ライフサイエンスコーパス: sodium channel blocker

1 eptors but are unaffected by tetrodotoxin, a sodium channel blocker.

2 acerbated by GS967, a potent, unconventional sodium channel blocker.

3 e effect would persist after withdrawal of a sodium channel blocker.

4 dicarboxamide (CDA54), a peripherally acting sodium channel blocker.

5 cluding antiepileptics, antidepressants, and sodium channel blockers.

6 indings may also inspire redesign of cardiac sodium channel blockers.

7 synthesized as voltage-gated skeletal muscle sodium channel blockers.

8 e treatment of pain using novel and existing sodium channel blockers.

9 Lubeluzole moieties were modest sodium channel blockers.

10 Both riluzole and propranolol are efficient sodium channel blockers.

11 ch as carbamazepine and phenytoin, which are sodium channel blockers.

12 ut the side effect profile of broad spectrum sodium channel blockers.

13 opioid analgesics, such as subtype-selective sodium channel blockers.

14 ate onset epilepsies and lack of response to sodium channel blockers.

15 ncreased from 32.7% to 78.6% with the use of sodium channel blockers.

16 By contrast, the sodium channel blocker 1 microM tetrodotoxin had no effe

17 oncealed and may be unmasked or modulated by sodium channel blockers, a febrile state, vagotonic agen

18 Sodium channel blockers also rescued the I1660V current,

19 on of sodium was minimized by the epithelial sodium channel blocker amiloride.

20 he degree seen with mM concentrations of the sodium channel blocker amiloride.

21 The epithelial sodium-channel blocker amiloride has been shown to inhib

22 CFM6104 was shown to be a state-selective, sodium channel blocker and a fluorescent p-glycoprotein

23 found that oxcarbazepine and Huperzine A, a sodium channel blocker and reversible acetylcholinestera

24 del of multiple sclerosis using conventional sodium channel blockers and a novel central nervous syst

25 on between age at disease onset, response to sodium channel blockers and the functional properties of

26 ating recombinant strains expressing AaIT1(a sodium channel blocker) and hybrid-toxin (a blocker of b

27 tes, sodium channel antagonists (also called sodium channel blockers), and sympathomimetics.

28 (SDLs) containing saxitoxin (STX), a site 1 sodium channel blocker, and the glucocorticoid agonist d

29 Sodium channel blockers are effective for seizure contro

30 Sodium channel blockers are effective in unmasking carri

31 ribed to treat cardiac arrhythmias, but many sodium channel blockers are known to have pro-arrhythmic

32 Sodium channel blockers are largely used to shorten QT i

33 State-dependent sodium channel blockers are often prescribed to treat ca

34 Several clinical studies of sodium channel blockers are under way in patients with m

35 Sodium channel blockers are used as gene-specific treatm

36 Sodium channel blockers are used clinically to treat a n

37 Several sodium channel blockers are used clinically to treat neu

38 iate action potentials in brain neurons, and sodium channel blockers are used in therapy of epilepsy.

39 l hemiplegic migraine type 3, and identifies sodium channel blockers as potentially efficacious thera

40 Considered as a sodium channel blocker, BBG is remarkably potent, acting

41 voked depolarisation was inhibited by Nav1.8 sodium channel blockers but was refractory to the applic

42 nist for ASICs), tetrodotoxin (0.5 microM, a sodium channel blocker), cadmium (100 microM, a nonselec

43 Sodium channel blockers can potentiate these findings an

44 Here we show that charged sodium-channel blockers can be targeted into nociceptors

45 BIIB074, a Nav1.7-selective, state-dependent sodium-channel blocker, can be administered at therapeut

46 length was ameliorated by the use-dependent sodium channel blocker carbamazepine and by a blocker of

47 r trigeminal neuralgia is treatment with the sodium channel blockers carbamazepine and oxcarbazepine,

48 We previously showed that the sodium-channel blocker carbamazepine (Carb) corrects K(A

49 Thus, the peripheral nerve sodium channel blocker CDA54 selectively inhibits sensor

50 and a novel central nervous system-excluded sodium channel blocker (CFM6104) that was synthesized wi

51 Further, a good response to sodium channel blockers clinically was found to be assoc

52 the efficacy of both drugs to mexiletine, a sodium channel blocker currently used to treat myotonia.

