ライフサイエンスコーパス: chlorzoxazone

1 the CYP2E1 enzyme affinity for the substrate chlorzoxazone.

2 rat microsomes at varying concentrations of chlorzoxazone.

3 ed the ability to stimulate CYP2E1-catalyzed chlorzoxazone 6-hydroxylation.

4 Finally, treatment of the patient with chlorzoxazone, a BK/SK channel activator, partially impr

5 rm-selective substrates and inhibitors, only chlorzoxazone, a cytochrome P-450 2E1 (CYP2E1) substrate

6 of 4-AP was comparable, and not additive, to chlorzoxazone, an activator of Ca(2+)-dependent K(+) cha

7 ndicated by the increased production of 6-OH-chlorzoxazone and by glutathione depletion after incubat

8 al NOS oxygenase domains cocrystallized with chlorzoxazone and four nitroindazoles: 5-nitroindazole,

9 Chlorzoxazone and mephenytoin metabolism correlated with

10 evant therapeutic drugs (nicotine, coumarin, chlorzoxazone, and acetaminophen) and the prodrug (tamox

11 cs of a cytochrome P450 (CYP2E1) probe drug, chlorzoxazone, and to investigate the mechanism of these

12 ctivated potassium channels (SK channels) by chlorzoxazone (CHZ) combined with the folic acid (FA) on

13 ssessed using the oral clearance (CL(PO)) of chlorzoxazone (CHZ) in 20 NDN and 17 age, gender, and bo

14 d to measure the in vivo CYP3A activity, and chlorzoxazone (CHZ) oral clearance was used to assess in

15 ong-term injections of SK channels activator chlorzoxazone (CHZ) together and separately with the fol

16 f Ca(2+)-dependent K(+) channels, 1-EBIO and chlorzoxazone (CHZ).

17 Drug Administration (FDA)-approved compound, chlorzoxazone (CHZ).

18 ssessed by determination of the clearance of chlorzoxazone (CLZ), an in vivo CYP2E1-selective probe.

19 sing the probe drugs mephenytoin (CYP-2C19), chlorzoxazone (CYP-2E1), dapsone (multiple CYP enzymes),

20 In the case of chlorzoxazone, elimination was essentially unchanged.

21 was estimated by the fractional excretion of chlorzoxazone (fe(6-OH)) for 50 cases of BP and 50 contr

22 lot analysis, and rates of p-nitrophenol and chlorzoxazone hydroxylation were elevated 3- to 4-fold i

23 Rates of p-nitrophenol and chlorzoxazone hydroxylation were elevated approximately

24 a markedly reduces the systemic clearance of chlorzoxazone in cardiac arrest rats.

25 ncreased during postinjury recovery, whereas chlorzoxazone metabolism was suppressed to a lesser degr

26 The lowest energy docked configurations of chlorzoxazone, p-nitrophenol, and N-nitrosodimethylamine

27 Autodock was used to dock chlorzoxazone, p-nitrophenol, N-nitrosodimethylamine, ac

28 No changes in chlorzoxazone protein binding were observed at 37 degree

29 The binding of chlorzoxazone to iNOS and human and rat liver microsomal

30 Although the binding of chlorzoxazone to iNOS and its inhibition of iNOS activit

31 e (HCZ), the metabolite of the CYP2E1 probe, chlorzoxazone, under negative API.

32 Chlorzoxazone was administered as an intravenous bolus,

33 Chlorzoxazone was not a substrate for iNOS but was a pot

34 systemic clearance of the CYP2E1 substrate, chlorzoxazone, when compared with normothermia after car