1101113-39-6
Chemical Structure
MitoTEMPOL
- CAS No.: 1101113-39-6
- Formula:C32H42BrNO2P*
- Molecular Weight:583.56
IUPAC Name: triphenyl(5-((2,2,6,6-tetramethyl-1-(l1-oxidanyl)piperidin-4-yl)oxy)pentyl)phosphonium bromide
InChIKey: NCMZESLTQCMFES-UHFFFAOYSA-M
SMILES: [O]N1C(C)(CC(CC1(C)C)OCCCCC[P+](C2=CC=CC=C2)(C3=CC=CC=C3)C4=CC=CC=C4)C.[Br-]
Biological Activity: MitoTEMPOL is a mitochondria-targeted superoxide scavenger. MitoTEMPOL accumulates in mitochondria via membrane potential and locally scavenges superoxide anions. MitoTEMPOL alleviates hepatic oxidative stress and alterations in genes related to autophagy in STZ (HY-13753)-induced diabetic models. MitoTEMPOL inhibits diaphragmatic mitochondrial dysfunction and activation of proteolytic pathways in sepsis models. MitoTEMPOL also alleviates AGEs (HY-NP165)-induced ferritinophagy-dependent ferroptosis in human umbilical vein endothelial cells. MitoTEMPOL is used in research related to diabetes, sepsis, and vascular endothelial ferroptosis[1][2][3].
| Cat. No. | Product Name | Purity | Description | Pricing | |||||||||||||||||||
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MitoTEMPOL | 99.9% | MitoTEMPOL is a mitochondria-targeted superoxide scavenger. MitoTEMPOL accumulates in mitochondria via membrane potential and locally scavenges superoxide anions. MitoTEMPOL alleviates hepatic oxidative stress and alterations in genes related to autophagy in STZ (HY-13753)-induced diabetic models. MitoTEMPOL inhibits diaphragmatic mitochondrial dysfunction and activation of proteolytic pathways in sepsis models. MitoTEMPOL also alleviates AGEs (HY-NP165)-induced ferritinophagy-dependent ferroptosis in human umbilical vein endothelial cells. MitoTEMPOL is used in research related to diabetes, sepsis, and vascular endothelial ferroptosis. | ||||||||||||||||||||
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References
- [1]. Virgana R, et al. MitoTEMPOL modulates mitophagy and histopathology of Wistar rat liver after streptozotocin injection. Iranian journal of basic medical sciences. 2022 Nov;25(11):1382-1388.
- [2]. Supinski GS, et al. MitoTEMPOL, a mitochondrial targeted antioxidant, prevents sepsis-induced diaphragm dysfunction. American journal of physiology. Lung cellular and molecular physiology. 2020 Aug 01;319(2):L228-L238.
- [3]. Huang Y, et al. Ferritinophagy Is Involved in the Advanced Glycation End Products-Induced Ferroptosis of Vascular Endothelial Cells in Diabetes Mellitus. Journal of cellular and molecular medicine. 2025 Oct;29(20):e70857. [Content Brief]
