ライフサイエンスコーパス: aminopyridine

1 C) amplitude and/or K(+) channel-blockade (4-aminopyridine).

2 seizures induced by topical application of 4-aminopyridine.

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

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

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

6 by local injection of the chemoconvulsant 4-aminopyridine.

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

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

9 the potassium channel blockers barium and 4-aminopyridine.

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

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

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

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

14 tion on epileptiform discharges induced by 4-aminopyridine.

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

16 increased after blocking Kv channels with 4-aminopyridine.

17 rescent assays for FAAH based on substituted aminopyridines.

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

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

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

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

25 2-Aminopyridines 1a-c and 1-aminoisoquinoline with 1-chlor

26 rmal window width I(CaL,D-C) or subsequent 4-aminopyridine (2 mm), window I(CaL,D-C) narrowing (10 mV

27 of halogenation has been also extended to 2-aminopyridines, 2-aminopyrimidine, indole, and isoquinol

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

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

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

31 3-aminopyridine-2-carboxaldehyde thiosemicarbazone (3-AP;

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

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

34 reaction between arylglyoxal monohydrates, 2-aminopyridines/2-aminopyrimidine, and barbituric/N,N-dim

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

36 2-Aminopyridine-3,5-dicarbonitrile compounds were previous

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

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

39 Specifically, 3-methyl-4-aminopyridine (3Me4AP) was found to be approximately 7-f

40 nd 3F4AP; 3-methoxy- and 3-trifluoromethyl-4-aminopyridine (3MeO4AP and 3CF(3)4AP) were found to be a

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

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

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

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

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

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

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

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

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 the FDA-approved potassium channel blocker 4-aminopyridine (4-AP) improves motor behavior in both sex

53 ical acute seizure focus with injection of 4-aminopyridine (4-AP) in somatosensory cortex.

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

55 4-aminopyridine (4-AP) is used and licensed as a symptomat

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

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

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

59 f para-hydrogen ( p-H(2)) and a substrate (4-aminopyridine (4-AP) or 4-methylpyridine (4-MP)) into [I

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

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

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

63 neuronal activity by the FDA-approved drug 4-aminopyridine (4-AP) rescues the number and function of

64 2-3 PNs, using alpha-dendrotoxin (DTX) or 4-aminopyridine (4-AP) to block these conductances.

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

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

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

68 4-Aminopyridine (4-AP), a nonselective blocker of K(v) vol

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

90 4-Aminopyridine (4-AP, >= 5 mM) caused continuous spiking.

91 4-aminopyridine (4-AP, 0.5 mM) reduced the threshold for s

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

93 4-Aminopyridine (4-AP, 2 mm) attenuated I(A) in both whole

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

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

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

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

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

102 4-Aminopyridine (4AP) is a specific blocker of voltage-gat

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 cript reports on the sustained delivery of 4-Aminopyridine (4AP, molecular weight 94.1146 g/mol), a p

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

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

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

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

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

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

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

115 4-Aminopyridine, a K+ channel blocker, broadened the compo

116 4-Aminopyridine, a powerful modulator of sperm motility, b

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

118 2+)-activated K(+) channel blocker, and by 4-aminopyridine, a voltage-gated K(+) (KV) channel blocker

119 1-s pacing cycle length in the absence of 4-aminopyridine, adding a virtual Ito-like current (n=1113

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

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

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

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

124 Other aminopyridine analogs reduced attack frequency but, cons

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

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

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

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

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

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

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

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

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

134 ampal epileptiform activity is promoted by 4-aminopyridine and inhibited by GABA(B) receptor agonists

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 ther and renders this channel sensitive to 4-aminopyridine and Zn(2+).

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

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

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

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

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

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

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

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

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

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

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

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

153 4-Aminopyridines are valuable scaffolds for the chemical i

154 )2(Apy)2](2+), Apy = 4-aminopyridine and 3,4-aminopyridine, are stable in aqueous solution with stron

155 the need for an excess of alkene and with 2-aminopyridine as an ammonia surrogate to give the Markov

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

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

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

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

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

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

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

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

164 2-elicited dilation to a similar extent as 4-aminopyridine, but the selective KV1.3 blocker phenoxyal

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

166 Aminopyridines can directly target presynaptic HVACCs to

167 gard, for a new CO(2)-to-CO reduction cobalt aminopyridine catalyst, a detailed experimental and theo

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

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

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

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

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

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

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

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

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

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

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

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

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

181 4-Aminopyridine derivatives yielded oligoadenylates as lon

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

183 4-Aminopyridine did not change DeltaV(-)(m)/DeltaV(+)(m).

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

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

186 le-cell resolution, the dynamics of acute (4-aminopyridine) focal cortical seizures as they originate

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

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

189 4-aminopyridine, gaboxadol hydrochloride and N-acetylneura

190 4-Aminopyridine gave extensive protection against a number

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

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

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

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

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

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

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

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

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

200 While aminopyridines have demonstrated varying efficacy in tra

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

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

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

204 action between N-alkylnitriliumboranes and 2-aminopyridines, imidazoles, oxazoles, or isoxazoles lead

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

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

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

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

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

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

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

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

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

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

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

216 5 nM iberiotoxin, and unmodified by 0.8 mM 4-aminopyridine, indicating that LC causes vasodilation vi

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

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

219 4-Aminopyridine-induced hyperactivation even in cells susp

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

221 lar electrophysiological recordings during 4-aminopyridine-induced neocortical spikes and seizures.

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

223 our previously reported potent and selective aminopyridine inhibitors.

224 Aminopyridine is employed as a recyclable directing grou

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

245 4-Aminopyridine or depolarized conditioning blocked the TO

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

247 4-aminopyridine or related voltage-dependent K channel blo

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

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

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

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

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

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

254 iadiazine dioxides using readily available 2-aminopyridines/pyrazines/pyridazine and 2-chloro benzene

255 volves the chemoselective sulfonylation of 2-aminopyridines/pyrazines/pyridazine with 2-chloro benzen

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

298 nzoxazole and hydrogen-bonded complexes of 2-aminopyridine with protic substrates] vary depending on

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

300 t conversion of pyridines to Boc-protected 2-aminopyridines with exquisite site selectivity and chemo