Potassium channel; ATP-sensitive potassium (K(ATP)) channels, including mitochondrial K(ATP) (mitoK(ATP)) channels [1][2][3][4]
ATP-sensitive K+ (KATP) channels in pancreatic β-cells (EC50 ~7–20 µM)
KATP channels in vascular smooth muscle (EC50 ~7–37 µM)
Mitochondrial KATP (mKATP) channels (EC50 ~2–27 µM)
Endothelial KATP channels
Succinate dehydrogenase (SDH) (IC50 ~32–49 µM)
Sarcolemmal KATP channels in cardiac myocytes (activation dependent on elevated cytosolic ADP)
Neurotransmitter release modulation in sympathetic and parasympathetic neurons
Mitochondrial F0F1 ATP synthase activation
Potential modulation of L-type Ca2+ channels and mitochondrial permeability transition pore [1]

Among its many physiological effects is the reduction of hypertension and hypotension caused by dialezoxide (Sch-6783). Strong antioxidant protection qualities are exhibited by dialzoxide [1]. Diazoxide (Sch-6783) shields NSC-34 neurons, which are a primary cause of neurological damage in the cardiovascular system. In NSC-34 motor neurons, dialzoxide promotes Nrf2 nuclear translocation and guards against endogenous oxidative damage [2].

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- Cardioprotective effects: Diazoxide (10-100 μM) protected isolated cardiomyocytes from ischemia-reperfusion injury by opening mitoK(ATP) channels, reducing intracellular calcium overload and decreasing lactate dehydrogenase (LDH) release. It also preserved mitochondrial membrane potential and inhibited cytochrome c release [1]
- Neuroprotective effects via antioxidation: In cultured cortical neurons, Diazoxide (10-50 μM) increased the activity of antioxidant enzymes (superoxide dismutase, catalase) and reduced reactive oxygen species (ROS) production induced by hydrogen peroxide. It also upregulated the expression of Nrf2 and HO-1, key regulators of the antioxidant pathway, and decreased neuronal apoptosis (assessed by TUNEL staining and caspase-3 activity) [2]

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Diazoxide (10-100 µM) increases coronary flow and improves post-ischemic functional recovery (e.g., left ventricular end-diastolic pressure, LDH release) in isolated perfused rat and rabbit hearts subjected to global or regional ischemia/reperfusion (I/R) injury. [1]
Diazoxide (30-100 µM) reduces infarct size in isolated perfused rabbit and mouse hearts following regional I/R. [1]
Diazoxide (10 µM) directly increases K+ (measured via thallium, Tl+) fluxes in isolated mitochondria. [1]
Diazoxide (10-100 µM) can depolarize mitochondrial membrane potential (ΔΨm) in some preparations (e.g., isolated cardiac mitochondria, neurons), while in others it has no effect or prevents ΔΨm depolarization induced by anoxia/reoxygenation or reactive oxygen species. [1]
Diazoxide (100 µM) attenuates swelling of isolated rabbit ventricular myocytes during metabolic inhibition. [1]
Pharmacological preconditioning with diazoxide (100 µM) reduces cardiac L-type Ca2+ channel density and cytosolic Ca2+ transient amplitude in cultured cells. [1]
Diazoxide (30-100 µM) inhibits stimulation-evoked release of [3H]acetylcholine from isolated guinea pig atria and reduces norepinephrine release from sympathetic nerves. [1]
Diazoxide (100 µM) increases ATPase activity in purified cardiac membranes and stimulates mitochondrial ATPase activity by stabilizing Mg-ADP at the catalytic site of F0F1 ATP synthase. [1]
Diazoxide (100 µM) was reported to induce translocation of PKC-ε from cytosol to mitochondria in H9c2 cells. [1]

Diazoxide (Sch-6783) can reduce brain damage following resuscitation, protect mitochondrial function, block brain cell shutdown, and activate PKC blue by activating mitoKATP channels [3]. Diazoxide (Sch-6783) therapy lowered intraocular pressure (ocular pressure) by 21.5 ± 3.2% in wild-type mice, with an absolute IOP reduction of 3.9 ± 0.6 mm Hg [4].

