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Chemical Compound Review

AC1L98DZ     3-chloro-10-hydroxy-8-methyl- 10$l^{6}-thia...

Synonyms: NCIOpen2_003907, 8-chloro-5-hydroxy-3-methyl-5
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Disease relevance of diazoxide


Psychiatry related information on diazoxide


High impact information on diazoxide


Chemical compound and disease context of diazoxide


Biological context of diazoxide


Anatomical context of diazoxide


Associations of diazoxide with other chemical compounds

  • Both glibenclamide and sodium 5-hydroxydecanoic acid inhibited K+ flux through the diazoxide-opened mitochondrial KATP [31].
  • Application of the K(ATP) channel opener diazoxide or the ob gene product leptin mimicked the effect of glucose removal in a reversible manner; moreover, hyperpolarizations evoked by either agent were inhibited by tolbutamide [32].
  • Patch-clamping of matched chimeric human SUR1-SUR2A/K(IR)6.2 channels was used to identify the SUR regions that specify the selective response of sarcolemmal versus beta-cell channels to cromakalim or pinacidil versus diazoxide [33].
  • Furthermore, we have shown previously that 5-hydroxydecanoate is partially metabolized, and we hypothesized that fatty acid metabolism may explain the ability of this putative mitochondrial K(ATP) channel blocker to inhibit diazoxide-induced flavoprotein fluorescence, commonly used as an assay of K(ATP) channel activity [34].
  • Sustained depolarization (by tolbutamide, arginine, or high K+) and hyperpolarization (by diazoxide) of B-cells caused sustained increases and decreases of Ca2+i, respectively [35].

Gene context of diazoxide

  • SUR1- and SUR2-based channels are distinguished by their differential sensitivity to sulfonylureas, whereas SUR2A-based channels are distinguished from SUR2B channels by their differential sensitivity to diazoxide [36].
  • Constitutive activation of ATP-sensitive potassium channels by diazoxide does not alter leptin inhibition of preproinsulin mRNA levels [37].
  • Importantly, both mutant channels rescued to the cell surface have normal ATP, MgADP, and diazoxide sensitivities, demonstrating that SUR1 harboring either the A116P or the V187D mutation is capable of associating with Kir6.2 to form functional K(ATP) channels [38].
  • Diazoxide that attenuates voltage-activated Ca(2+) currents inhibited MIN6N8 cell death by IFN-gamma/TNF-alpha, while glibenclamide that accentuates voltage-activated Ca(2+) currents augmented insulinoma cell death [39].
  • Diazoxide increased the levels of Bcl2 and inhibited the association of Bax with mitochondria in neurons exposed to an apoptotic insult, suggesting that activation of mitochondrial ATP-sensitive potassium channels may stabilize mitochondrial function by differentially modulating proapoptotic and antiapoptotic proteins [40].

