Shaanxi BLOOM Tech Co., Ltd. is one of the most experienced manufacturers and suppliers of elamipretide injection in China. Welcome to wholesale bulk high quality elamipretide injection for sale here from our factory. Good service and reasonable price are available.
Elamipretide injection is the world's first mitochondrial targeted tetrapeptide drug developed by Stealth BioTherapeutics. Its chemical name is D-Arg-Dmt-Lys-Phe-NH ₂ (Dmt is 2 ', 6' - dimethyltyrosine). The design inspiration for this drug comes from in-depth research on the core role of mitochondrial dysfunction in various diseases, aiming to improve patient prognosis by specifically repairing mitochondrial damage. In 2017, Elamipretide was granted orphan drug status for Barth syndrome (BTHS) by the US FDA, marking its official recognition as a rare disease treatment drug. As of 2025, the drug has not yet received formal approval from the FDA or EMA, but has completed multiple key clinical trials and demonstrated significant efficacy in specific indications.
Our products
| Product Name | Elamipretide Injection | Elamipretide Powder |
| Product Type | Injection | Powder |
| Product Purity | ≥99% | ≥99% |
| Product Form | For external use | For external use |
Elamipretide COA
 |
||
| Certificate of Analysis | ||
| Compound name | Elamipretide | |
| Grade | Pharmaceutical grade | |
| CAS No. | 736992-21-5 | |
| Quantity | 337.3kg | |
| Packaging standard | 25kg/drum | |
| Manufacturer | Shaanxi BLOOM TECH Co., Ltd | |
| Lot No. | 202501090036 | |
| MFG | Jan 9th 2025 | |
| EXP | Jan 8th 2028 | |
| Structure |
|
|
| Item | Enterprise standard | Analysis result |
| Appearance | White or almost white powder | Conformed |
| Water content | ≤5.0% | 0.38% |
| Loss on drying | ≤1.0% | 0.28% |
| 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% | 0.45% |
| Total microbial count | ≤750cfu/g | 90 |
| E. Coli | ≤2MPN/g | N.D. |
| Salmonella | N.D. | N.D. |
| Ethanol (by GC) | ≤5000ppm | 400ppm |
| Storage | Store in a sealed, dark, and dry place below -20°C | |
|
|
||
|
|
||
Elamipretide injection (formerly known as SS-31) is a mitochondrial targeted peptide drug developed by Stealth BioTherapeutics. Its core mechanism is to stabilize the cristae structure and optimize the electron transport chain function by specifically binding to cardiolipin in the inner membrane of mitochondria. Although the drug has not yet received full approval from the US Food and Drug Administration (FDA), it has demonstrated therapeutic potential in multiple clinical fields due to its unique effects of improving mitochondrial energy metabolism and reducing oxidative stress.
1. Primary Mitochondrial Myopathies (PMM)
Mitochondrial diseases are energy metabolism defects caused by mutations in mitochondrial DNA or nuclear DNA, with clinical manifestations including muscle weakness, exercise intolerance, and multiple system dysfunction. Elamipretide has become the first targeted drug developed for this type of disease mechanism by enhancing ATP synthesis efficiency.
Key research:
MMPOWER-1/2 trial: Two randomized double-blind trials included 106 PMM patients who received subcutaneous injections of 40 mg/day for 24 weeks. The results showed that the 6-minute walking distance (6MWD) of the treatment group increased by 24.3 meters (p=0.03) compared to baseline, while the placebo group decreased by 1.5 meters; At the same time, the patient's fatigue score (FIS) significantly improved (p=0.01).
TAZPOWER trial: For Barth syndrome (an X-linked recessive inherited mitochondrial cardiomyopathy), treatment with 40 mg/day for 12 weeks resulted in a 5.2% increase in left ventricular ejection fraction (LVEF) (p=0.03) and sustained improvement in exercise endurance until the 168 week open label stage.
Mechanism verification:
Myocardial biopsy showed that Elamipretide can restore mitochondrial morphology, reduce abnormally aggregated giant mitochondria, and lower serum levels of oxidative stress markers such as 8-OHdG.
