ライフサイエンスコーパス: aminopyridine

1 seizures induced by topical application of 4-aminopyridine.

2 al events elicited with focal injection of 4-aminopyridine.

3 less sensitive to the K(+) channel blocker 4-aminopyridine.

4 r can be easily obtained in two steps from 2-aminopyridine.

5 increased after blocking Kv channels with 4-aminopyridine.

6 by charybdotoxin, iberiotoxin, apamin, or 4-aminopyridine.

7 IC50 of 5.2 mM and was unaffected by 1 mM 4-aminopyridine.

8 the potassium channel blockers barium and 4-aminopyridine.

9 firing induced by the K(+)-channel blocker 4-aminopyridine.

10 ion was reduced by 46.2 +/- 10.3 % in 5 mM 4-aminopyridine.

11 ing K+ currents with extracellular TEA and 4-aminopyridine.

12 shold current steps was greatly reduced by 4-aminopyridine.

13 g brain with the potassium channel blocker 4-aminopyridine.

14 tion on epileptiform discharges induced by 4-aminopyridine.

15 ctive cyclization promoted by N,N-dimethyl-4-aminopyridine.

16 rescent assays for FAAH based on substituted aminopyridines.

17 utward current that was also suppressed by 4-aminopyridine (0.5 mM).

18 IPO was blocked by Ba2+ (1 mM), 4-aminopyridine (1 mM) and tetraethylammonium (TEA; 20 mM)

19 Application of 4-aminopyridine (1 mM) to normal TTX-resistant bladder aff

20 ansient outward current (I(to)) block with 4-aminopyridine (1 to 2 mmol/L) or quinidine (5 micromol/L

21 llergic rats treated with 4-aminopyridine (4-aminopyridine) (1 mg/kg) (n = 6); and allergic rats trea

22 s identified (1st step, neat, 2.3 equiv of 2-aminopyridine, 1.20 equiv of I(2), 4 h, 110 degrees C; 2

23 el blockers tetraethylammonium (10 mM) and 4-aminopyridine (10 mM) markedly increased the amplitude o

24 cells were disclosed after application of 4-aminopyridine (100 microM), indicating that these synaps

25 with oral, extended-release dalfampridine (4-aminopyridine) 10mg twice daily.

26 2-Aminopyridines 1a-c and 1-aminoisoquinoline with 1-chlor

27 Using a xenograft model, we found that 3-aminopyridine-2-carboxaldehyde thiosemicarbazone (3-AP)

28 Importantly, 3-aminopyridine-2-carboxaldehyde thiosemicarbazone (3-AP)

29 Triapine(R) (3-aminopyridine-2-carboxaldehyde thiosemicarbazone (3-AP))

30 3-aminopyridine-2-carboxaldehyde thiosemicarbazone (3-AP;

31 Triapine (3-AP; 3-aminopyridine-2-carboxaldehyde thiosemicarbazone), a rib

32 electronic spectrum of the gas-phase dimer 2-aminopyridine.2-pyridone, an analog of the adenine.thymi

33 was antagonized by a high concentration of 4-aminopyridine (3 mM).

34 2-Aminopyridine-3,5-dicarbonitrile compounds were previous

35 ructure-activity relationship study of the 6-aminopyridine-3,5-dicarbonitrile scaffold.

36 compound able to increase axon conduction, 4-aminopyridine-3-methanol, promotes further improvement i

37 rized potentials was reversibly blocked by 4-aminopyridine (4 mM) but not tetraethylammonium chloride

38 kylamino)pyridines (1) in three steps from 2-aminopyridine (4) is reported.

39 trols) (n = 6); allergic rats treated with 4-aminopyridine (4-aminopyridine) (1 mg/kg) (n = 6); and a

40 oltage-dependent K(+) (K(V)) currents with 4-aminopyridine (4-AP) an outward current containing inact

41 potassium channels [blocked by 100 microM 4-aminopyridine (4-AP) and 0.5-1 microM alpha-dendrotoxin

42 ed by Cs+, Ba2+ and high concentrations of 4-aminopyridine (4-AP) and TEA.

43 del also accounts for selective effects of 4-aminopyridine (4-AP) and tetraethylammonium (TEA), which

44 The A-type current was blocked by 4-aminopyridine (4-AP) and was inhibited by flecainide, wi

45 f the dendrites similar to those seen with 4-aminopyridine (4-AP) application.

