1334850-99-5
Chemical Structure
Mito-TEMPO
- CAS No.: 1334850-99-5
- Formula:C29H35ClN2O2P
- Molecular Weight:510.03
InChIKey: WKKFJIJNGHNQQW-UHFFFAOYSA-N
SMILES: [O]N1C(C)(C)CC(NC(C[P+](C2=CC=CC=C2)(C3=CC=CC=C3)C4=CC=CC=C4)=O)CC1(C)C.[Cl-]
Biological Activity: Mito-TEMPO is a mitochondria-targeted antioxidant. Mito-TEMPO induces mitophagy by activating the PINK1/Parkin pathway, inhibits NLRP3 inflammasome activation, restores mitochondrial membrane potential, and improves renal function and podocyte injury. Mito-TEMPO regulates Ca2+ homeostasis, inhibits Bnip3 overexpression, shortens action potential duration, and exerts antiarrhythmic effects. Mito-TEMPO reverses premature senescence, reduces trabecular bone loss, and decreases cell apoptosis. Mito-TEMPO can be used in studies of chronic kidney disease, age-related cardiac dysfunction, postmenopausal osteoporosis, and ischemic stroke[1][2][3][4].
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Mito-TEMPO | 99.19% | Mito-TEMPO is a mitochondria-targeted antioxidant. Mito-TEMPO induces mitophagy by activating the PINK1/Parkin pathway, inhibits NLRP3 inflammasome activation, restores mitochondrial membrane potential, and improves renal function and podocyte injury. Mito-TEMPO regulates Ca2+ homeostasis, inhibits Bnip3 overexpression, shortens action potential duration, and exerts antiarrhythmic effects. Mito-TEMPO reverses premature senescence, reduces trabecular bone loss, and decreases cell apoptosis. Mito-TEMPO can be used in studies of chronic kidney disease, age-related cardiac dysfunction, postmenopausal osteoporosis, and ischemic stroke. | ||||||||||||||||||||
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- [1]. Liu B, et al. MitoTEMPO protects against podocyte injury by inhibiting NLRP3 inflammasome via PINK1/Parkin pathway-mediated mitophagy. Eur J Pharmacol. 2022;929:175136. [Content Brief]
- [2]. Olgar Y, et al. MitoTEMPO provides an antiarrhythmic effect in aged-rats through attenuation of mitochondrial reactive oxygen species. Exp Gerontol. 2020;136:110961. [Content Brief]
- [3]. Li J, et al. Mitochondria-specific antioxidant MitoTEMPO alleviates senescence of bone marrow mesenchymal stem cells in ovariectomized rats. J Cell Physiol. 2024;239(8):e31323. [Content Brief]
- [4]. Akkoca A, et al. Protective effect of MitoTEMPO against cardiac dysfunction caused by ischemia-reperfusion: MCAO stroke model study. Int J Neurosci. 2024;134(12):1582-1593. [Content Brief]
Keywords