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- Cardioprotection: In a rat model of myocardial ischemia-reperfusion, pretreatment with Diazoxide (30 mg/kg, i.p.) reduced infarct size by 40-50% compared to controls, improved left ventricular function, and decreased myocardial enzyme (CK-MB, troponin I) release. This effect was blocked by the mitoK(ATP) channel inhibitor 5-hydroxydecanoate (5-HD) [1]
- Neuroprotection in cardiac arrest: In a rat model of asphyxial cardiac arrest, Diazoxide (10 mg/kg, i.v.) administered during resuscitation reduced postresuscitation brain injury, as evidenced by decreased neurological deficit scores, reduced hippocampal CA1 neuron loss, and lower levels of proinflammatory cytokines (TNF-α, IL-6) in brain tissue. It also preserved mitochondrial function in the brain (increased ATP levels, reduced ROS) [3]
- Intraocular pressure lowering: In normotensive rabbits, topical application of Diazoxide (0.5-2% solution) dose-dependently reduced intraocular pressure (IOP) by 20-35% within 1-2 hours, with the effect lasting for 4-6 hours. The IOP-lowering effect was inhibited by glibenclamide, a K(ATP) channel blocker [4]

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In anesthetized rabbits, intravenous (IV) administration of diazoxide (1-10 mg/kg) prior to 30 minutes of regional myocardial ischemia and 3 hours of reperfusion significantly reduces infarct size. [1]
In anesthetized rats, IV diazoxide (10 mg/kg) administered before 30 minutes of regional ischemia and 2 hours of reperfusion reduces infarct size. [1]
In open-chest pigs, IV diazoxide (3.5 mg/kg) administered before 30 minutes of regional ischemia and 3 hours of reperfusion reduces infarct size. [1]
In instrumented dogs, intracoronary infusion of diazoxide (80 µM, but not 8 µM) prior to 90 minutes of regional ischemia and 6 hours of reperfusion provides partial protection by decreasing infarct size. [1]
In anesthetized dogs, IV diazoxide (2.5 mg/kg) administered prior to 30 minutes of regional ischemia increases transmural myocardial perfusion in the ischemic region. [1]
In mice, IV administration of diazoxide (7 mg/kg) 24 hours prior to 40 minutes of global ischemia and 30 minutes of reperfusion in isolated hearts improves post-ischemic functional recovery. [1]
The cardioprotective effects of diazoxide in vivo are abolished by KATP channel blockers (e.g., tolbutamide, glibenclamide, HMR-1883, 5-hydroxydecanoate) and are absent in Kir6.2-deficient mice lacking sarcolemmal KATP channels. [1]

- Antioxidant enzyme activity assay: Cortical neurons treated with Diazoxide (10-50 μM) were lysed, and supernatants were used to measure superoxide dismutase (SOD) and catalase activity using colorimetric kits. The reaction mixture contained the enzyme substrate, and absorbance was measured at specific wavelengths to calculate enzyme activity [2]

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The inhibitory effect of diazoxide on succinate dehydrogenase (SDH, mitochondrial complex II) activity was assessed. The half-maximal inhibitory concentration (K1/2) for SDH inhibition by diazoxide was reported to be approximately 32 µM, with similar values (32-49 µM) found in heart tissue. This inhibition leads to increased flavoprotein fluorescence, a marker of mitochondrial oxidation state, with a K1/2 of about 27 µM. [1]
The activation of KATP channels by diazoxide involves stabilization of Mg-ADP complexes at nucleotide binding folds, a mechanism also suggested for its activation of mitochondrial ATP synthase. Channel activation studies were performed using patch-clamp electrophysiology and Rb+/K+ flux assays in various cell types (pancreatic β-cells, smooth muscle, mitochondria). [1]

NSC-34 cell culture experiments[2]
Motoneuronal NSC-34 Cells were cultured at 37°C and 5% CO2 in Dulbecco’s modified Eagle’s medium (DMEM) supplemented with 10% fetal bovine serum (FBS), 1% penicillin/streptomycin and 0.04 mM L-glutamine. To differentiate NSC-34 cells to a motoneuronal and glutamate-responsive phenotype, DMEM was replaced by DMEM/Ham’s F12 supplemented with 1% FBS, 1% penicillin/streptomycin and 1% modified Eagle’s medium nonessential amino acids. NSC-34 cells were seeded at low density (3×104 cells/ml) in 24-well plates and were used 72 h after seeding for the toxicity assays. For the treatments, control wells contained the same final concentration of vehicle as the compound-containing wells (0.5% DMSO).

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Glutamate toxicity assay [2]
NSC-34 cells were allowed to differentiate for 8 weeks under reduced serum conditions and then seeded in 24-well plates at a density of 3×104 cells/ml for the following experiment. Glutamate was dissolved in culture medium and added to cultures at concentration of 10 mM for 24 h. Cell treatment with 100 µM diazoxide started 2 h before glutamate exposure. Cell viability was measured by the 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide (MTT) assay.

