SS-31
Price range: $120.00 through $260.00
Description
A single-component research material supplied for controlled research environments. Suitable for studies involving mitochondrial-targeting peptide characterization and method development in model systems.Not for human use.
Documentation & Quality Assurance
Each lot is sourced through our verified global supply chain with emphasis on traceability and quality control.These documents are reviewed internally and displayed as they become available. Independent third-party testing is also performed on select lots to confirm identity, purity, and alignment with our internal specifications.
Important Notice
This product is intended for laboratory research use only. It is not intended for human or veterinary use, and must not be used for diagnostic, therapeutic, or clinical purposes.
This material is not a drug, medical device, or dietary supplement, and has not been evaluated by the U.S. Food and Drug Administration.
Quality & Manufacturing
All materials are sourced from carefully vetted domestic and international manufacturing partners who follow quality systems consistent with ISO and cGMP principles. Each supplier is reviewed for reliability, documentation integrity, and transparency in testing.
We require a verified purity of 99% or higher and perform independent third-party spot testing to confirm that select lots meet our internal standards for identity, purity, and composition. Where available, endotoxin testing results are included on Certificates of Analysis to verify laboratory purity; their inclusion is for research quality assessment only and does not imply suitability for human or veterinary use.
All research materials are sealed for integrity and packaged for stability during storage and transport from manufacturing through final delivery.
Additional information
| Weight | 0.0625 lbs |
|---|---|
| Dosage | 10mg, 50mg |
Certificate of Analysis
Every batch undergoes independent third-party laboratory analysis to verify identity, potency, and safety. Testing includes quantitative assay verification, heavy metals screening, and comprehensive microbial analysis.
All Available COAs
Storage Instructions
All products from Apex Health Performance are manufactured using a lyophilization (freeze-drying) process. This method is designed to maintain product integrity and allows vials to remain stable during shipping for approximately 3–4 months.
Once a vial is reconstituted with bacteriostatic water, it should be stored in the refrigerator to help maintain stability. Under these conditions, reconstituted material is generally considered stable for up to 30 days.
Lyophilization is a dehydration technique in which compounds are frozen and then exposed to low pressure. This causes the water in the vial to sublimate directly from solid to gas, leaving behind a stable, crystalline white structure. This powder can be kept at room temperature until reconstitution.
Upon receipt, products should be stored away from heat and light. For short-term use, refrigeration at approximately 4°C (39°F) is suitable. For long-term storage (several months to years), vials may be placed in a freezer at approximately -80°C (-112°F). Freezing is the preferred method for preserving product stability over extended periods.
⚠️ Important Notice:
These products are intended for research use only. Not for human consumption.
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MOTS-c
Price range: $100.00 through $200.00Select options This product has multiple variants. The options may be chosen on the product page -
Research Use Only
The following peer-reviewed publications reference compounds for laboratory and in vitro research purposes only. Not for human or animal use. Not intended to diagnose, treat, cure, or prevent any disease or condition.
Published Scientific Research
Peer-reviewed laboratory studies investigating metabolic research peptides
SS-31 improves post-cardiac arrest brain injury by inhibiting microglial ferroptosis and polarization.
SS-31, a novel mitochondria-targeting peptide, has demonstrated protective effects against mitochondrial dysfunction induced by ischemia/reperfusion injury. This study aimed to investigate the neuroprotective effects of SS-31 in post-CA brain injury and clarify the underlying signaling mechanisms.
View Full Study on PubMedEnhanced Parkin-mediated mitophagy mitigates adverse left ventricular remodelling after myocardial infarction: role of PR-364.
To reveal the mechanism of PR-364, a multi-omic strategy was deployed in combination with classical functional assays using in vivo MI and in vitro cardiomyocyte models. RESULTS: In vitro cell data indicated that Parkin activation by PR-364 increased mitophagy and mitochondrial biogenesis, enhanced adenosine triphosphate production via improved citric acid cycle, altered accumulation of calcium localization to the mitochondria, and initiated translational reprogramming with increased expression of mitochondrial translational proteins.
View Full Study on PubMedMitochondrial Cardiolipin-Targeted Tetrapeptide, SS-31, Exerts Neuroprotective Effects Within In Vitro and In Vivo Models of Spinal Cord Injury.
