| Identification | Back Directory | [Name]
Mito-TEMPO | [CAS]
1334850-99-5 | [Synonyms]
Mito-TEMPO
MitoTEMPO >=98% (HPLC)
(2-(2,2,6,6-Tetramethylpiperidin-1-oxyl-4-ylamino)-2-oxoethyl)triphenylphosphonium chloride | [Molecular Formula]
C29H35N2O2P.Cl | [MDL Number]
MFCD26406410 | [MOL File]
1334850-99-5.mol | [Molecular Weight]
510.03 |
| Chemical Properties | Back Directory | [storage temp. ]
-20°C | [solubility ]
H2O: soluble10mg/mL, clear | [form ]
powder | [color ]
white to light brown | [Water Solubility ]
H2O: 10mg/mL, clear | [Stability:]
Stable for 2 years from date of purchase as supplied | [InChI]
InChI=1S/C29H34N2O2P.ClH/c1-28(2)20-23(21-29(3,4)31(28)33)30-27(32)22-34(24-14-8-5-9-15-24,25-16-10-6-11-17-25)26-18-12-7-13-19-26;/h5-19,23H,20-22H2,1-4H3;1H | [InChIKey]
WKKFJIJNGHNQQW-UHFFFAOYSA-N | [SMILES]
[P+](C1C=CC=CC=1)(C1C=CC=CC=1)(C1C=CC=CC=1)CC(=O)NC1CC(N(C(C1)(C)C)[O])(C)C.[Cl-] |^1:31| |
| Hazard Information | Back Directory | [Description]
Mito-TEMPO (1334850-99-5) is a mitochondria-targeted antioxidant. Partially prevents mitochondrial permeability transition pore opening, necrosis and mitochondrial apoptosis after ATP depletion recovery.1?Resolves mitochondrial oxidative stress and rescues coronary collateral growth in Zucker obese fatty rats.2?Protects mitochondrial membrane potential and attenuates reperfusion-induced ROS production in a mouse ventricular myocyte model.3?Abrogates the induction of senescence in a human vascular smooth muscle cell model.4 | [Uses]
MitoTEMPO has been used as a mitochondria-targeted antioxidant. | [Biochem/physiol Actions]
MitoTEMPO is a mitochondrially targeted antioxidant, a specific scavenger of mitochondrial superoxide. MitoTEMPO is a combination of the antioxidant piperidine nitroxide TEMPO with the lipophilic cation triphenylphosphonium, giving MitoTEMPO the ability to pass through lipid bilayers with ease and accumulate several hundred-fold in mitochondria. Mitochondrial dysfunction and oxidative stress contribute to a variety of disorders involving cardiovascular, kidney, liver disorders, Parkinson′s and Alzheimer′s disease. | [in vivo]
Mito-TEMPO (MT) greatly attenuates the increase in ALT activities and reduces the areas of necrosis at both time points, indicating that the protection by Mito-TEMPO is sustained until at least 24 h post-APAP. Mito-Tempo could induce secondary apoptosis in the late phase of APAP hepatotoxicity. Mito-Tempo induces secondary apoptosis after APAP overdose by inhibition of RIP3[1]. | [References]
1) Liang?et al.?(2010)?SOD1 and MitoTEMPO partially prevent mitochondrial permeability transition pore opening, necrosis and mitochondrial apoptosis after ATP depletion recovery; Free Radic. Biol. Med.?49?1550
2) Pung?et al.?(2012)?Resolution of mitochondrial oxidative stress rescues coronary collateral growth in Zucker obese fatty rats; Arterioscler. Thromb. Vasc. Biol.?32?325
3) DeSantiago?et al.?(2013)?Ischemia/Reperfusion injury protection by mesenchymal stem cell derived antioxidant capacity; Stem Cells Dev.?22?2497
4) Mistri?et al.?(2013)?A role for mitochondrial oxidants in stress-induced premature senescence of human vascular smooth muscle cells; Redox. Biol.?1?411 |
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