53 otent than anticonvulsant and antiarrhythmic sodium channel blockers currently used to treat neuropat

54 tes the high-affinity binding site for these sodium channel blocker drugs, and block may be mainly el

55 reased mortality risk, consistent with known sodium channel blocker effects, which, however, normaliz

56 Internal perfusion with a fast sodium channel blocker eliminated spontaneous bursting b

57 d of two enantiomers that are equally potent sodium-channel blockers; however, (R)-propafenone is an

58 s demonstrate unexpected efficacy of a novel sodium channel blocker in Dravet syndrome and suggest a

59 (NavMs) binds and is inhibited by eukaryotic sodium channel blockers in a manner similar to the human

60 ts, together with results showing effects of sodium channel blockers in immune cells, raise questions

61 ise questions about the long-term effects of sodium channel blockers in neuroinflammatory disorders,

62 The potential role of sodium channel blockers in patients with potassium chann

63 orders, and suggest that clinical studies of sodium channel blockers in these disorders should be pla

64 combination with aerosolized amiloride, the sodium channel blocker, in normal human volunteers.

65 affected individuals and can be unmasked by sodium channel blockers, including antiarrhythmic drugs

66 Sodium channel blockers increase STE.

67 The response to sodium channel blockers indicates a therapeutic overlap

68 ines even in the presence of Tetrodotoxin, a sodium channel blocker, indicating that the morphine's e

69 Local perfusion of tetrodotoxin, a sodium channel blocker, into the striatum of an anesthet

70 le the anti and proarrhythmic potential of a sodium channel blocker is thought to depend on the chara

71 Clinical utility of nonselective sodium channel blockers is limited due to serious advers

72 s show that CNS penetration by voltage-gated sodium channel blockers is not required for efficacy in

73 Na(v)1.1-1.8 demonstrated that the standard sodium channel blocker lamotrigine had modest activity a

74 hase 2 trial, we aimed to assess whether the sodium-channel blocker lamotrigine is also neuroprotecti

75 we examine the rate-dependent effects of the sodium channel blocker lidocaine by constructing and ana

76 of MD, visual cortices were infused with the sodium channel blocker lidocaine in vehicle or vehicle o

77 Perfusion of the DRG with a sodium channel blocker (lidocaine) at a dose much less t

78 ike cationic derivatives of local anesthetic sodium channel blockers like QX-314, this cationic compo

79 for most patients, concomitant therapy with sodium channel blockers, like mexiletine, is often utili

80 Nevertheless, compared with other known sodium channel blockers, lubeluzole adds a third pharmac

81 me pathophysiology, these data indicate that sodium channel blockers may be considered therapeutic fo

82 ta are converging to suggest next generation sodium channel blockers may offer the potential for nove

83 We report the characterization of a new sodium channel blocker, mu-conotoxin PIIIA(mu-PIIIA).

84 ort the discovery of two novel TTX-resistant sodium channel blockers, mu-conotoxins SIIIA and KIIIA,

85 d surgical antiadrenergic interventions with sodium channel blockers often accompanied by an implanta

86 litis (EAE) have shown protective effects of sodium channel blockers on central nervous system axons

87 eived HS containing a long acting epithelial sodium channel blocker (P308); isotonic saline; or no tr

88 Two sodium channel blockers, phenytoin and flecainide, have

89 Our pharmacological data indicate that sodium channel blockers present a treatment option in SC

90 induced type 1 Brugada ECG pattern following sodium channel blocker provocation (SCBP) are not fully

91 the calcium channel blocker nifedipine, the sodium channel blocker quinidine, etc.

92 lencing motor neurons with the intracellular sodium channel blocker QX-314 also disrupted premotor rh

93 vity, by introducing the membrane-impermeant sodium channel blocker QX-314 into these axons via the T

94 Most sodium channel blockers reduce the early (peak) and late

95 icacy in some GoF SCN2A patients, phenytoin (sodium channel blocker) reduced the excitability of neur

96 f tetrodotoxin (TTX), a potent voltage-gated sodium channel blocker, reduces neurological deficits an

97 esensitization blocker cyclothiazide and the sodium channel blockers riluzole, mexiletine and QX-314

98 nd carvedilol), flecainide, and the neuronal sodium-channel blocker riluzole; a direct antiarrhythmic

99 Site-1 sodium channel blockers (S1SCBs) act as potent local ana

100 ionally, inhibition of sodium influx using a sodium channel blocker saxitoxin completely prevented th

101 Antiepileptic drugs were categorized by MOA: sodium channel blockers (SC), gamma-aminobutyric acid an

102 two individuals with GoF variants, while the sodium-channel blocker (SCB) lamotrigine exacerbated sei

103 Intravenous infusion of sodium-channel blockers (SCB) with either ajmaline, flec

104 After administration in combination with sodium channel blockers, status epilepticus was interrup

105 in many patients, but can be unmasked using sodium channel blockers such as flecainide, ajmaline or

106 Site 1 sodium channel blockers such as tetrodotoxin (TTX) are e

107 hysiological effects as some pharmacological sodium channel blockers, such as significantly shortenin

108 Amiloride, an epithelial sodium channel blocker, suppresses the responsiveness of

109 produce SLRs followed by an injection of the sodium channel blocker tetrodotoxin (TTX) into the MCP.

