Diazoxide - CAS 364-98-7

Diazoxide - CAS 364-98-7 Catalog number: BADC-00171

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Diazoxide is a potassium channel activator that causes local relaxation in smooth muscle by increasing membrane permeability to potassium ions. The cellular release of potassium switches off voltage-gated calcium ion channels which inhibits the generation of an action potential.

General Information

Category
ADCs Cytotoxin
Product Name
Diazoxide
CAS
364-98-7
Catalog Number
BADC-00171
Molecular Formula
C8H7ClN2O2S
Molecular Weight
230.7

Chemical Structure

  • Diazoxide

Ordering Information

Catalog Number Size Price Stock Quantity
BADC-00171 2 g $199 In stock
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Purity
98% (TLC).
Appearance
white solid.
Synonyms
7-Chloro-3-methyl-4H-1,2,4-benzothiadiazine 1,1-dioxide
Solubility
in methanol; slightly in dilute aqueous base; insoluble in water.
Storage
Store at room temperature.
Application
ADCs Cytotoxin
Shelf Life
As supplied, 2 years from the QC date provided on the Certificate of Analysis, when stored properly
Shipping
-20°C (International: -20°C)
Melting Point
330-331 °C.
Density
1.61g/cm3
Canonical SMILES
CC1=NS(=O)(=O)C2=C(N1)C=CC(=C2)Cl
InChI Key
GDLBFKVLRPITMI-UHFFFAOYSA-N
InChI
InChI=1S/C8H7ClN2O2S/c1-5-10-7-3-2-6(9)4-8(7)14(12,13)11-5/h2-4H,1H3,(H,10,11)
Quantity
Milligrams-Grams
Current Developer
Mercury
1.Impaired glucose-stimulated insulin secretion and reduced beta cell mass in pancreatic islets of hyperthyroid rats.
Karbalaei N1,2, Noorafshan A1, Hoshmandi E2. Exp Physiol. 2016 Apr 6. doi: 10.1113/EP085627. [Epub ahead of print]
To clarify mechanism behind the effect of thyroid hormone excess on pancreatic insulin secretion and abnormal glucose tolerance induced by hyperthyroidism, we investigated the effect of hyperthyroidism on the pancreatic beta cell mass and two key components of insulin secretion pathway, ATP-sensitive K+ (KATP) and L-type Ca2+ channels. In the control and levothyroxine-treated hyperthyroid rats, intraperitoneal glucose tolerance test (IPGTT) was performed and insulin secretion and content of the isolated islets were assayed. In order to determine the effect of hyperthyroidism on KATP and L-type Ca2+ channels, isolated islets were exposed to specific pharmacological drugs including glibenclamide (KATP channel blocker), diazoxide (KATP channel opener), and nifedipine (L-type Ca2+ channel blocker). Histomorphometric changes and histochemistry of the islet in both groups were compared. Our data indicated that plasma glucose and insulin concentrations during IPGTT in the hyperthyroid group was respectively higher and lower than the controls.
2.Isosteviol Sensitizes sarcKATP Channels towards Pinacidil and Potentiates Mitochondrial Uncoupling of Diazoxide in Guinea Pig Ventricular Myocytes.
Fan Z1, Wen T2, Chen Y2, Huang L2, Lin W2, Yin C2, Tan W1. Oxid Med Cell Longev. 2016;2016:6362812. doi: 10.1155/2016/6362812. Epub 2016 Feb 2.
KATP channel is an important mediator or factor in physiological and pathological metabolic pathway. Activation of KATP channel has been identified to be a critical step in the cardioprotective mechanism against IR injury. On the other hand, desensitization of the channel to its opener or the metabolic ligand ATP in pathological conditions, like cardiac hypertrophy, would decrease the adaption of myocardium to metabolic stress and is a disadvantage for drug therapy. Isosteviol, obtained by acid hydrolysis of stevioside, has been demonstrated to play a cardioprotective role against diseases of cardiovascular system, like anti-IR injury, antihypertension, antihyperglycemia, and so forth. The present study investigated the effect of isosteviol (STV) on sarcKATP channel current induced by pinacidil and mitochondrial flavoprotein oxidation induced by diazoxide. Our results showed that preincubating cells with STV not only increased the current amplitude and activating rate of sarcKATP channels induced by pinacidil but also potentiated diazoxide-elicited oxidation of flavoprotein in mitochondria.
3.Depolarization of Mitochondria in Neurons Promotes Activation of Nitric Oxide Synthase and Generation of Nitric Oxide.
Katakam PV1, Dutta S2, Sure VN2, Grovenburg SM2, Gordon AO2, Peterson NR2, Rutkai I2, Busija DW2. Am J Physiol Heart Circ Physiol. 2016 Mar 4:ajpheart.00759.2015. doi: 10.1152/ajpheart.00759.2015. [Epub ahead of print]
The diverse signaling events following mitochondrial depolarization in neurons are not clear. We examined for the first time the effects of mitochondrial depolarization on mitochondrial function, intracellular calcium, neuronal nitric oxide synthase (nNOS) activation, and nitric oxide (NO) production in cultured neurons and perivascular nerves. Cultured rat primary cortical neurons were studied on 7-10 days in vitro and endothelium-denuded cerebral arteries of adult Sprague Dawley rats were studied ex vivo. Diazoxide and BMS-191095 (BMS), activators of mitochondrial KATP channels, depolarized mitochondria in cultured neurons and increased cytosolic calcium levels. However, mitochondrial oxygen consumption rate was unaffected by mitochondrial depolarization. In addition, diazoxide and BMS not only increased the nNOS phosphorylation at positive regulatory serine 1417 but also decreased nNOS phosphorylation at negative regulatory serine 847.
4.Rosuvastatin Treatment Affects Both Basal and Glucose-Induced Insulin Secretion in INS-1 832/13 Cells.
Salunkhe VA1, Elvstam O1, Eliasson L1, Wendt A1. PLoS One. 2016 Mar 17;11(3):e0151592. doi: 10.1371/journal.pone.0151592. eCollection 2016.
Rosuvastatin is a member of the statin family. Like the other statins it is prescribed to lower cholesterol levels and thereby reduce the risk of cardiovascular events. Rosuvastatin lowers the cholesterol levels by inhibiting the key enzyme 3-hydroxy-3-methyl-glutaryl-CoA reductase (HMG-CoA reductase) in the cholesterol producing mevalonate pathway. It has been recognized that apart from their beneficial lipid lowering effects, statins also exhibit diabetogenic properties. The molecular mechanisms behind these remain unresolved. To investigate the effects of rosuvastatin on insulin secretion, we treated INS-1 832/13 cells with varying doses (20 nM to 20 μM) of rosuvastatin for 48 h. At concentrations of 2 μM and above basal insulin secretion was significantly increased. Using diazoxide we could determine that rosuvastatin did not increase basal insulin secretion by corrupting the KATP channels. Glucose-induced insulin secretion on the other hand seemed to be affected differently at different rosuvastatin concentrations.

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