Analytical, diagnostic and therapeutic context of diazoxide


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  2. Neonatal hyperglycemia following maternal diazoxide administration. Milsap, R.L., Auld, P.A. JAMA (1980) [Pubmed]
  3. Hypotension and bradycardia following diazoxide and hydralazine therapy. Mizroch, S., Yurasek, M. JAMA (1977) [Pubmed]
  4. Hyperinsulinism in short-chain L-3-hydroxyacyl-CoA dehydrogenase deficiency reveals the importance of beta-oxidation in insulin secretion. Clayton, P.T., Eaton, S., Aynsley-Green, A., Edginton, M., Hussain, K., Krywawych, S., Datta, V., Malingre, H.E., Berger, R., van den Berg, I.E. J. Clin. Invest. (2001) [Pubmed]
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  8. Gender differences in effects of pinacidil but not diazoxide on heart automatism in the isolated guinea pig right atria. Kocić, I., Gruchała, M., Petrusewicz, J. Polish journal of pharmacology. (2003) [Pubmed]
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  10. Hypertrichosis lanuginosa acquisita associated with autoimmune hepatitis. Roh, M.R., Chung, H.J., Cho, Y.H., Chung, K.Y. J. Dermatol. (2006) [Pubmed]
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  12. Truncation of Kir6.2 produces ATP-sensitive K+ channels in the absence of the sulphonylurea receptor. Tucker, S.J., Gribble, F.M., Zhao, C., Trapp, S., Ashcroft, F.M. Nature (1997) [Pubmed]
  13. Synaptic activity becomes excitotoxic in neurons exposed to elevated levels of platelet-activating factor. Bellizzi, M.J., Lu, S.M., Masliah, E., Gelbard, H.A. J. Clin. Invest. (2005) [Pubmed]
  14. Therapy for persistent hyperinsulinemic hypoglycemia of infancy. Understanding the responsiveness of beta cells to diazoxide and somatostatin. Kane, C., Lindley, K.J., Johnson, P.R., James, R.F., Milla, P.J., Aynsley-Green, A., Dunne, M.J. J. Clin. Invest. (1997) [Pubmed]
  15. ATP-sensitive potassium channels mediate contraction-induced attenuation of sympathetic vasoconstriction in rat skeletal muscle. Thomas, G.D., Hansen, J., Victor, R.G. J. Clin. Invest. (1997) [Pubmed]
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  18. Effect of streptozotocin on red-blood-cell-reduced glutathione: modification by glucose, nicotinamide, and epinephrine. Slonim, A.E., Fletcher, T., Burke, V., Burr, I.M. Diabetes (1976) [Pubmed]
  19. Chlorpropamide-induced hypoglycemia: successful treatment with diazoxide. Johnson, S.F., Schade, D.S., Peake, G.T. Am. J. Med. (1977) [Pubmed]
  20. The use of human skin fibroblasts to obtain potency estimates of drug binding to androgen receptors. Eil, C., Edelson, S.K. J. Clin. Endocrinol. Metab. (1984) [Pubmed]
  21. Hyperlipidemic Mice Present Enhanced Catabolism and Higher Mitochondrial ATP-Sensitive K(+) Channel Activity. Alberici, L.C., Oliveira, H.C., Patr??cio, P.R., Kowaltowski, A.J., Vercesi, A.E. Gastroenterology (2006) [Pubmed]
  22. Angina-like syndrome with diazoxide therapy for hypertensive crisis. Kanada, S.A., Kanada, D.J., Hutchinson, R.A., Wu, D. Ann. Intern. Med. (1976) [Pubmed]
  23. Mitochondrial ATP-dependent potassium channels: novel effectors of cardioprotection? Liu, Y., Sato, T., O'Rourke, B., Marban, E. Circulation (1998) [Pubmed]
  24. Activation of mitochondrial K(ATP) channel elicits late preconditioning against myocardial infarction via protein kinase C signaling pathway. Takashi, E., Wang, Y., Ashraf, M. Circ. Res. (1999) [Pubmed]
  25. Non-beating HL-1 cells for confocal microscopy: application to mitochondrial functions during cardiac preconditioning. Pelloux, S., Robillard, J., Ferrera, R., Bilbaut, A., Ojeda, C., Saks, V., Ovize, M., Tourneur, Y. Prog. Biophys. Mol. Biol. (2006) [Pubmed]
  26. A family of sulfonylurea receptors determines the pharmacological properties of ATP-sensitive K+ channels. Inagaki, N., Gonoi, T., Clement, J.P., Wang, C.Z., Aguilar-Bryan, L., Bryan, J., Seino, S. Neuron (1996) [Pubmed]
  27. Protection of cardiac mitochondria by diazoxide and protein kinase C: implications for ischemic preconditioning. Korge, P., Honda, H.M., Weiss, J.N. Proc. Natl. Acad. Sci. U.S.A. (2002) [Pubmed]