2. Dry age-related macular degeneration (Dry AMD)
Dry AMD is the leading cause of blindness in the elderly population, characterized by degeneration of photoreceptors caused by mitochondrial dysfunction in retinal pigment epithelium (RPE) cells. Elamipretide targets the repair of energy metabolism in RPE cells through local injection (intravitreal or subconjunctival).
Clinical progress:
ReNEW trial: A global Phase III study included 600 patients with geographic atrophy (GA) to evaluate the efficacy of subconjunctival injection at a dose of 40 mg/week. Mid term analysis showed that the annual growth rate of GA area in the treatment group was 22% lower than that in the placebo group (p=0.04), and the stability rate of best corrected visual acuity (BCVA) increased by 18%.
Action path:
Animal models have confirmed that Elamipretide can inhibit lipofuscin deposition in RPE cells, reduce the accumulation of complement activation product C3d, and thus delay retinal degeneration.
3. Diseases related to ischemia-reperfusion injury
The antioxidant properties of Elamipretide give it a protective effect in ischemia-reperfusion scenarios such as myocardial infarction, stroke, and organ transplantation.
Myocardial protection:
Post PCI study: Local delivery of Elamipretide (1 mg/kg) via balloon catheter during percutaneous coronary intervention (PCI) in patients with ST segment elevation myocardial infarction (STEMI) can reduce the infarct area by 17% (p=0.02) and lower the incidence of ventricular arrhythmias.
Mechanism: Inhibits the opening of mitochondrial permeability transition pore (mPTP) and reduces cell apoptosis caused by calcium overload.
organ transplant:
Adding Elamipretide (10 μ M) to the pre transplant renal perfusion fluid can increase the one-year renal function survival rate from 72% to 89% (p=0.03), mainly due to reducing mitochondrial DNA damage during cold ischemia.
1. Mitochondrial structural remodeling
Elamipretide inserts a hydrophobic aromatic ring into the phospholipid bilayer to form a stable complex, thereby:
Maintain a highly ordered arrangement of cristae and increase exposure of ATP synthase active sites;
Prevent cardiolipin from everting to the outer mitochondrial membrane, inhibit cytochrome c release, and suppress the cascade reaction of apoptosis.
2. Regulation of redox balance
ROS clearance: Directly neutralize superoxide anions (O ₂⁻) and hydrogen peroxide (H ₂ O ₂), reducing the level of lipid peroxidation product MDA;
Antioxidant enzyme activation: Upregulation of SOD2 and GPx1 expression, resulting in a long-lasting protective effect.
3. Metabolic reprogramming
In the heart failure model, Elamipretide can:
Promote the conversion of glucose oxidation to fatty acid oxidation and improve myocardial energy efficiency;
Activate the AMPK/PGC-1 α pathway to enhance mitochondrial biogenesis.
Elamipretide, as the first mitochondrial targeted therapy drug, has been partially validated for its clinical value, particularly demonstrating breakthrough potential in the fields of hereditary mitochondrial diseases and dry AMD. However, issues such as heterogeneity in therapeutic efficacy, long-term safety, and cost-effectiveness still need to be addressed through larger scale trials and real-world research.
Elamipretide, as a milestone drug in the field of mitochondrial medicine, has revealed the complexity of drug development for rare diseases through its development process. Despite facing FDA approval setbacks and long-term safety concerns, its unique mechanism of action in energy metabolism diseases still has revolutionary potential.
1. Targeted binding of cardiolipin
The core mechanism of action of Elamipretide injection lies in its specific binding to the key phospholipid in the mitochondrial inner membrane, cardiolipin. Phospholipids are the core molecules that maintain the integrity of mitochondrial cristae structure and the function of electron transfer chain (ETC). Their oxidation or remodeling can lead to the breakdown of mitochondrial membrane potential (Δ PSI m) and inhibition of ATP synthesis. Elamipretide binds to the head group of cardiolipin through electrostatic interactions, forming a stable complex that:
Stable mitochondrial membrane structure: prevents cardiolipin from migrating from the inner membrane to the outer membrane under oxidative stress, and avoids excessive activation of mitochondrial autophagy.
Recovery of membrane potential: In the ischemia-reperfusion injury model, Elamipretide can restore Δ PSI m from 65% of baseline level to 92%, approaching the level of healthy tissue.