110 ked this large outward component because the sodium channel blocker tetrodotoxin (TTX) is typically u

111 e tested this by measuring the effect of the sodium channel blocker tetrodotoxin (TTX) on depolarizat

112 nvestigated this concept with the reversible sodium channel blocker tetrodotoxin (TTX) to determine (

113 DMPP persisted following application of the sodium channel blocker tetrodotoxin (TTX), and in the pr

114 ither in the presence or absence of the fast sodium channel blocker tetrodotoxin (TTX).

115 using glutamate receptor antagonists and the sodium channel blocker tetrodotoxin (TTX).

116 ivation of the basolateral amygdala with the sodium channel blocker tetrodotoxin disrupted both the a

117 Conversely, the sodium channel blocker tetrodotoxin fully abolished the

118 mpletely abolished by the application of the sodium channel blocker tetrodotoxin or by replacement of

119 In all experiments the sodium channel blocker tetrodotoxin was used to prevent

120 The astrocytic responses were blocked by the sodium channel blocker tetrodotoxin, the voltage-depende

121 with small hydrophilic molecules, the site 1 sodium channel blockers tetrodotoxin and saxitoxin.

122 ught to induce hyperpolarized arrest) or the sodium-channel blocker tetrodotoxin (which induces polar

123 The highly selective sodium channel blocker, tetrodotoxin (TTX) has been inst

124 f the study was to examine the effect of the sodium channel blocker, tetrodotoxin (TTX), in order to

125 The sodium channel blocker, tetrodotoxin (TTX), is an effect

126 intravitreal injections of the voltage-gated sodium channel blocker, tetrodotoxin (TTX), the metabotr

127 Then, the BC was microinjected with a sodium channel blocker, tetrodotoxin, during 4 extinctio

128 The sodium-channel blocker, tetrodotoxin (TTX; 2 micromol/l)

129 t carriers responded significantly better to sodium channel blockers than to other anti-seizure medic

130 S represents a structurally novel and potent sodium channel blocker that may be used as a template fo

131 We report here the discovery of A-803467, a sodium channel blocker that potently blocks tetrodotoxin

132 Evenamide is a selective voltage-gated sodium channel blocker that reduces neuronal hyperexcita

133 Tetrodotoxin (TTX) is a sodium channel blocker that temporarily inactivates both

134 , we demonstrated that tetrodotoxin (TTX), a sodium channel blocker that temporarily inactivates neur

135 after incubation with tetrodotoxin (TTX), a sodium channel blocker, there was a significant increase

136 The development of subtype-specific sodium channel blockers, though clearly desirable, has b

137 ranch block, as well as the effectiveness of sodium channel blockers to unmask the syndrome and, thus

138 orms of the disease and the effectiveness of sodium channel blockers to unmask the syndrome and, thus

139 The clinical suspicion and use of a sodium-channel blocker to unmask BrS has allowed earlier

140 with a reduction in seizures in response to sodium channel blocker treatment (carbamazepine, oxcarba

141 gically silencing action potentials with the sodium channel blocker tricaine.

142 receptor antagonist CNQX (20 microM) or the sodium channel blocker TTX (1 microM) did not.

143 Application of the voltage-gated sodium channel blocker TTX enhanced the on-centre respon

144 Third, the sodium channel blocker TTX mimicked the effects of D2 re

145 Application of the voltage-gated sodium channel blocker TTX produced effects on AII amacr

146 ted dilation was inhibited completely with a sodium channel blocker (TTX), an NOS inhibitor (L-NNA),

147 ist, bicuculline (10 microM) and by the fast sodium channel blocker, TTX, suggesting that 5-HT had in

148 We find that the use of sodium channel blockers was often associated with clinic

149 sory axons by targeted delivery of a charged sodium-channel blocker, we found that functional blockad

150 -onset forms and an insufficient response to sodium channel blockers were associated with loss-of-fun

151 In contrast, sodium channel blockers were rarely effective in epileps

152 nderstood and may differ from those of other sodium channel blockers with greater potencies.

153 subtle differences among three subclasses of sodium channel blockers with sub-millisecond accuracy.

154 Mexiletine is a well-known sodium channel blocker, with proven efficacy in patients