ライフサイエンスコーパス: mibefradil

1 T-type calcium channel antagonists Ni2+ and mibefradil.

2 ic acid) (DTNB) and the T channel antagonist mibefradil.

3 functional LVA Ca(2+) currents sensitive to mibefradil.

4 of D.42 plasma induced ALI with WEB 2170 or mibefradil.

5 Mibefradil (1 microM) increased the duration of the two

6 ow inactivation with a 60-s pulse to -10 mV, mibefradil (1 microM) produced 45% fractional block in N

7 At high concentrations, mibefradil (10 microM) and Ni+ (1 mM) blocked I(Na).

8 hibited by Ni(2+) (IC(50) = 1.4 x 10(-5) M), mibefradil (10(-6) to 10(-5) M), and extracellular Ba(2+

9 Mibefradil, a blocker of T-type Ca2+ channels attenuated

10 Incubation of LPS pre-tx rats with mibefradil, a Ca2+ channel blocker, or WEB 2170, a plate

11 Mibefradil, a new calcium antagonist that selectively bl

12 The alpha1H channel is sensitive to mibefradil, a nondihydropyridine Ca2+ channel blocker, w

13 La3+ and mibefradil, agents interfering with low-threshold Ca2+ c

14 Mibefradil also failed to reduce the size of the unitary

15 Mibefradil also inhibited P-type calcium channels in Pur

16 channel patch-clamp recording, we found that mibefradil also potently blocked an ATP-activated K(+) c

17 Mibefradil also reversibly blocked, with similar potency

18 ced oscillations were resistant to 50 microM mibefradil, an I(T) blocker, in contrast to spontaneous

19 Partial sensitivity to 1 micrometer mibefradil and an enhanced sensitivity of the GVIA-resis

20 Patients comedicated with mibefradil and antiarrhythmics (class I or III), includi

21 ases of cardiogenic shock in patients taking mibefradil and beta-blockers who began taking dihydropyr

22 aled a potential serious interaction between mibefradil and beta-blockers, digoxin, verapamil, and di

23 Ca(2+) antagonists including penfluridol and mibefradil and by 8-(4-chlorophenylthio)-cAMP.

24 changed by the Ca2+ and HCN channel blockers mibefradil and ZD7288, respectively.

25 ced by blocking T-type Ca(2+) channels (e.g. mibefradil) and by blocking the Na(+)/Ca(2+) exchanger (

26 ly) after block of T-type calcium current by mibefradil, and most cells continued to fire after block

27 Total mortality was similar between mibefradil- and placebo-treated patients (P=0.151).

28 preclinical proof of concept for repurposing mibefradil as a mechanism-based treatment strategy for G

29 These results identify mibefradil as a potent inhibitor of ATP-activated K(+) c

30 ed A-type K(+) current was also inhibited by mibefradil at concentrations approximately 10-fold highe

31 er cell growth, and that NPPB, tamoxifen and mibefradil at their IC50 for growth do not suppress the

32 the idea that Asn406 lies within or near the mibefradil binding site.

33 The structural determinants controlling mibefradil block have not been identified, although evid

34 Using whole-cell voltage clamp, we examined mibefradil block of four Na+ channel isoforms expressed

35 We have recently reported state-dependent mibefradil block of Na(+) channels in which apparent aff

36 e, and hydrophobicity had minimal effects on mibefradil block, but all mutations dramatically altered

37 ation lid (Nav1.5 ICM + MTSET) did not alter mibefradil block, confirming that the drug does not pref

38 vate, however, at the voltages used to assay mibefradil block, supporting the idea that Asn406 lies w

39 Mibefradil blocked currents of all Na+ channel isoforms

40 Mibefradil blocked Nav1.5 in a use/frequency-dependent m

41 Our results suggest that mibefradil blocks Na+ channels in a state-dependent mann

42 d mEPSC frequency; an increase suppressed by mibefradil but not by HVA Ca2+ channel antagonists.

43 The antihypertensive agent mibefradil completely and reversibly inhibited T-type ca

44 When used as adjunct therapy, mibefradil did not affect the usual outcome of CHF.

45 Ca(2+) channel blockers NiCl2 (50 microM) or mibefradil dihydrochloride (10 microM) affected the ampl

46 l/L, consistent with the reported potency of mibefradil for T-type Ca2+ channels.

47 M), and the T-type Ca(2+) channel antagonist mibefradil (IC(50) = 5 microM), whereas other metals (in

48 1 microM), tamoxifen (IC50 = 1.3 microM) and mibefradil (IC50 = 7 microM) inhibited proliferative gro

49 produce some of the toxicity associated with mibefradil in cardiovascular pharmacology.

50 The 14% increased risk of mortality with mibefradil in the first 3 months was not statistically s

51 DTNB alone and in combination with mibefradil induces thermal analgesia.

52 The T-type Ca(2+) channel blocker mibefradil inhibited Ca(2+) spikes and waves on cells an

53 Oral administration of mibefradil inhibited growth of GSC-derived GBM murine xe

54 opylamino) benzoic acid (NPPB), tamoxifen or mibefradil inhibited swelling-activated anionic current.

55 T-type Ca2+ channel blockers (Ni2+ and mibefradil) inhibited large-amplitude SMOCs without affe

56 a holding potential of -70 mV, the Kapp for mibefradil inhibition of P-type channels was approximate

57 rendipine and PN200-110, but 1-10 micrometer mibefradil inhibits reversibly.

58 We also tested whether mibefradil interacted with slow-inactivated state(s).

59 We tested whether mibefradil interacts with the local anesthetic (LA) bind

60 Mibefradil is a novel Ca(2+) channel antagonist that pre

61 Mibefradil is a T-type and L-type calcium channel blocke

62 Mibefradil is a T-type Ca2+ channel antagonist with repo

63 Mibefradil is a tetralol derivative once marketed to tre

64 s selective block of T-type Ca(2+) channels, mibefradil may be a potent but less-selective K(+) chann

65 The manufacturer voluntarily withdrew mibefradil on June 8, 1998.

66 In addition, mibefradil reduced action potential-mediated synaptic tr

67 Only the inhibitory effects of NPPB and mibefradil reversed with the drug washout.

68 , thus conferring T-type Ca(2+) channel-like mibefradil sensitivity to the Na(+) channel.

69 Mibefradil should be a useful compound for distinguishin

70 eparing to switch patients' medications from mibefradil to other antihypertensive agents should be aw

71 Mibefradil treatment or RNAi-mediated attenuation of Cav

72 The potency of mibefradil was increased at less hyperpolarized holding

73 The inhibition of I(AC) by mibefradil was independent of the membrane potential.

74 The initial 50-mg daily dose of mibefradil was uptitrated to 100 mg after 1 month and co

75 SCs can be targeted by the FDA-approved drug mibefradil, which inhibits the T-type calcium channel Ca

76 I(AC) channels were inhibited by mibefradil with an IC(50) value of 0.50 microM, a concen

77 We further probed the interaction of mibefradil with inactivated Nav1.5 channels.

78 ter, randomized, double-blind study compared mibefradil with placebo as adjunct to usual therapy in 2