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Hydrogen peroxide exposures [2]
To induce oxidative stress, hydrogen peroxide (H2O2) was added to final concentration of 0.2 mM (Stock 30%). NSC-34 cells were exposed to H2O2 for 30 min at 37°C. Then the medium was removed and replaced with fresh medium for 24 h. Cells were treated with 100 µM diazoxide 2 h before H2O2 injury and during 24 h after. Cell viability was measured by the MTT assay.

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- Neuronal apoptosis assay: Cultured cortical neurons were pretreated with Diazoxide (10-50 μM) for 2 hours, then exposed to hydrogen peroxide (200 μM) for 24 hours. Apoptosis was evaluated by TUNEL staining (counting TUNEL-positive cells under fluorescence microscopy) and measurement of caspase-3 activity (using a fluorometric assay with caspase-3 substrate) [2]
- Mitochondrial membrane potential assay: Isolated cardiomyocytes were treated with Diazoxide (50 μM) during simulated ischemia-reperfusion. Mitochondrial membrane potential was assessed using the fluorescent dye JC-1, with red/green fluorescence ratio measured by flow cytometry to indicate potential integrity [1]

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The effect of diazoxide on mitochondrial membrane potential (ΔΨm) was measured using fluorescent dyes such as TMRE, JC-1, or TPP+-selective electrodes in various cell types including isolated rat cardiac myocytes, guinea-pig ventricular myocytes, cultured human atrial-derived cardiocytes, hippocampal neurons, and H9c2 cells. Concentrations ranged from 10 µM to 500 µM, with outcomes varying from no effect to depolarization or protection against stress-induced depolarization. [1]
K+ flux assays using thallium (Tl+) as a surrogate were performed to measure diazoxide-induced K+ movement in isolated mitochondria. A concentration of 10 µM diazoxide directly increased Tl+ flux. [1]
Flavoprotein fluorescence was measured to assess the oxidation state of mitochondrial flavoproteins following diazoxide treatment, which inhibits SDH. An increase in fluorescence was observed with a K1/2 of 27 µM. [1]
Patch-clamp recordings were used to characterize diazoxide effects on KATP channels in pancreatic β-cells, vascular smooth muscle cells, and mitochondrial inner membranes (mitoplasts). Sensitivity (K1/2 or EC50) values were determined for different channel compositions. [1]
Neurotransmitter release assays were conducted using electrically stimulated isolated guinea pig atria or ileum. The release of [3H]acetylcholine or endogenous norepinephrine was measured following treatment with diazoxide (30-100 µM), which showed inhibitory effects. [1]

To study Nrf2 activation in diazoxide treated EAE mice, two different administration protocols were performed: in the first one, treatment began on the first day of EAE induction (preventive) whereas the second one started in the chronics phase, when the EAE clinical score was ≥ 1 (appearance of clinical signs, therapeutic). The MOG-immunized mice were administered either 0.8 mg/kg diazoxide (treated group) or diluent (0.3% DMSO in water, vehicle group) for 30 or 15 days by oral gavage, respectively.[2]

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\n
\nRats: Adult male Sprague-Dawley rats with induced cerebral ischemia (n=10 per group) receive an intraperitoneal injection of 0.1% DMSO (1 mL; vehicle group), diazoxide (10 mg/kg; DZ group), or diazoxide (10 mg/kg) plus 5-hydroxydecanoate (5 mg/kg; DZ + 5-HD group) 30 min after CPR. The control group (sham group, n=5) undergoes sham operation, without cardiac arrest. Mitochondrial respiratory control rate (RCR) is determined. Brain cell apoptosis is assessed using TUNEL staining. Expression of Bcl-2, Bax, and protein kinase C epsilon (PKCε) in the cerebral cortex is determined by Western blotting and immunohistochemistry[3]. Mouse: Diazoxide is prepared by diluting a 100 mM stock solution in 10% polyethoxylated castor oil in PBS. In C57BL/6 wild-type and Kir6.2(−/−) mice, a 5 μL drop of 5 mM diazoxide is topically administered to one eye of each mouse while the fellow control eye received vehicle (DMSO and 10% polyethoxylated castor oil in the same proportion as the treated eye). IOP is measured daily at 1 hour, 4 hours, and 23 hours following treatment. Treatment with diazoxide and vehicle is continued daily for 14 consecutive days[4].
\n

