SS-31 injection is a novel drug molecule and a pioneering mitochondrial targeted therapy drug. It is mainly used in clinical treatment to improve muscle strength in adult and pediatric patients with Bart's syndrome weighing at least 30 kilograms (approximately 66 pounds). It is a synthetic peptide that targets mitochondria and specifically binds to cardiolipin on the inner membrane of mitochondria. It is a therapeutic drug that can be used to treat diseases such as Alzheimer's disease, skeletal muscle atrophy, and cardiovascular disease.
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SS-31 COA
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| Certificate of Analysis | ||
| Compound name | SS-31/Elamipretide | |
| Grade | Pharmaceutical grade | |
| CAS No. | 736992-21-5 | |
| Quantity | 80g | |
| Packaging standard | PE bag+Al foil bag | |
| Manufacturer | Shaanxi BLOOM TECH Co., Ltd | |
| Lot No. | 202601090056 | |
| MFG | Jan 9th 2026 | |
| EXP | Jan 8th 2029 | |
| Structure |
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| Item | Enterprise standard | Analysis result |
| Appearance | White or almost white powder | Conformed |
| Water content | ≤5.0% | 0.25% |
| Loss on drying | ≤1.0% | 0.17% |
| Heavy Metals | Pb≤0.5ppm | N.D. |
| As≤0.5ppm | N.D. | |
| Hg≤0.5ppm | N.D. | |
| Cd≤0.5ppm | N.D. | |
| Purity (HPLC) | ≥99.0% | 99.80% |
| Single impurity | <0.8% | 0.26% |
| Total microbial count | ≤750cfu/g | 233 |
| E. Coli | ≤2MPN/g | N.D. |
| Salmonella | N.D. | N.D. |
| Ethanol (by GC) | ≤5000ppm | 419ppm |
| Storage | Store in a sealed, dark, and dry place below -20°C | |
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| Chemical Formula | C32H49N9O5 |
| Exact Mass | 639 |
| Molecular Weight | 640 |
| m/z | 639 (100.0%), 640 (34.6%), 641 (3.1%), 641 (2.7%), 640 (2.2%), 640 (1.1%), 641 (1.0%) |
| Elemental Analysis | C, 60.07; H, 7.72; N, 19.70; O, 12.50 |
SS-31 injection, as a pioneering mitochondrial targeted therapy drug, has shown significant efficacy in the treatment of cardiovascular disease and Barth's syndrome. In cardiovascular disease, it protects myocardial cells from damage and delays the progression of heart failure by improving mitochondrial function, regulating energy metabolism, and inhibiting inflammatory responses. In Bart's syndrome, direct targeting of the root cause of the disease (defects in cardiolipin synthesis) restores mitochondrial function, significantly improving muscle strength, exercise endurance, and cardiac function, enhancing patients' quality of life, and prolonging survival. Its approval for market launch provides the first effective treatment for patients with Barth's syndrome and opens up new directions for the treatment of mitochondrial diseases.
Application in the treatment of cardiovascular diseases
1. Improving heart function and treating heart failure
By targeting the inner membrane of mitochondria and specifically binding to cardiac phospholipids, the mitochondrial membrane structure is stabilized and the assembly of respiratory chain hypercomplex is promoted, thereby enhancing the efficiency of mitochondrial energy generation. This mechanism plays a crucial role in the treatment of heart failure. The myocardial cells of heart failure patients have decreased contractile function due to energy metabolism disorders, while the restoration of mitochondrial function significantly enhances the ATP production ability of myocardial cells.
In a canine heart failure model, long-term use can improve left ventricular systolic function, reduce cardiac load, and decrease levels of inflammatory factors. In addition, it can alleviate cardiac fibrosis, inhibit myocardial cell apoptosis, and thus delay the progression of heart failure.
2. Protect myocardial cells from ischemia-reperfusion injury
Myocardial ischemia-reperfusion injury is a common complication in cardiovascular events such as acute myocardial infarction, and its core mechanism is oxidative stress and cell apoptosis caused by mitochondrial dysfunction.
By stabilizing mitochondrial membrane potential, reducing reactive oxygen species (ROS) generation, and inhibiting the opening of mitochondrial permeability transition pores (mPTP), myocardial cells are protected from ischemia-reperfusion injury. In the rat heart ischemia-reperfusion model, pretreatment can significantly reduce the myocardial infarction area, improve cardiac function recovery, and reduce the expression of myocardial cell apoptosis markers (such as caspase-3).
3. Regulating cardiac energy metabolism and fatty acid oxidation
The energy metabolism pattern of myocardial cells in heart failure patients changes, with reduced fatty acid oxidation and increased glucose utilization, leading to a decrease in energy generation efficiency. By promoting the assembly of mitochondrial respiratory chain hypercomplex and enhancing the activity of fatty acid oxidase, the balance of cardiac energy metabolism can be restored. In the pig model of hypercholesterolemia induced renal vascular hypertension, it can improve left ventricular diastolic function, alleviate cardiac hypertrophy, and does not affect blood pressure and systolic function. Its mechanism is closely related to regulating cardiac energy metabolism.
4. Inhibit cardiac inflammatory response
Chronic inflammation is an important driving factor for the progression of cardiovascular disease. SS-31 injection reduces mitochondrial ROS generation and inhibits the activation of NLRP3 inflammasome, thereby lowering the expression of cardiac inflammatory factors such as IL-6 and TNF - α. In fibroblasts of patients with dilated cardiomyopathy with ataxia syndrome (DCMA), mitochondrial fragmentation and excessive ROS generation can be reversed, inflammatory cytokine release can be reduced, and cardiac function can be improved.