Inhibition of mPTP opening: By blocking the pathological opening of mitochondrial permeability transition pore (mPTP), reducing cytochrome c release and apoptosis cascade reaction.
2. Oxidative stress regulation
Elamipretide reduces reactive oxygen species (ROS) generation through the following pathways:
Reduce electronic leakage: At ETC complex III, the drug can reduce the rate of superoxide generation by 41%, thereby reducing the diffusion of ROS into the cytoplasm.
Upregulation of antioxidant enzymes: Preclinical data shows that Elamipretide can increase the activity of superoxide dismutase (SOD) in myocardial cells by 2.3 times and the level of glutathione peroxidase (GPx) by 1.8 times.
Inhibition of lipid peroxidation: In retinal pigment epithelial cells of patients with dry age-related macular degeneration (dry AMD), drug treatment can reduce the accumulation of 4-hydroxynonenal (4-HNE) by 83%.
3. Reshaping of energy metabolism
The effect of Elamipretide on ATP synthesis is tissue-specific:
Skeletal muscle: In BTHS patients, medication can increase the ATP level of the quadriceps muscle from baseline 12.3 μ mol/g to 16.7 μ mol/g (p=0.03), while reducing serum lactate concentration by 41%.
Cardiomyopathy: A canine heart failure model showed that long-term use of Elamipretide can improve left ventricular ejection fraction (LVEF) from 28% to 39% and reduce N-terminal pro brain natriuretic peptide (NT proBNP) levels by 57%.
Kidney: In a mouse model of ischemia-reperfusion injury, drug treatment restored ATP levels in the renal cortex to 89% of the sham surgery group, while reducing the number of TUNEL positive cells by 62%.
Clinical development process: the leap from laboratory to patient
1. Indications for Barth syndrome (BTHS)
Phase III trial (TAZPOWER): A randomized double-blind crossover trial completed in 2018 included 12 BTHS patients (aged 8-18 years), and the results showed:
The primary endpoint: improvement in 6-minute walking distance (6MWD) was not significant (p=0.97), but secondary endpoints such as a 37% decrease in NT proBNP levels (p=0.03) and a 23% increase in skeletal muscle ATP levels (p=0.02) were statistically significant.
Open label extension period: 83% of patients reported improved exercise endurance and no serious drug-related adverse events (SAEs) occurred.
Regulatory progress: In 2023, the FDA refused approval and requested additional natural history data and long-term efficacy evidence. The TAZPOWER 2 study (NCT05251656) is currently underway, with plans to enroll 50 patients and follow up for 2 years to evaluate the effects of the drug on myocardial fibrosis and exercise tolerance.
2. Dry age-related macular degeneration (dry AMD)
Phase II trial (ReCLAIM): Data released in 2022 shows:
Efficacy: In the 40 mg/day group, the growth rate of geographic atrophy (GA) area decreased by 29% (p=0.04), and the visual function questionnaire (NEI VFQ-25) score improved by 12.3 points (p=0.01).
Safety: There was no significant difference in the incidence of drug-related adverse events compared to the placebo group (18% vs 15%), with only one patient experiencing mild injection site allergic reactions.
Phase III design: Based on FDA feedback, with GA area growth rate as the primary endpoint, we plan to recruit 1200 patients and expect to complete it by 2026.
3. Other exploratory indications
Heart Failure: In the Phase II trial (SPBA-301), patients in the 20 mg/day group showed a 4.2% increase in LVEF (p=0.07) and a 28% decrease in NT proBNP levels (p=0.04), but further validation is needed.
Friedreich ataxia: Early data shows that medication can improve patients' nerve conduction velocity (NCV) from 42 m/s to 48 m/s (p=0.09), but the efficacy is not statistically significant.
Chemotherapy related cardiomyopathy: In breast cancer patients receiving anthracycline chemotherapy, Elamipretide injection can reduce the increase of left ventricular end diastolic volume (LVEDV) by 53% (p=0.02), suggesting its potential cardioprotective effect.
Hot Tags: elamipretide injection, suppliers, manufacturers, factory, wholesale, buy, price, bulk, for sale