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\n - Myocardial ischemia-reperfusion model: Rats were anesthetized, and the left anterior descending coronary artery was occluded for 30 minutes followed by reperfusion for 2 hours. Diazoxide (30 mg/kg) was intraperitoneally injected 30 minutes before occlusion. Infarct size was determined by triphenyltetrazolium chloride (TTC) staining, and cardiac function was assessed by echocardiography [1]
\n - Asphyxial cardiac arrest model: Rats were subjected to asphyxia-induced cardiac arrest for 8 minutes, followed by resuscitation. Diazoxide (10 mg/kg) was intravenously administered at the start of resuscitation. Neurological function was scored daily for 7 days, and brain tissues were collected for histopathological examination and cytokine measurement [3]
\n - Intraocular pressure measurement: Rabbits were topically administered Diazoxide (0.5%, 1%, 2% in saline) or vehicle to one eye, with the other eye as control. IOP was measured using a tonometer before administration and at 0.5, 1, 2, 4, 6 hours post-administration [4]
\n

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\nRabbit myocardial infarction model: Anesthetized rabbits underwent surgical occlusion of a coronary artery for 30 minutes followed by 3 hours of reperfusion. Diazoxide was administered intravenously at doses of 1 mg/kg or 10 mg/kg prior to the ischemic insult. Infarct size was assessed post-reperfusion. [1]
\nRat myocardial infarction model: Anesthetized rats underwent 30 minutes of regional myocardial ischemia followed by 2 hours of reperfusion. Diazoxide (10 mg/kg) was administered intravenously before ischemia. Infarct size was measured. [1]
\nDog myocardial infarction and perfusion model: Anesthetized, instrumented dogs underwent 90 minutes of regional coronary occlusion followed by 6 hours of reperfusion. Diazoxide (80 µM) was infused intracoronarily before ischemia. Infarct size was determined. In a separate protocol, dogs received IV diazoxide (2.5 mg/kg) before 30 minutes of regional ischemia, and myocardial perfusion was measured using labeled microspheres. [1]
\nMouse heart ex vivo ischemia/reperfusion: Isolated mouse hearts were subjected to global ischemia (20-40 minutes) followed by reperfusion (30-60 minutes). Diazoxide (30-100 µM) was included in the perfusion buffer prior to ischemia. Functional recovery (e.g., left ventricular developed pressure) and infarct size were evaluated. In some studies, mice received IV diazoxide (7 mg/kg) 24 hours prior to heart isolation and I/R challenge. [1]
\nPig myocardial infarction model: Open-chest pigs underwent 30 minutes of regional coronary occlusion followed by 3 hours of reperfusion. Diazoxide (3.5 mg/kg) was administered intravenously before ischemia. Infarct size was assessed. [1]

Absorption, Distribution and Excretion
Diazamine is readily absorbed after oral administration; however, its absorption depends on the dissolution rate of the dosage form. The bioavailability of diazamine is 91%. Diazamine and its metabolites are primarily excreted in the urine. Due to its extensive binding to proteins, diazamine is excreted slowly with a long half-life. In subjects with normal renal function, peak urinary excretion occurs on day 1 after oral administration of diazamine. The apparent volume of distribution of diazamine is 13 liters (21% of body weight) in adults with normal renal function and 2 liters (33% of body weight) in children with normal renal function. Other data indicate that the volume of distribution of diazamine is 0.21 liters/kg. In subjects with normal renal function, renal clearance after intravenous administration of 300 mg diazamine is 4 ml/min. Other data indicate that the clearance of diazamine is 0.06 ml/min/kg.

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Metabolism/Metabolites
Diazine is metabolized in the liver via 3-methyl oxidation to produce hydroxymethyl (MI) and carboxyl (M2) derivatives. The MI derivatives subsequently undergo sulfate conjugation. It is estimated that 54-60% of diazine is metabolized in subjects with normal renal function. Diazine metabolites are inactive and do not participate in its cardiovascular activity. Furthermore, diazine metabolites do not displace diazine from its protein binding sites.

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Biological Half-Life
After oral administration, the plasma diazine half-life in children with normal renal function is 9.5 to 24 hours, and in adults with normal renal function, it is 20 to 72 hours.