46 Aminopyridines such as 4-aminopyridine (4-AP) are widely used as voltage-activate

47 h L2 and L5 are not considered part of the 4-aminopyridine (4-AP) binding site, unlike the L4 heptad

48 blockers tetraethyl ammonium chloride and 4-aminopyridine (4-AP) both inhibited short-term copper-in

49 was sensitive to the K(+) channel blocker 4-aminopyridine (4-AP) but not tetraethylammonium (TEA) or

50 ntly, the potassium (K(+)) channel blocker 4-aminopyridine (4-AP) constitutes the most promising trea

51 4-Aminopyridine (4-AP) has been used extensively to study

52 However, although 4-aminopyridine (4-AP) inhibited peak I(A) activated by st

53 4-Aminopyridine (4-AP) is a well known convulsant that enh

54 he voltage-gated K(+) (Kv) channel blocker 4-aminopyridine (4-AP) is used to target symptoms of the n

55 Perfusion of 4-aminopyridine (4-AP) mimicked a known effect of behavior

56 In this study we analyzed the effect of 4-aminopyridine (4-AP) on free cytosolic calcium concentra

57 erotonin or the potassium channel blockers 4-aminopyridine (4-AP) or alpha-dendrotoxin (DTX).

58 Inhibition of KV1 channels with 4-aminopyridine (4-AP) or treatment with the epidermal gro

59 ) channels vary in sensitivity to block by 4-aminopyridine (4-AP) over a 1000-fold range.

60 2-3 PNs, using alpha-dendrotoxin (DTX) or 4-aminopyridine (4-AP) to block these conductances.

61 ty that uses the potassium channel blocker 4-aminopyridine (4-AP) to induce large amplitude populatio

62 l studies have demonstrated the ability of 4-aminopyridine (4-AP) to restore electrophysiological and

63 ine (RAMH), tetraethyl ammonium (TEA), and 4-aminopyridine (4-AP) were applied in the superfusate.

64 thylammonium (TEA) and variably blocked by 4-aminopyridine (4-AP) with half-inactivation near -85 mV,

65 in the presence of a K(+) channel blocker, 4-aminopyridine (4-AP), 5-HT left unaltered the presynapti

66 4-Aminopyridine (4-AP), a nonselective blocker of K(v) vol

67 artificial cerebrospinal fluid containing 4-aminopyridine (4-AP), a potassium channel blocker.

68 t silver ion (Ag(+)) uptake is enhanced by 4-aminopyridine (4-AP), a well known voltage-sensitive pot

69 e that is blocked selectively by 50 microM 4-aminopyridine (4-AP), and a 4-AP-insensitive component t

70 g step using the potassium channel blocker 4-aminopyridine (4-AP), at a low (50 microM) and at a high

71 '-tetraacetic acid (BAPTA), application of 4-Aminopyridine (4-AP), expression of a Kv4.2 dominant neg

72 locked by 3,4-diaminopyridine (3,4-DAP) or 4-aminopyridine (4-AP), inhibitors of K(V) channels.

73 ibitors of IK, tetraethylammonium (TEA) or 4-aminopyridine (4-AP), reduced the control current elicit

74 trical and chemical synapses in sustaining 4-aminopyridine (4-AP)-evoked network activity recorded ex

75 F-actin and cofilin in hippocampus due to 4-aminopyridine (4-AP)-induced seizures/epileptiform activ

76 d a fivefold increase in susceptibility to 4-aminopyridine (4-AP)-induced spontaneous ectopic firing.

77 K(+) channel mKv1.5 is thought to encode a 4-aminopyridine (4-AP)-sensitive component of the current

78 -cell patch clamping showed a reduction of 4-aminopyridine (4-AP)-sensitive current (Kv current) from

79 cerebellar Purkinje cell dendrites, and a 4-aminopyridine (4-AP)-sensitive potassium channel underli

80 I(D) is a slowly inactivating 4-aminopyridine (4-AP)-sensitive potassium current of hipp

81 produced by the potassium channel blocker 4-aminopyridine (4-AP).

82 presence of the weak K(+) channel blocker 4-aminopyridine (4-AP).

83 K+ current that is largely insensitive to 4-aminopyridine (4-AP).

84 ocked by both tetraethylammonium (TEA) and 4-aminopyridine (4-AP).

