Diazoxide | K-ATP channel activator
NMR (Conforms)
Available Options
| Size : | Price | Quantity | |
|---|---|---|---|
| 100 mg | $50.00 | ||
| 500 mg | $150.00 |
Diazoxide (364-98-7) activates ATP-dependent K+ channels1 via inducing translocation of PKC-epsilon from the cytosol to the mitochondria2. Hyperglycemic agent. Induces powerful protective effects against cardiac ischemia via multiple mechanisms.3 Stimulates mitochondrial ATP synthase activity conferring cardioprotection in a streptozotocin-induced acute diabetes model.4 Prevents alterations in memory and synaptic plasticity induced by Amyloid-ß.5
References:
1) Trube et al. (1986), Opposite effects of tolbutamide and diazoxide on the ATP-dependent K+ channel in mouse pancreatic beta-cells.l; Pflugers Arch., 407 493
2) Kim et al. (2006), Diazoxide acts more as a PKC-epsilon activator, and indirectly activates the mitochondrial K(ATP) channel conferring cardioprotection against hypoxic injury; Br. J. Pharmacol, 149 1059
3) Coetzee (2013), Multiplicity of effectors of the cardioprotective agent, diazoxide; Pharmacol. Ther., 140 167
4) Jasova et al. (2016), Stimulation of mitochondrial ATP synthase activity – a new diazoxide-mediated mechanism of cardioprotection; Physiol. Res., 65 Suppl 1 S119
5) Salgado-Puga et al. (2017), Subclinical Doses of ATP-sensitive Potassium channel Modulators Prevent Alterations in Memory and Synaptic Plasticity Induced by Amyloid-β; J. Alzheimers Dis., 57 205
NMR (Conforms)
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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
Diazoxide (364-98-7) activates ATP-dependent K+ channels1 via inducing translocation of PKC-epsilon from the cytosol to the mitochondria2. Hyperglycemic agent. Induces powerful protective effects against cardiac ischemia via multiple mechanisms.3 Stimulates mitochondrial ATP synthase activity conferring cardioprotection in a streptozotocin-induced acute diabetes model.4 Prevents alterations in memory and synaptic plasticity induced by Amyloid-ß.5
References:
1) Trube et al. (1986), Opposite effects of tolbutamide and diazoxide on the ATP-dependent K+ channel in mouse pancreatic beta-cells.l; Pflugers Arch., 407 493
2) Kim et al. (2006), Diazoxide acts more as a PKC-epsilon activator, and indirectly activates the mitochondrial K(ATP) channel conferring cardioprotection against hypoxic injury; Br. J. Pharmacol, 149 1059
3) Coetzee (2013), Multiplicity of effectors of the cardioprotective agent, diazoxide; Pharmacol. Ther., 140 167
4) Jasova et al. (2016), Stimulation of mitochondrial ATP synthase activity – a new diazoxide-mediated mechanism of cardioprotection; Physiol. Res., 65 Suppl 1 S119
5) Salgado-Puga et al. (2017), Subclinical Doses of ATP-sensitive Potassium channel Modulators Prevent Alterations in Memory and Synaptic Plasticity Induced by Amyloid-β; J. Alzheimers Dis., 57 205
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