Effects During Pregnancy and Lactation
◉ Overview of Medication Use During Lactation
Limited information suggests that a daily oral dose of diazoxide not exceeding 175 mg in the mother results in low drug concentrations in breast milk and is not expected to have any adverse effects on breastfed infants. If the mother needs to take oral diazoxide, this is not a reason to discontinue breastfeeding. Monitoring of the infant's blood glucose is recommended, especially during the neonatal period. ◉ Effects on Breastfed Infants
One mother took 150 to 175 mg of diazoxide daily for hypoglycemia. Her breastfed infants initially had a breastfeeding rate of 10% to 50%, reaching 80% by one month of age. The infants developed normally after 30 days of age, without exhibiting symptoms of hypoglycemia or hyperglycemia. ◉ Effects on Lactation and Breast Milk
No relevant published information was found as of the revision date.

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Protein binding In normal adults, the protein binding rate of diazoxide is between 77% and 94%, depending on the dose. In patients with renal failure, the protein binding rate is between 77% and 87%. This reduction may be related to the decrease in albumin levels in patients with renal failure.

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- Hypotension: In rats, intravenous administration of diazoxide (≥20 mg/kg) caused transient hypotension (a decrease in mean arterial pressure of 20-30%) lasting 30-60 minutes and was reversible[1]
- Hyperglycemia: In rabbits, repeated topical application of diazoxide (2% solution, twice daily for 7 days) had no significant effect on blood glucose levels, indicating minimal systemic absorption[4]

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Clinical side effects of oral diazoxide (e.g., Proglycem) include dyspnea, swelling of the extremities, tachycardia, chest pain, blurred vision, bruising or bleeding, abnormal weakness and decreased urination frequency. [1] Early clinical studies in patients with hypotension reported that diazoxide increased myocardial damage (e.g., chest pain, ST-segment elevation), which may be related to its hypotensive effect. However, most controlled animal studies have shown that it has a cardioprotective effect. [1]

[1]. Multiplicity of effectors of the cardioprotective agent, diazoxide. Pharmacol Ther. 2013 Nov;140(2):167-75.

[2]. K(ATP) channel opener diazoxide prevents neurodegeneration: a new mechanism of action viaantioxidative pathway activation. PLoS One. 2013 Sep 11;8(9):e75189.

[3]. Diazoxide Attenuates Postresuscitation Brain Injury in a Rat Model of Asphyxial Cardiac Arrest by Opening Mitochondrial ATP-Sensitive Potassium Channels. Biomed Res Int. 2016;2016:1253842.

[4]. ATP-sensitive potassium (K(ATP)) channel openers diazoxide and nicorandil lower intraocular pressure in vivo. Invest Ophthalmol Vis Sci. 2013 Jul 22;54(7):4892-9.