85 sium and potassium conductances blocked by 4-aminopyridine (4-AP).

86 the induction of epileptiform activity by 4-aminopyridine (4-AP).

87 in the adult mouse SVZ: type 1 cells, with 4-aminopyridine (4-AP)/tetraethylammonium (TEA)-sensitive

88 4-Aminopyridine (4-AP, >= 5 mM) caused continuous spiking.

89 4-aminopyridine (4-AP, 0.5 mM) reduced the threshold for s

90 ge-dependent potassium conductance blocker 4-aminopyridine (4-AP, 100 microM) abolished the inhibitor

91 4-Aminopyridine (4-AP, 2 mm) attenuated I(A) in both whole

92 nels was blocked by a low concentration of 4-aminopyridine (4-AP, 40 microM), a significant facilitat

93 4-Aminopyridine (4-AP, 5 mM) decreased the amplitude of th

94 nclusion of the A-type K+ current blocker, 4-aminopyridine (4-AP, 5 mM) in the pipette also antagonis

95 s were inhibited by applications of either 4-aminopyridine (4-AP, at micromolar levels), alpha-dendro

96 e Ca2+-activated K+ (KCa) channel blocker; 4-aminopyridine (4-AP; 1 mM), a voltage-gated K+ (KV) chan

97 by 65% with the potassium channel blocker 4-aminopyridine (4-AP; 100 microM) and a 12-lipoxygenase i

98 nsitive to application of TEA (0.5 mm) and 4-aminopyridine (4-AP; 30 mum).

99 vating I(Kv) which was potently blocked by 4-aminopyridine (4-AP; IC50, 232 microM), but was almost i

100 of IK1-like and other potassium channels by aminopyridines (4-AP and 3,4-DAP) may also explain the p

101 vity included the alpha-amino derivative 29, aminopyridine 47, isothiourea 67, and aminoguanidine 69.

102 The convulsant 4-aminopyridine (4AP) facilitates the synchronous firing o

103 We present a model for the action of 4-aminopyridine (4AP) on K channels.

104 the two channel types were also found for 4-aminopyridine (4AP).

105 ls and using the potassium channel blocker 4-aminopyridine (4AP).

106 of either bicuculline methiodide (BMI) or 4-aminopyridine (4AP).

107 zations were significantly attenuated with 4-aminopyridine (5 mM) but unaffected by tetraethylammoniu

108 identity of I(A) was confirmed by applying 4-aminopyridine (5 mM), which significantly inhibited I(A)

109 The utility of a 2-aminopyridine-5-boronic acid pinacol ester as a robust a

110 us epileptiform activity induced in CA3 by 4-aminopyridine (50-100 microM) was investigated.

111 c-efficiency-focused drug design resulted in aminopyridine 8e, which was potent across a broad panel

112 Application of 2 mM 4-aminopyridine (a dose sufficient to cause channel blocka

113 e opening and is absent in the presence of 4-aminopyridine, a compound that prevents the last gating

114 4-Aminopyridine, a K+ channel blocker, broadened the compo

115 4-Aminopyridine, a powerful modulator of sperm motility, b

116 2+)-activated K(+) channel blocker, and by 4-aminopyridine, a voltage-gated K(+) (KV) channel blocker

117 2+)-activated K(+) channel blocker, and by 4-aminopyridine, a voltage-gated K(+) (KV) channel blocker

118 1-s pacing cycle length in the absence of 4-aminopyridine, adding a virtual Ito-like current (n=1113

119 Titration of MlTrxR-Trx and MlTrxR with 3-aminopyridine adenine dinucleotide phosphate (AADP+), an

120 oxidase with oxidized 3-acetylpyridine and 3-aminopyridine adenine dinucleotides further support the

121 The K(v) channel blocker 4-aminopyridine also inhibited oxyhb-induced cerebral arte

122 iodine-catalyzed oxidative cyclization of 2-aminopyridine/amidine and isothiocyanate via N-S bond fo

123 were induced by neocortical injections of 4-aminopyridine, an inhibitor of voltage-gated K+ channels

124 vein myocytes, in the presence of 5 mmol/L 4-aminopyridine, an outwardly rectifying K+ current was re

125 Other aminopyridine analogs reduced attack frequency but, cons

126 specificity of the effect for K(v) channels, aminopyridine analogs were assessed for their ability to

127 n, and tetraethylammonium but sensitive to 4-aminopyridine and 0.5 mM Ba2+, consistent with A-type po

128 prepared in short, modular sequences from 2-aminopyridine and 2-aminopyrimidine wherein aminations o

129 complexes cis-[Ru(phen)2(Apy)2](2+), Apy = 4-aminopyridine and 3,4-aminopyridine, are stable in aqueo

130 Ureas 1 and 7 were prepared by reacting 2-aminopyridine and aminonaphthyridine 25, respectively, w

131 e, and increased survival were observed in 4-aminopyridine and EPI groups.

