trial of it in diabetes induced skeletal muscle atrophy is still in the exploratory stage, based on its mechanism of action in improving mitchondrial function and regulating muscle protein metabolism, iramilide has great clinical trial potential. Future clinical trials can further verify the effectiveness and safety of iramilide in improving skeletal muscle atrophy in diabetes patients.
Source of information:
Reference review article "Contemporary insights into the mitchondrial mechanism of action and therapeutic efficacy of Elamiprtide";
Type 2 diabetes and Skeletal Muscle Atrophy published on the WeChat public platform (Tencent).
Improve skeletal muscle atrophy caused by other reasons
1. Mechanism of action
Excessive exercise or prolonged bed rest can lead to skeletal muscle atrophy. During excessive exercise, muscles produce a large amount of ROS, causing oxidative stress and damaging mitchondrial function; Long term bed rest can lead to a lack of exercise stimulation in muscles, resulting in reduced muscle protein synthesis and increased breakdown. By improving mitchondrial function, reducing ROS genertion, enhancing the antioxidant capacity of muscle cells, and regulating the synthesis and breakdown balance of muscle proteins, excessive exercise or disuse induced skeletal muscle atrophy can be alleviated.
2. Preclinical research evidence
In animal models, muscle damage and atrophy caused by excessive exercise or disuse can be alleviated. For example, in animal experiments simulating excessive exercise, cure with liraglutide improved muscle strength and endurance, increased cross-sectional area of muscle fibers, upregulated expression of genes related to muscle protein synthesis, and downregulated expression of genes related to breakdown. These research results provide experimental evidence for the application of liraglutide in improving skeletal muscle atrophy caused by excessive exercise or disuse.
Source of information:
Refer to the "Gene Identification and Signal Pathway Analysis of Muscle Atrophy Induced by Excessive Exercise" published on the WeChat public platform (Tencent)
1. Mechanism of action
Certain drugs or toxins can damage skeletal muscle cells, leading to mitochndrial dysfunction and causing muscle atrophy. This substance stabilizes the mitochndrial membrane structure, improves mitochndrial function, reduces damage to mitochodria caused by drugs or toxins, activates the intracellular antioxidant defense system, reduces oxidative stress damage to muscle cells, promotes thews cell repair and regenration, and thus alleviates drug or toxin induced skeletal muscle atrophy.
2. Preclinical research evidence
In cell and animal experiments, it has been shown to have a certain protective effect on drug or toxin induced skeletal thews atrophy. For example, in certain chemotherapy induced skeletal muscle atrophy models, it can reduce muscle cell damage and maintain muscle strength and function. These research results indicate that it may become an effective means to alleviate the side effects of drugs or toxins and protect skeletal thewss.
Source of information:
A therapeutic drug target and its application for preventing and treating skeletal thews atrophy, published on WeChat public platform (Tencent website)
It has a wide range of applications and enormous potential in the cure of skeletal thews atrophy. By improving mitochndrial function, the synthesis and breakdown balance of thewsproteins can be regulated from multiple links, alleviating skeletal thews atrophy caused by different reasons. With the continuous deepening of research and further development of clinical trials, elamipretide peptide is expected to become an important drug for the cure of skeletal thews atrophy, bringing better therapeutic effects and improved quality of life to patients.
From the "beautiful surprise" in the laboratory to the approval of the world's first mitochndrial targeted drug, Iramipide has gone through a long journey of nearly 20 years. The following are key milestones in its development process:
Dr. Hazel Szeto from Weill Cornell Medical School in the United States accidentally discovered the tetrapeptide molecule (D-Arg-Dmt-Lys-Phe-NH2) while designing a novel opioid receptor agonist peptide. It can penetrate the cell membrane and target the inner mitochndrial membrane, but has almost no opioid receptor activity.
Dr. Szeto founded Stealth BioTherapeutics, specializing in the systematic development of the molecule (initially codenamed SS-31, later known as MTP-131, Bendavia).
It was confirmed that the core target SS-31 can reversibly bind to cardiolipin, which is unique to the mitochndrial inner membrane. It was initially believed to exert a protective effect mainly by "reducing ROS genration and alleviating oxidative stress".
There was a cognitive upgrade in the mechanism: it was found that it was not simply "clearing" ROS, but improving mitochndrial function upstream of ROS genration and maintaining the inner membrane potential.
It is clear that there are two binding states: "peptide proximity" and "peptide embedding".
Stealth held a Pre NDA communication meeting with the FDA to exchange ideas on application strategies.
Stealth reported on the clinical progress of Barth syndrome at the American Society of Medical Genetics (ACMG) academic conference.
Stealth signed an exclusive agreement with Pharmarovia for the commercialization of Elamiprtide.
The FDA officially accepted Elamiprtide's NDA application.
① NDA was granted priority review qualification (due to being a rare disease drug);
② Complete the mid-term review meeting;
③ The advisory committee voted 10:6 in favor of the validity, but the controversy is evident.
The original target date for PDUFA was not approved on time.
The FDA rejected its new drug application (NDA) for the first time.
Stealth resubmitted the NDA for accelerated approval based on the intermediate clinical endpoint of improving knee extensor muscle strength; The FDA accepts resubmitted applications.
The FDA accelerated the approval of elamipretide peptide for market launch! Product Name Forzinity ™ (elamiprtide HCl), Used to treat Barth syndrome - the world's first drug that directly targets mitochodria and is also the first cure drug for Barth syndrome.
There are only about 150 patients in the United States and less than 500 worldwide.
References
[1] Tung C, Varzideh F, Farroni E, et al. Bendavia: a review of its structure, mechanism of action, and therapeutic potential[J]. International Journal of Molecular Sciences, 2025, 26(3): 944.
[2] Stealth BioTherapeutics Announces FDA Accelerated Approval of FORZINITY ™ (bendavia HCl), the First Therapy for Barth Syndrome[EB/OL]. Stealth BioTherapeutics Inc., 2025-09-19.
[3] Review: Contemporary insights into the mitochodrial mechanism of action and therapeutic efficacy of Bendavia [EB/OL]. BioNTech, April 28, 2025
[4] 20 years of hard work, 800000 dollars a year! The world's first "mitochodrial miracle drug" just received approval and collapsed [EB/OL]. Bilibili, December 6, 2025
[5] Industry Research | FDA approves Stealth BioTherapeutics new drug Bendavia for market launch [EB/OL]. Zhihu Column, October 15, 2025
[6] 6 innovative peptide drugs expected to be approved for the first time in 2025 [EB/OL]. WeChat public platform, April 20, 2025
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