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 Mibefradil, an inhibitor of calcium channels, was also f

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

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

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

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

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

25 Unlike the channel blockers mibefradil and ML218, which reduced total and progressiv

26 We conclude that the effects of mibefradil and Ni(2+) in other lymphatic preparations ar

27 out lymphatic vessels responded similarly to mibefradil and Ni(2+), which substantially reduced contr

28 e reputedly selective T-type VGCC inhibitors mibefradil and Ni(2+).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

44 Mibefradil blocked currents of all Na+ channel isoforms

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

46 cium channel blocker ML218 acts similarly to mibefradil, blocking CatSper channels activated by both

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

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

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

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

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

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

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

54 1 microM), tamoxifen (IC50 = 1.3 microM) and mibefradil (IC50 = 7 microM) inhibited proliferative gro

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

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

57 We also demonstrated that the TTCC blocker mibefradil induces apoptosis and impairs migration and i

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

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

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

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

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

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

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

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

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

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

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

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

70 Mibefradil is a tetralol derivative once marketed to tre

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

72 Bay K 8644 (Ca(V)1.3 inhibitor, activator), mibefradil, Ni(2+) (Ca(V)3.2 inhibitors) and high K(+) d

73 TTCC in vitro (such as tetralol derivatives mibefradil/NNC-55-096, or different 3,4-dihydroquinazoli

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

75 acological inhibition of CatSper with either mibefradil or NNC 55-0396 leads to the same loss in swim

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

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

78 (2+)-transients; ADT-treated LNCaP exhibited mibefradil-sensitive or, occasionally, nifedipine-sensit

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

80 Mibefradil should be a useful compound for distinguishin

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

82 Mibefradil treatment or RNAi-mediated attenuation of Cav

83 The potency of mibefradil was increased at less hyperpolarized holding

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

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

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

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

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

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