132 F2 increased in controls but decreased in 4-aminopyridine and EPI groups.

133 Leukotriene B4 decreased in 4-aminopyridine and EPI groups.

134 ication of neuromodulators such as DCG IV, 4-aminopyridine and forskolin as well as a paired train st

135 efer and less frequent upon coinjection of 4-aminopyridine and leptin.

136 )) antagonized completely by clofilium and 4-aminopyridine and partially by tetraethylammonium, chary

137 inhibition by hypoxia, low sensitivity to 4-aminopyridine and quinine and insensitivity to tetraethy

138 e in both rat and human nNOS, in which the 2-aminopyridine and the fluorobenzene linker form crucial

139 Two c-Met clinical candidates from aminopyridine and triazolopyrazine chemical series (PF-0

140 by potassium ions that was reduced by 1 mM 4-aminopyridine and/or 100 nM iberiotoxin but unaffected b

141 road range of imidazo[1,2-a]pyridines from 2-aminopyridines and acetophenones is achieved by a tandem

142 olid state, isolated as (P) in (IO)3 (from 2-aminopyridine) and (R) in (26IO)3 (from 2-aminopyrimidin

143 mm tetraethylammonium, 100 nm apamin, 1 mm 4-aminopyridine, and 10 microm glybenclamide.

144 ptiform bursts induced by 7.5mM [K(+)](o), 4-aminopyridine, and bicuculline, and electrographic seizu

145 eliminated by tetrodotoxin, reinstated by 4-aminopyridine, and blocked by ionotropic glutamate recep

146 blockers, including tetraethylammonium and 4-aminopyridine, and insensitive to intracellular Ca2+.

147 midazo[1,2-a]pyridines from benzaldehydes, 2-aminopyridines, and propiolate derivatives catalyzed by

148 ribe the preparation of a series of 2-acyl-4-aminopyridines, and their use as catalysts for the hydro

149 vasoconstriction stimulated by Psora-4 or 4-aminopyridine, another KV channel inhibitor.

150 element, |H(DA)|, for electron transfer from aminopyridine (ap) to the 4-carbonyl-2,2'-bipyridine (cb

151 We found that during 4-aminopyridine application, both spontaneous seizure-like

152 4-Aminopyridines are valuable scaffolds for the chemical i

153 )2(Apy)2](2+), Apy = 4-aminopyridine and 3,4-aminopyridine, are stable in aqueous solution with stron

154 orescent assay for LAPs based on substituted aminopyridines as fluorescent reporters.

155 gned with the hope that they could (a) mimic aminopyridines as potent, isoform-selective arginine iso

156 ating, fast inactivating, and sensitive to 4-aminopyridine at 3 mm), and I(K) (slowly activating, non

157 ing, slowly inactivating, and sensitive to 4-aminopyridine at 30 microm), I(A) (fast activating, fast

158 pairs with high affinity, (Me)P (3-methyl-2 aminopyridine) binds to GC at higher pHs than cytosine,

159 These results suggest that aminopyridines block tottering mouse attacks via cerebel

160 K(+) antagonists used in animal research, 4-aminopyridine blocked E. coli chemotaxis between 10(-3)

161 ngth, EADs were blocked by the Ito blocker 4-aminopyridine, but reappeared when a virtual current wit

162 2-elicited dilation to a similar extent as 4-aminopyridine, but the selective KV1.3 blocker phenoxyal

163 Internal 4-aminopyridine, Ca2+ (10(-8) to 10(-6) M), and tetraethyl

164 Aminopyridines can directly target presynaptic HVACCs to

165 Enhancement of transmitter release with 4-aminopyridine caused a significant increase in quantal s

166 The 2-aminopyridine/CBrCl3 system acts as an alpha-bromination

167 ries of novel ALK2 inhibitors based on the 2-aminopyridine compound K02288.