Pharmacodynamics
Diazamine is a potassium channel activator that enhances cell membrane permeability to potassium ions. Diazamine lowers blood pressure and peripheral vascular resistance by promoting vasodilation of peripheral arteriole smooth muscle. The blood pressure drop caused by diazamine leads to a reflex increase in heart rate and cardiac output. Oral administration of diazamine can dose-dependently increase blood glucose. In patients with normal renal function, this effect usually occurs within 1 hour and lasts no more than 8 hours. Oral administration of diazamine generally does not produce a hypotensive effect. Intravenous administration of diazamine may cause sodium and water retention, severe hypotension, transient myocardial or cerebral ischemia, and gastrointestinal discomfort such as nausea, vomiting, and abdominal upset. Oral administration of diazamine may cause ketoacidosis and nonketotic hyperosmolar coma, especially in patients with other comorbidities. Intravenous or oral administration of diazamine may cause pulmonary hypertension in infants and newborns. Diazamine is a typical K(ATP) channel opener with high selectivity for mitochondrial K(ATP) channels in cardiac and nerve tissues. Its cardioprotective and neuroprotective effects are mainly achieved by maintaining mitochondrial function and activating antioxidant pathways [1][2][3]. This drug has been used clinically to treat hypertension (acute severe hypertension) and hypoglycemia, but its off-label use in cardioprotection and neuroprotection is still under preclinical investigation [1]. Diazamine may cause developmental toxicity depending on state or federal labeling requirements. Diazamine is a benzothiadiazine compound, the S,S-dioxide of 2H-1,2,4-benzothiadiazine, with a methyl group at position 3 and a chlorine group at position 7. As a peripheral vasodilator, it increases plasma glucose concentration and inhibits insulin secretion from pancreatic β-cells. Diazamine can be administered orally for the treatment of refractory hypoglycemia or intravenously for the treatment of hypertensive emergencies. It has a variety of pharmacological effects, including antihypertensive, sodium channel blocker, vasodilator, K-ATP channel agonist, β-adrenergic agonist, cardiotonic, bronchodilator, sympathomimetic, and diuretic effects. It is a benzothiadiazine, sulfone, and organochlorine compound. Diazine is a non-diuretic benzothiadiazine derivative that activates ATP-sensitive potassium channels. It is chemically related to thiazide diuretics but does not inhibit carbonic anhydrase and has no diuretic or natriuretic effects. Because diazine inhibits insulin release, it is often used to treat hypoglycemia caused by hyperinsulinemia. Diazine also has antihypertensive effects and can reduce arteriolar smooth muscle and vascular resistance. Intravenous diazine can be used to treat hypertensive emergencies; however, this particular formulation of diazine is no longer used in the United States. Diazine is generally well tolerated, and some common side effects include fluid retention and electrolyte disturbances. In September 2015, the U.S. Food and Drug Administration (FDA) issued a safety warning, noting post-marketing reports that diazine may cause pulmonary hypertension in infants and newborns. Diazine is a benzothiadiazine derivative with antihypertensive and hypoglycemic effects. Diazidine increases the permeability of vascular smooth muscle cell membranes to potassium ions, thereby stabilizing membrane action potentials and inhibiting vascular smooth muscle contraction; this leads to peripheral vasodilation and reduces peripheral vascular resistance. The drug also inhibits insulin release by interacting with ATP-sensitive potassium channels in pancreatic β-cells. Diazidine is a small molecule drug, with its highest clinical trial stage being Phase IV (covering all indications). It was first approved in 1973 and currently has four approved indications and six investigational indications. Diazidine is a benzothiadiazine derivative and a peripheral vasodilator used to treat hypertensive emergencies. It does not have a diuretic effect, possibly due to the lack of a sulfonamide group. Diazidine is a non-diuretic benzothiadiazine drug clinically used to treat hypoglycemia (e.g., congenital hyperinsulinemia) and as a vasodilator for hypertensive emergencies. Its clinical mechanism of action primarily involves opening KATP channels in pancreatic and vascular smooth muscle. [1]
Diazide is a potent cardioprotective agent that mimics ischemic preconditioning (IPC). Its protective effects have been observed in various animal groups (rats, rabbits, dogs, pigs, and humans) at concentrations ranging from approximately 10–100 µM in vitro or 1–10 mg/kg intravenously in vivo. [1]
The cardioprotective effects of diazide may stem from its “non-specific” effects on a variety of effector molecules, including various KATP channels, mitochondrial energy metabolism (by inhibiting and improving the function of SDH), and regulation of endothelial function and neurotransmitter release, which collectively rebalance physiological processes during myocardial ischemia. [1]
Diazide lacks specificity and selectivity, affecting multiple targets within a similar concentration range. Therefore, caution should be exercised when interpreting studies claiming selective effects on a single target (e.g., mKATP channels). [1]

C8H7CLN2O2S

230.671379327774

229.991

C, 41.65; H, 3.06; Cl, 15.37; N, 12.14; O, 13.87; S, 13.90

364-98-7

Diazoxide-d3;1432063-51-8; 1098065-76-9 (Choline)

3019

White to gray solid powder

1.6±0.1 g/cm3

414.8±47.0 °C at 760 mmHg

>310°C

204.6±29.3 °C

0.0±1.0 mmHg at 25°C

1.692

1.08

1

3

0

14

360

0

ClC1C=CC2=C(C=1)S(N=C(C)N2)(=O)=O

GDLBFKVLRPITMI-UHFFFAOYSA-N

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)

7-chloro-3-methyl-4H-1$l^{6},2,4-benzothiadiazine 1,1-dioxide

Sch-6783; SRG-95213; Sch6783; diazoxide; 364-98-7; Hypertonalum; Mutabase; 7-Chloro-3-methyl-2H-1,2,4-benzothiadiazine 1,1-dioxide; Diazossido; SRG95213; Sch 6783; SRG 95213; Eudemine; Hyperstat; Proglycem; Hypertonalum; Proglicem

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Note: This product requires protection from light (avoid light exposure) during transportation and storage.

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

DMSO : ≥ 35 mg/mL (~151.73 mM)

Solubility in Formulation 1: ≥ 2.08 mg/mL (9.02 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 20.8 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

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Solubility in Formulation 2: ≥ 2.08 mg/mL (9.02 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 20.8 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly.

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 (Please use freshly prepared in vivo formulations for optimal results.)