  28. Pharmacological plasticity of cardiac ATP-sensitive potassium channels toward diazoxide revealed by ADP. D'hahan, N., Moreau, C., Prost, A.L., Jacquet, H., Alekseev, A.E., Terzic, A., Vivaudou, M. Proc. Natl. Acad. Sci. U.S.A. (1999) [Pubmed]
  29. ATP-modulated K+ channels sensitive to antidiabetic sulfonylureas are present in adenohypophysis and are involved in growth hormone release. Bernardi, H., De Weille, J.R., Epelbaum, J., Mourre, C., Amoroso, S., Slama, A., Fosset, M., Lazdunski, M. Proc. Natl. Acad. Sci. U.S.A. (1993) [Pubmed]
  30. Vasodilator administration in the presence of beta-adrenergic blockade. Mroczek, W.J., Lee, W.R., Davidov, M.E., Finnerty, F.A. Circulation (1976) [Pubmed]
  31. Cardioprotective effect of diazoxide and its interaction with mitochondrial ATP-sensitive K+ channels. Possible mechanism of cardioprotection. Garlid, K.D., Paucek, P., Yarov-Yarovoy, V., Murray, H.N., Darbenzio, R.B., D'Alonzo, A.J., Lodge, N.J., Smith, M.A., Grover, G.J. Circ. Res. (1997) [Pubmed]
  32. Identification and characterization of glucoresponsive neurons in the enteric nervous system. Liu, M., Seino, S., Kirchgessner, A.L. J. Neurosci. (1999) [Pubmed]
  33. Pharmaco-topology of sulfonylurea receptors. Separate domains of the regulatory subunits of K(ATP) channel isoforms are required for selective interaction with K(+) channel openers. Babenko, A.P., Gonzalez, G., Bryan, J. J. Biol. Chem. (2000) [Pubmed]
  34. K+-independent actions of diazoxide question the role of inner membrane K(ATP) channels in mitochondrial cytoprotective signaling. Dröse, S., Brandt, U., Hanley, P.J. J. Biol. Chem. (2006) [Pubmed]
  35. Influence of membrane potential changes on cytoplasmic Ca2+ concentration in an electrically excitable cell, the insulin-secreting pancreatic B-cell. Gilon, P., Henquin, J.C. J. Biol. Chem. (1992) [Pubmed]
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  37. Leptin inhibits insulin gene transcription and reverses hyperinsulinemia in leptin-deficient ob/ob mice. Seufert, J., Kieffer, T.J., Habener, J.F. Proc. Natl. Acad. Sci. U.S.A. (1999) [Pubmed]
  38. Sulfonylureas correct trafficking defects of ATP-sensitive potassium channels caused by mutations in the sulfonylurea receptor. Yan, F., Lin, C.W., Weisiger, E., Cartier, E.A., Taschenberger, G., Shyng, S.L. J. Biol. Chem. (2004) [Pubmed]
  39. Role of calcium in pancreatic islet cell death by IFN-gamma/TNF-alpha. Chang, I., Cho, N., Kim, S., Kim, J.Y., Kim, E., Woo, J.E., Nam, J.H., Kim, S.J., Lee, M.S. J. Immunol. (2004) [Pubmed]
  40. Activation of mitochondrial ATP-dependent potassium channels protects neurons against ischemia-induced death by a mechanism involving suppression of Bax translocation and cytochrome c release. Liu, D., Lu, C., Wan, R., Auyeung, W.W., Mattson, M.P. J. Cereb. Blood Flow Metab. (2002) [Pubmed]
  41. Somatic deletion of the imprinted 11p15 region in sporadic persistent hyperinsulinemic hypoglycemia of infancy is specific of focal adenomatous hyperplasia and endorses partial pancreatectomy. de Lonlay, P., Fournet, J.C., Rahier, J., Gross-Morand, M.S., Poggi-Travert, F., Foussier, V., Bonnefont, J.P., Brusset, M.C., Brunelle, F., Robert, J.J., Nihoul-Fékété, C., Saudubray, J.M., Junien, C. J. Clin. Invest. (1997) [Pubmed]
  42. Preconditioning by mitochondrial ATP-sensitive potassium channel openers: An effective approach for improving the preservation of heart transplants. Kevelaitis, E., Oubénaïssa, A., Peynet, J., Mouas, C., Menasché, P. Circulation (1999) [Pubmed]
  43. K(ATP) channels and pancreatic islet blood flow in anesthetized rats: increased blood flow induced by potassium channel openers. Jansson, L., Kullin, M., Karlsson, F.A., Bodin, B., Hansen, J.B., Sandler, S. Diabetes (2003) [Pubmed]
  44. Glucose-induced [Ca2+]i abnormalities in human pancreatic islets: important role of overstimulation. Björklund, A., Lansner, A., Grill, V.E. Diabetes (2000) [Pubmed]
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