168 iated by the activation of N-Boc-protected 2-aminopyridine-containing amides by triflic anhydride (Tf

169 In the novel series, the 2-aminopyridine core allowed a 3-benzyloxy group to reach

170 pid construction of the highly substituted 2-aminopyridine core.

171 In the presence of 4-aminopyridine, depolarizing pulses evoked transient outw

172 a high-throughput screening lead afforded an aminopyridine derivative 13 with significant NR2B antago

173 of these leads was developed into the novel aminopyridine derivative 9, a low micromolar inhibitor o

174 on in muscle cells, we identified a unique 4-aminopyridine derivative exhibiting an embedded partial

175 A series of alpha-amino functionalized aminopyridine derivatives (3-8) were designed to probe t

176 ion of members of a new series of 3-alkoxy-5-aminopyridine derivatives that display good selectivity

177 nner compounds, a number of new 3,5-diaryl-2-aminopyridine derivatives were synthesized.

178 4-Aminopyridine derivatives yielded oligoadenylates as lon

179 dification by immunization with biotinylated aminopyridine-derivatized glycans enriched for the anion

180 However, 4-aminopyridine did not affect the adaptation of rapidly a

181 4-Aminopyridine did not change DeltaV(-)(m)/DeltaV(+)(m).

182 tion was inhibited by paxilline but not by 4-aminopyridine, diphenylphosphine oxide-1, or 5-(4-phenyl

183 Addition of bicuculline and 4-aminopyridine facilitated the occurrence of large events

184 ermediate and facilitates the synthesis of 2-aminopyridines for which other methods fail.

185 nt method for the synthesis of substituted 2-aminopyridines from pyridine N-oxides is reported.

186 4-aminopyridine, gaboxadol hydrochloride and N-acetylneura

187 4-Aminopyridine gave extensive protection against a number

188 ot blocked by tetraethylammonium chloride, 4-aminopyridine, glibenclamide, apamin or MK-499.

189 para position relative to the amino group in aminopyridines greatly increased the fluorescence (i.e.,

190 amine level was higher in controls and the 4-aminopyridine group but reduced in the EPI group.

191 Metabolic acidosis was prevented in the 4-aminopyridine group.

192 in controls and EPI group and decreased in 4-aminopyridine group; prostaglandin F2 increased in contr

193 hylammonium (half-block by 150 microm) and 4-aminopyridine (half-block by 110 microm).

194 mbination with low, subepileptic levels of 4-aminopyridine, Halorhodopsin activation rapidly induced

195 tment of central vestibular disorders with 4-aminopyridine has been extended to patients with ataxia-

196 s of orally active antimalarial 3,5-diaryl-2-aminopyridines has been identified from phenotypic whole

197 While aminopyridines have demonstrated varying efficacy in tra

198 in nystagmus treatment, like the usage of 4-aminopyridine, have added potent medications to the phys

199 One of the derivatives contains a 2-aminopyridine heterocycle (d2APy) while the second conta

200 y its sensitivity to low concentrations of 4-aminopyridine (IC50 <100 mum) and block by the peptide i

201 linical studies suggested that fampridine (4-aminopyridine) improves motor function in people with mu

202 ate outward current was eliminated by 1 mM 4-aminopyridine in Kv1.4+/+, Kv1.4+/- and Kv1.4-/- myocyte

203 rfusion with the potassium channel blocker 4-aminopyridine in Mg(2+)-free medium.

204 zations were observed after application of 4-aminopyridine in Tg mice.

205 We induced focal neocortical seizures with 4-aminopyridine in transgenic mice expressing green fluore

206 Pyridine N-oxides were converted to 2-aminopyridines in a one-pot fashion using Ts2O-t-BuNH2 f

207 ] cycloaddition to form highly substituted 2-aminopyridines in an atom-efficient manner that is both

208 macological manipulations (bicuculline and 4-aminopyridine) in the entorhinal cortex and in the hippo

209 a straightforward synthesis of a variety of aminopyridines, including known estrogen receptor ligand

210 These results suggest that the aminopyridines increase the threshold for attack initiat

211 with TBOA and the Sk blocker apamin, only 4-aminopyridine increased the frequency of dopamine transi