5. Clinical research evidence
TAZPOWER trial: In patients with Bart's syndrome, a genetic disease characterized by cardiomyopathy, treatment with liraglutide significantly improved left ventricular stroke volume (by over 40%) and reduced N-terminal pro brain natriuretic peptide (NT proBNP) levels, suggesting its cardioprotective effect.
Elderly heart failure model: In an elderly mouse model of left ventricular diastolic dysfunction, treatment with liraglutide for 8 weeks can normalize left ventricular diastolic function, improve exercise endurance, and reduce cardiac hypertrophy.
Chronic cardiac stress overload model: Enramiside can prevent stress-induced myocardial necrosis and apoptosis, prevent premature animal death, and its mechanism is related to the inhibition of mitochondrial ROS generation and inflammatory response.
Source of information:
BioNTech Review: Contemporary Insights into the Mitochondrial Mechanisms and Therapeutic Effects of Elamipretide "(published on April 28, 2025)
WeChat Public Platform (Tencent) "FDA Approval of Forzinity: A New Hope for Patients with Barth's Syndrome" (Published on October 12, 2025)
WeChat public platform (Tencent) "Elamipretide, a potential new drug for Barth syndrome, re enters review in the United States" (published on August 25, 2025)
Application in the treatment of Barth's syndrome
1. Improve muscle strength and exercise endurance
Bart's syndrome is an X-linked inherited mitochondrial disease caused by mutations in the TAFAZZIN gene leading to defects in cardiolipin synthesis and mitochondrial dysfunction. Patients present with severe muscle weakness, exercise intolerance, and fatigue, with 85% of children dying before the age of 5. Ilamiside targets the inner membrane of mitochondria, stabilizes the structure of cardiac phospholipids, promotes the assembly of respiratory chain hypercomplex, and thus restores the energy generation ability of muscle cells.
In the TAZPOWER clinical trial, 12 patients with Barth's syndrome were subcutaneously injected with 40mg of liraglutide daily. After 12 weeks, the knee extensor muscle strength increased by 45%, the average six minute walking distance increased by 95.9 meters, and the left ventricular stroke volume increased by over 40%. Long term use resulted in continuous improvement of patient function, while the heart function of the control group of patients with natural disease course continued to deteriorate.
2. Relieve abnormal heart function
Patients with Bart's syndrome often have cardiomyopathy, manifested as dysfunction of left ventricular contraction and relaxation. Ilamiside improves mitochondrial function in myocardial cells, enhances cardiac energy supply, and thus reduces cardiac burden. In a canine heart failure model, long-term use of liraglutide can reduce NT proBNP levels (a biomarker of heart failure) and decrease the expression of pro-inflammatory cytokines (such as IL-6), suggesting its cardioprotective effect.
3. Reduce oxidative stress and inflammatory response
The TAFAZZIN gene mutation leads to defects in cardiolipin synthesis, causing increased mitochondrial ROS production and oxidative stress, further damaging muscle and heart tissues. SS-31 injection stabilizes mitochondrial membrane structure, reduces ROS leakage, and inhibits NLRP3 inflammasome activation, thereby reducing levels of inflammatory factors. In fibroblasts of DCMA patients, imatinib can reverse mitochondrial fragmentation and excessive ROS generation, reduce the release of inflammatory factors, and improve tissue damage.
4. Improve quality of life and prognosis
Patients with Bart's syndrome have significantly reduced quality of life due to muscle weakness and abnormal heart function, requiring assistance with daily activities such as dressing and climbing stairs. Treatment can significantly improve patients' exercise endurance and muscle strength, thereby improving their daily life functions. In the TAZPOWER trial, patients' overall impression score of symptoms significantly improved, and long-term use can delay disease progression and reduce mortality.
5. Clinical application and regulatory approval
On September 19, 2025, the US FDA accelerated the approval of Forzinity, a peptide used to improve muscle strength in patients with Bart's syndrome weighing ≥ 30 kilograms. This is the world's first mitochondrial targeted therapy drug and the first approved therapy for Bart's syndrome. Approved open label extension data based on the TAZPOWER trial, showing sustained improvement in knee extensor muscle strength and significant correlation with the results of the six minute walk test.
Source of information:
WeChat public platform (Tencent) "FDA grants FORZINITY accelerated approval for the treatment of Barth syndrome" (published on September 22, 2025)
WeChat public platform (Tencent) "20 years of hard work, 800000 US dollars a year! The world's first 'mitochondrial miracle drug' just got approved and collapsed" (published on December 6, 2025)
ChemicalBook (Booker Chemical Network) "Mechanism of Action and Indications of Ilamiside" (published on January 20, 2026)
Arterial network (arterial orange) "FDA grants FORZINITY accelerated approval for the treatment of Barth syndrome" (published on September 19, 2025)
FAQ
What does peptide SS-31 do?
SS-31 Peptide and Kidney Disease | Causes of Kidney Disease ...SS-31 (Elamipretide) is a synthetic peptide used to enhance mitochondrial function, reduce reactive oxygen species (ROS), and prevent cellular apoptosis (cell death). It primarily acts as a mitochondria-targeted antioxidant, improving ATP production and managing conditions related to energy failure, including kidney, heart, eye, and neurodegenerative diseases.
Is SS-31 peptide legal?
The FDA has officially approved SS-31 (elamipretide), a mitochondria-targeted peptide previously popular in the longevity space, for the treatment of Barth syndrome, a rare genetic disorder.
Can SS-31 reverse aging?
Mitochondrial function was assessed in vivo using 31P and optical spectroscopy. SS-31 reversed age-related decline in maximum mitochondrial ATP production (ATPmax) and coupling of oxidative phosphorylation (P/O).
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