ライフサイエンスコーパス: retigabine

1 ation (-33.1 +/- 2.6 mV, n = 4, by 10 microM retigabine).

2 mes more potent and also more selective than retigabine.

3 lly restored by the neuronal K(v)7 activator retigabine.

4 nted by incubation with the M-channel opener retigabine.

5 uction of deactivation distinct from that of retigabine.

6 ) and absence (7.6 +/- 0.01 pS) of 10 microM retigabine.

7 reby influences the unique gating effects of retigabine.

8 r by local infusion of the M-channel opener, retigabine.

9 ng that KCNQ2 may be the molecular target of retigabine.

10 Retigabine (0.1 to 10 microM) also slowed the rate of ch

11 Retigabine (0.1 to 10 microM) induced a potassium curren

12 The M-current enhancers Retigabine (10 and 30muM) and Flupirtine (30muM) had a d

13 ain slices, whereas KCNQ channel activation (retigabine, 2-40 mum) silenced these neurons.

14 re, it can be rescued by bath perfusion with retigabine, a KCNQ channel activator, and chronic treatm

15 ardiac conduction blocks can be prevented by retigabine, a Kv7 channel opener.

16 technique was used to examine the effects of retigabine, a novel anticonvulsant drug, on the electror

17 Application of retigabine, a recently marketed KV 7 channel opener, par

18 Retigabine, a small molecule that activates KCNQ2-5 chan

19 specific chemical interactions required for retigabine action.

20 In conclusion, we have shown that retigabine acts as a KCNQ potassium channel opener.

21 Retigabine also had a marked effect on KCNQ current kine

22 Intra-LHb infusion of retigabine also reduced ethanol consumption and preferen

23 al moieties of the KCNQ2-5 channel activator retigabine, an anticonvulsant approved by the U.S. Food

24 Retigabine, an M-channel opener that does not open recep

25 In addition, potency of numerous retigabine analogues correlates with the negative electr

26 c-scale interaction essential for effects of retigabine and provide stringent constraints that may gu

27 KCNQ2/Q3 channels as a molecular target for retigabine and suggest that activation of KCNQ2/Q3 chann

28 Retigabine and zinc pyrithione are two activators for KC

29 Here we report that retigabine and zinc pyrithione recognize two different s

30 An activator (retigabine) and an inhibitor (XE991) of the M-current we

31 nsing domains (VSDs) in response to voltage, retigabine, and PIP2.

32 In the presence of retigabine at 0 mV the combined duration and contributio

33 that SF0034 was five times more potent than retigabine at shifting the voltage dependence of KCNQ2/3

34 To elucidate how the retigabine binding site is coupled to changes in voltage

35 eveal an important role for PIP2 in coupling retigabine binding to altered VSD function.

36 Retigabine binds to the pore-forming domain, causing a h

37 resent study, we sought to determine whether retigabine could enhance current through M-like currents

38 els and coapplication of zinc pyrithione and retigabine could restore a disease mutant channel simila

39 ent for use as anti-epileptic drugs, such as retigabine (D-23129, N-(2-amino-4-(4-fluorobenzylamino)-

40 cker linopirdine and anticonvulsant enhancer retigabine display increased and decreased potency, resp

41 x was potentiated by the anticonvulsant drug retigabine (EC(50)=0.5 microM).

42 lishes channel potentiation, indicating that retigabine effects rely strongly on formation of a H-bon

43 In differentiated PC12 cells, retigabine enhanced a linopirdine-sensitive current.

44 The mechanism by which retigabine enhanced KCNQ2/Q3 currents involved large, dr

45 channel openers, including FDA-approved drug retigabine (ezogabine), show antidepressant efficacy.

46 Both potassium-induced and retigabine-facilitated efflux were blocked by TEA (IC(50

47 We investigated four M channel enhancers (retigabine, flupirtine, zinc pyrithione and H(2)O(2)) fo

48 In control experiments retigabine had no effect on either resting membrane pote

49 This effect was limited to IPSCs; retigabine had no significant effect on excitatory posts

50 Although KCNQ channel openers, such as retigabine, have emerged as anti-epilepsy drugs, their e

51 ions to -85 mV in the presence of 100 microM retigabine (IC(50) = 5.2 microM).