212 ng a dominant-negative Kv4.2 construct and 4-aminopyridine, increased the amplitude of plateau potent

213 5 nM iberiotoxin, and unmodified by 0.8 mM 4-aminopyridine, indicating that LC causes vasodilation vi

214 Potassium channel blockers, such as 4-aminopyridine, induce vasoconstriction.

215 However, the 4-aminopyridine-induced GABA-dependent negative potentials

216 4-Aminopyridine-induced hyperactivation even in cells susp

217 cker) decreased the cumulative duration of 4-aminopyridine-induced ictal-like activities, with a slow

218 ons from lean mice, the Kv channel blocker 4-aminopyridine inhibited leptin-induced changes in input

219 our previously reported potent and selective aminopyridine inhibitors.

220 IK1 was a 4-aminopyridine-insensitive current with a negative half-i

221 Aminopyridine is employed as a recyclable directing grou

222 d transmitter release could be reversed by 4-aminopyridine, it is suggested that the effect on releas

223 The strategy for optimization of the 2-aminopyridine lead series to potent inhibitors of BACE-1

224 e pyridine core of antimalarial 3,5-diaryl-2-aminopyridines led to the identification of a novel seri

225 Low doses of 4-aminopyridine (<100 microm) reduced the oscillations and

226 ide nucleic acids containing thymidine and 2-aminopyridine (M) nucleobases form stable and sequence-s

227 e efficient reduction of CO2 to CO by cobalt aminopyridine macrocycles.

228 on of cholinergic interneuron spiking with 4-aminopyridine mimicked the effects of exogenous agonist

229 We have addressed this issue in the 4-aminopyridine model of epilepsy in vitro by comparing GA

230 We conclude that, in the 4-aminopyridine model of epilepsy in vitro, connexin36 is

231 he mouse entorhinal cortex in the in vitro 4-aminopyridine model of epileptiform synchronization.

232 in the entorhinal cortex, in the in vitro 4-aminopyridine model.

233 ariety of differently substituted linker and aminopyridine moieties attached at the C-2 position.

234 cules which incorporated aminopyrimidine and aminopyridine moieties with ATP mimetic characteristics

235 he importance of alkyl substitution at the 2-aminopyridine moiety and electron deficient aromatic gro

236 Kv3.1b does not account for the effects of 4-aminopyridine on central myelinated tracts.

237 Application of 4-aminopyridine on slices resulted in spontaneous network

238 Indazoles attached to a 2-aminopyridine or 2-aminoimidazole by a propylene linker

239 e reaction of isophthaloyl dichloride with 2-aminopyridine or 2-aminopyrimidine provides a facile ent

240 intraocular pressure increases induced by 4-aminopyridine or a selective agonist of the A3 adenosine

241 Blockade of the current by low doses of 4-aminopyridine or alpha-dendrotoxin dramatically slows th

242 of neither sEPSCs nor mEPSCs stimulated by 4-aminopyridine or capsaicin differed significantly betwee

243 4-Aminopyridine or depolarized conditioning blocked the TO

244 ed epileptiform activity induced by either 4-aminopyridine or Mg(2+)-free medium alone.

245 4-aminopyridine or related voltage-dependent K channel blo

246 yields of 35-92% in one pot by reaction of 2-aminopyridines or 2-(or 4-)aminopyrimidines, respectivel

247 mpal slices perfused with 7.5mM [K(+)](o), 4-aminopyridine, or bicuculline, and in vivo against seizu

248 en, or broad-spectrum K(+) channel blocker 4-Aminopyridine, or by knockdown of Kv1.3 expression via t

249 targeting different convulsant mechanisms (4-Aminopyridine, Pentylenetetrazole, Pilocarpine and Stryc

250 regioselective, as only 4,6-disubstituted 2-aminopyridine products are formed in moderate to high yi

251 st, blockade of motor neuron K channels by 4-aminopyridine prolonged the action potential and introdu

252 Our data point to I(to) block (4-aminopyridine, quinidine) as an effective pharmacologica

253 Structure based design led to aminopyridine (R)-21, a potent and selective inhibitor a

254 the relatively broad K(+) channel blocker 4-aminopyridine reduced the fast repolarization, resulting

255 The potassium channel blocker 4-aminopyridine reliably induces seizure-like events in te

256 The aminopyridine ring mimics the guanidinium group of L-arg

257 w inhibitors consists of three fragments: an aminopyridine ring, a pyrrolidine, and a tail of various

258 mbin and the edges of the central phenyl and aminopyridine rings and the sulfonyl group of 1 such tha

259 rein a series of Nek2 inhibitors based on an aminopyridine scaffold.