Emerging evidence suggests that CL alterations contribute to secondary SCI pathology, but their precise role and underlying mechanisms remain fully understudied. The results showed that SS-31 reduced rotenone- and glutamate-induced mitochondrial dysfunction and neuronal death in a dose-dependent manner in vitro.
View Full Study on PubMedComprehensive dry eye therapy: overcoming ocular surface barrier and combating inflammation, oxidation, and mitochondrial damage.
Currently, anti-inflammatory drugs have shown promising efficacy in treating DED; however, such drugs are associated with side effects. This calls for investigations to overcome these challenges associated with ocular drug administration.
View Full Study on PubMedApplication research of novel peptide mitochondrial-targeted antioxidant SS-31 in mitigating mitochondrial dysfunction.
Due to the pivotal role of mitochondria in the generation of adenosine triphosphate (ATP) and the regulation of cellular homeostasis, mitochondrial dysfunction may exert a profound impact on various physiological systems, potentially precipitating a spectrum of distinct diseases. This article extensively expounds upon the superiority of SS-31 over natural antioxidants and traditional mitochondrial-targeted antioxidants, delves into its mechanisms of modulating mitochondrial function, and comprehensively summarizes its applications in alleviating mitochondrial dysfunction-associated disorders.
View Full Study on PubMedPodocyte senescence: from molecular mechanisms to therapeutics.
Therefore, understanding the aging process of podocytes will allow us to understand their susceptibility to injury and identify targeted protective mechanisms. In addition, CCAAT/enhancer-binding protein-α, transforming growth factor-β signaling, glycogen synthase kinase-3β, cycle-dependent kinase, programmed cell death protein 1, and plasminogen activator inhibitor-1 are closely related to aging.
View Full Study on PubMedResearch Use Only
The following peer-reviewed publications reference compounds for laboratory and in vitro research purposes only. Not for human or animal use. Not intended to diagnose, treat, cure, or prevent any disease or condition.
Published Scientific Research
Peer-reviewed laboratory studies investigating metabolic research peptides
SS-31 improves post-cardiac arrest brain injury by inhibiting microglial ferroptosis and polarization.
SS-31, a novel mitochondria-targeting peptide, has demonstrated protective effects against mitochondrial dysfunction induced by ischemia/reperfusion injury. This study aimed to investigate the neuroprotective effects of SS-31 in post-CA brain injury and clarify the underlying signaling mechanisms.
View Full Study on PubMedEnhanced Parkin-mediated mitophagy mitigates adverse left ventricular remodelling after myocardial infarction: role of PR-364.
To reveal the mechanism of PR-364, a multi-omic strategy was deployed in combination with classical functional assays using in vivo MI and in vitro cardiomyocyte models. RESULTS: In vitro cell data indicated that Parkin activation by PR-364 increased mitophagy and mitochondrial biogenesis, enhanced adenosine triphosphate production via improved citric acid cycle, altered accumulation of calcium localization to the mitochondria, and initiated translational reprogramming with increased expression of mitochondrial translational proteins.
View Full Study on PubMedMitochondrial Cardiolipin-Targeted Tetrapeptide, SS-31, Exerts Neuroprotective Effects Within In Vitro and In Vivo Models of Spinal Cord Injury.
Emerging evidence suggests that CL alterations contribute to secondary SCI pathology, but their precise role and underlying mechanisms remain fully understudied. The results showed that SS-31 reduced rotenone- and glutamate-induced mitochondrial dysfunction and neuronal death in a dose-dependent manner in vitro.
View Full Study on PubMedComprehensive dry eye therapy: overcoming ocular surface barrier and combating inflammation, oxidation, and mitochondrial damage.
Currently, anti-inflammatory drugs have shown promising efficacy in treating DED; however, such drugs are associated with side effects. This calls for investigations to overcome these challenges associated with ocular drug administration.
View Full Study on PubMedApplication research of novel peptide mitochondrial-targeted antioxidant SS-31 in mitigating mitochondrial dysfunction.