52 transfer were all significantly enhanced by retigabine in a dose-dependent manner.

53 on can explain the anticonvulsant actions of retigabine in animal models of epilepsy.

54 re potent and less toxic anticonvulsant than retigabine in rodents.

55 In contrast, the Kv7 channel opener retigabine increased I(M) amplitude and I(hold).

56 Retigabine increased mean maximal Po to 0.38 +/- 0.04 an

57 Consistent with the hypothesis that retigabine increases inhibitory neurotransmission via a

58 contrast, treatment of VPA-treated mice with retigabine induced anticonvulsant effects even when admi

59 rization and increased AP frequency, whereas retigabine induced hyperpolarization and arrested firing

60 Retigabine-induced currents in CHO-KCNQ2/Q3 cells were i

61 Retigabine is a novel anticonvulsant with an unknown mec

62 Retigabine is a recently approved anticonvulsant that ac

63 teromeric channel showed that application of retigabine leads to a concentration-dependent hyperpolar

64 It has recently been reported that retigabine modulates a potassium channel current in nerv

65 ut mice, and that the decay was sensitive to retigabine modulation, unlike in wild-type mice.

66 Retigabine [N-(2-amino-4-[fluorobenzylamino]-phenyl) car

67 local infusion or systemic administration of retigabine normalized neuronal hyperactivity and depress

68 resent study we have examined the effects of retigabine on recombinant human KCNQ2 and KCNQ3 potassiu

69 glion neurons did not reduce the efficacy of retigabine or flupirtine to hyperpolarize the resting me

70 Retigabine or similar drugs may be used as a personalize

71 or absence of the specific M-channel opener retigabine, or agonists of bradykinin B2 or purinergic P

72 increased H-bonding propensity, strengthens retigabine potency.

73 In addition, retigabine potentiated inhibitory postsynaptic currents

74 Therefore, retigabine potently reduces excitability in neural circu

75 Retigabine raised the threshold for activation of arteri

76 orted mutation that abolishes sensitivity to retigabine, remains fully sensitive to these compounds.

77 nel blocker XE991 or the KCNQ channel opener retigabine reverses the effects on consolidation caused

78 Retigabine (RTG) is a first-in-class antiepileptic drug

79 e we show that the novel anti-epileptic drug retigabine (RTG) modulates channel function of pore-only

80 olybasic motif in the proximal C terminus of retigabine-sensitive KCNQ channels that contributes to V

81 Moreover, unlike retigabine, SF0034 did not shift the voltage dependence

82 Retigabine shifted the voltage dependence of channel act

83 with its known action on potassium channels, retigabine significantly hyperpolarized the resting memb

84 Retigabine stabilizes the conducting conformation of the

85 We found that co-application of retigabine strongly decreased the nicotine-induced incre

86 paired-pulse depression, was not altered by retigabine, suggesting that its effect on IPSCs is prima

87 Exposure to the KCNQ channel activator retigabine suppressed the type II fiber's response to ha

88 Application of 10 microM retigabine to oocytes expressing the KCNQ2/3 heteromeric

89 Application of retigabine to speed KCNQ channel activation accelerated

90 The effect of retigabine was associated with a slowing of M-like tail

91 zylamino)-phenyl)-carbamic acid ethyl ester (retigabine) was abrogated.

92 Ezogabine (retigabine) was recently approved as an add-on drug for

93 he 3-position of the tri-aminophenyl ring of retigabine, we synthesized a small-molecule activator (S

94 Similar effects of retigabine were observed in oocytes expressing KCNQ2 alo

95 nsensitive to another Kv7 channel activator, retigabine, were also insensitive to ML213 (10 muM).

96 Retigabine, which opens KCNQ channels, diminishes axonal