260 ctivity of human nNOS inhibitors bearing a 2-aminopyridine scaffold.

261 evidence that oxyhb selectively decreases 4-aminopyridine sensitive, voltage-dependent K(+) channel

262 IK2 was a 4-aminopyridine-sensitive current (half-maximal block at a

263 IK,A was a 4-aminopyridine-sensitive current with a negative inactiva

264 Block of 4-aminopyridine-sensitive K(+) currents increased the ampl

265 requency of bicuculline-, picrotoxin-, and 4-aminopyridine-sensitive miniature IPSCs (mIPSCs) mediate

266 was the presence of very high conductance, 4-aminopyridine-sensitive multistate channels resembling t

267 nwardly rectifying K(+) (Kir) channels and 4-aminopyridine-sensitive outwardly rectifying voltage-gat

268 ant increase (approximately 1.5-fold) in a 4-aminopyridine-sensitive transient outward K+ current (I(

269 ing NTS neurons displayed large transient, 4-aminopyridine-sensitive, A-type currents (IKA).

270 receive, and the density of low-threshold, 4-aminopyridine-sensitive, transient K+ current.

271 to the discovery of a 3,4,5-trisubstituted-2-aminopyridine series and present the application of phys

272 pyrido[2,3-d]pyrimidin-7-ones to include a 2-aminopyridine side chain at the C2-position provides inh

273 rmation and parasite growth depends on its 4-aminopyridine substructure.

274 Aminopyridines such as 4-aminopyridine (4-AP) are widely

275 tructure and the fluorescence of substituted aminopyridines suggested that a methoxy group in the par

276 and with the potassium channel inhibitor, 4-aminopyridine, suggested that D1-type receptors enhanced

277 se duration and remains in the presence of 4-aminopyridine, suggesting the existence of an intrinsic

278 administration of the K(+) channel blocker 4-aminopyridine, suggesting the presence of latent connect

279 and caffeine-induced attacks were blocked by aminopyridines suggests that these triggers act via simi

280 T poisoning, the precise mechanisms by which aminopyridines symptomatically treat botulism are not un

281 The reaction of MBH bromides with 2-aminopyridines takes place in the absence of any reagent

282 K+ concentrations, the K+ channel blockers 4-aminopyridine, tetraethylammonium ions and XE991.

283 entry to a variety of secondary and tertiary aminopyridines that are otherwise not readily synthesize

284 turally diverse polycyclic fused and spiro-4-aminopyridines that are prepared in only three steps fro

285 vity relationships of a series of 6-phenyl-2-aminopyridines that potently and selectively inhibit the

286 imental condition (ie, bath application of 4-aminopyridine), the initiation of low-voltage, fast and

287 re decreased markedly by acetazolamide and 4-aminopyridine, the primary treatments for EA2, suggestin

288 e of this study was to test the ability of 4-aminopyridine to restore blood pressure and increase sur

289 All allergic 4-aminopyridine-treated rats survived after the induction

290 ltage-dependent K+ channel inhibition with 4-aminopyridine treatment restores blood pressure and incr

291 The IA channel blocker 4-aminopyridine triggered AP generation in TNs and prevent

292 However, only 4-aminopyridine was able to reduce the transient hyperpola

293 nse of [Ca2+]cyt to the KV channel blocker 4-aminopyridine was significantly attenuated in PPH-PASMCs

294 The convulsant 4-aminopyridine was used to induce interictal activity and

295 Nifedipine and 4-aminopyridine were applied to inhibit the L-type calcium

296 ons also abolished Shaker's sensitivity to 4-aminopyridine, which is a pharmacological tool to isolat

297 r the kinetics of AMPA EPSC was altered by 4-aminopyridine, while the maximal number of quanta increa

298 -phenylimidazo[1,2-a]pyridines by coupling 2-aminopyridine with phenylacetophenones, phenylacetones,

299 The reaction of 3-halo-4-aminopyridines with acyl chlorides and triethylamine is

300 sitive to quinine, tetraethylammonium, and 4-aminopyridine, with IC50 values of 21.7 micromol/L, 1.49