Mito-TEMPO | Mitochondria targeted antioxidant
HR Mass Spec. (Conforms)
Available Options
| Size : | Price | Quantity | |
|---|---|---|---|
| 5 mg | $60.00 | ||
| 25 mg | $230.00 |
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
References/Citations:
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
HR Mass Spec. (Conforms)
Safety Data Sheet:
Product Data Sheet:
Materials provided by Focus Biomolecules are for laboratory research use only and are not intended for human or veterinary applications. Please note that we do not sell to individuals and that all orders placed by non-research organizations will incur a $20 restocking/refund fee
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
References/Citations:
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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