Due to the pivotal role of mitochondria in the generation of adenosine triphosphate (ATP) and the regulation of cellular homeostasis, mitochondrial dysfunction may exert a profound impact on various physiological systems, potentially precipitating a spectrum of distinct diseases. This article extensively expounds upon the superiority of SS-31 over natural antioxidants and traditional mitochondrial-targeted antioxidants, delves into its mechanisms of modulating mitochondrial function, and comprehensively summarizes its applications in alleviating mitochondrial dysfunction-associated disorders.
View Full Study on PubMedPodocyte senescence: from molecular mechanisms to therapeutics.
Therefore, understanding the aging process of podocytes will allow us to understand their susceptibility to injury and identify targeted protective mechanisms. In addition, CCAAT/enhancer-binding protein-α, transforming growth factor-β signaling, glycogen synthase kinase-3β, cycle-dependent kinase, programmed cell death protein 1, and plasminogen activator inhibitor-1 are closely related to aging.
View Full Study on PubMedResearch Use Only
The following peer-reviewed publications reference compounds for laboratory and in vitro research purposes only. Not for human or animal use. Not intended to diagnose, treat, cure, or prevent any disease or condition.
Published Scientific Research
Peer-reviewed laboratory studies investigating metabolic research peptides
SS-31 improves post-cardiac arrest brain injury by inhibiting microglial ferroptosis and polarization.
SS-31, a novel mitochondria-targeting peptide, has demonstrated protective effects against mitochondrial dysfunction induced by ischemia/reperfusion injury. This study aimed to investigate the neuroprotective effects of SS-31 in post-CA brain injury and clarify the underlying signaling mechanisms.
View Full Study on PubMed →Enhanced Parkin-mediated mitophagy mitigates adverse left ventricular remodelling after myocardial infarction: role of PR-364.
To reveal the mechanism of PR-364, a multi-omic strategy was deployed in combination with classical functional assays using in vivo MI and in vitro cardiomyocyte models. RESULTS: In vitro cell data indicated that Parkin activation by PR-364 increased mitophagy and mitochondrial biogenesis, enhanced adenosine triphosphate production via improved citric acid cycle, altered accumulation of calcium localization to the mitochondria, and initiated translational reprogramming with increased expression of mitochondrial translational proteins.
View Full Study on PubMed →Mitochondrial Cardiolipin-Targeted Tetrapeptide, SS-31, Exerts Neuroprotective Effects Within In Vitro and In Vivo Models of Spinal Cord Injury.
Emerging evidence suggests that CL alterations contribute to secondary SCI pathology, but their precise role and underlying mechanisms remain fully understudied. The results showed that SS-31 reduced rotenone- and glutamate-induced mitochondrial dysfunction and neuronal death in a dose-dependent manner in vitro.
View Full Study on PubMed →Comprehensive dry eye therapy: overcoming ocular surface barrier and combating inflammation, oxidation, and mitochondrial damage.
Currently, anti-inflammatory drugs have shown promising efficacy in treating DED; however, such drugs are associated with side effects. This calls for investigations to overcome these challenges associated with ocular drug administration.
View Full Study on PubMed →Application research of novel peptide mitochondrial-targeted antioxidant SS-31 in mitigating mitochondrial dysfunction.
Due to the pivotal role of mitochondria in the generation of adenosine triphosphate (ATP) and the regulation of cellular homeostasis, mitochondrial dysfunction may exert a profound impact on various physiological systems, potentially precipitating a spectrum of distinct diseases. This article extensively expounds upon the superiority of SS-31 over natural antioxidants and traditional mitochondrial-targeted antioxidants, delves into its mechanisms of modulating mitochondrial function, and comprehensively summarizes its applications in alleviating mitochondrial dysfunction-associated disorders.
View Full Study on PubMed →Podocyte senescence: from molecular mechanisms to therapeutics.
Therefore, understanding the aging process of podocytes will allow us to understand their susceptibility to injury and identify targeted protective mechanisms. In addition, CCAAT/enhancer-binding protein-α, transforming growth factor-β signaling, glycogen synthase kinase-3β, cycle-dependent kinase, programmed cell death protein 1, and plasminogen activator inhibitor-1 are closely related to aging.
View Full Study on PubMed →Important Research Notice: These products are research chemicals intended exclusively for in vitro laboratory research by qualified professionals. Not for human or animal consumption. Not approved by the FDA for any therapeutic purpose. Sold strictly for scientific research applications only.