ライフサイエンスコーパス: cytisine

1 cerebral cortex, and hippocampus, using [3H]cytisine.

2 ChRs with relatively low affinity to ACh and cytisine.

3 behavioral responses to spinal nicotine and cytisine.

4 decreased the antidepressant-like effect of cytisine.

5 s serotonin depletion blocked the effects of cytisine.

6 ited differential activation by nicotine and cytisine.

7 similar agonist activity profile to that of cytisine.

8 a4beta2 nAChR subtype in binding assays than cytisine.

9 y of binding was measured in the presence of cytisine.

10 approximately 4-fold the number of sites for cytisine.

11 (-)-Cytisine (0.8 and 1.0 mg/kg) displaced 70% and 72% of th

12 paradigm with subcutaneous injection of (-)-cytisine (0.8 and 1.0 mg/kg).

13 l ATP release while alpha3* stimulation with cytisine (1-100 muM) caused a concentration-dependent, b

14 ditional agonists (acetylcholine, anabasine, cytisine, 1, 1-dimethyl-4-phenylpiperazinium, lobeline,

15 e and other activator ligands, including (-)-cytisine, 1,1-dimethyl-4-phenylpiperazinium, (S)-3-methy

16 Cytisine (100 microM), an agonist of nAChRs that contain

17 bladder reflexes in response to intravesical cytisine (100 muM) is blocked by systemic administration

18 ation and radioligand binding studies ([(3)H]cytisine, (125)I-alpha-bungarotoxin, and (125)I-alpha-co

19 s reported for 40% of participants receiving cytisine (264 of 655) and 31% of participants receiving

20 nd the cytisine-derivative 3-(pyridin-3'-yl)-cytisine (3-pyr-Cyt) on brain reward function in nicotin

21 Subcutaneous injection of 1 mg/kg cytisine 45 min after injection of the radiotracer reduc

22 Moreover, unlike epibatidine and cytisine, 5-[(125)I]iodo-A-85380 shows no binding in any

23 receptor agonists nicotine (5-100 microM) or cytisine (50-75 microM) and the P2X receptor agonists AT

24 Cytisine, a ligand formerly believed to be beta4-selecti

25 Placebo-controlled trials indicate that cytisine, a partial agonist that binds the nicotinic ace

26 Cytisine, a partial agonist that binds with high affinit

27 pibatidine binding sites with relatively low cytisine affinity ("cytisine-resistant" sites), resolvin

28 e, nicotine, dimethylphenylpiperazinium, and cytisine all produced a conductance increase.

29 Both cytisine and 1,1-dimethyl-4-phenylpiperazinium behaved a

30 [3H]Cytisine and 125I-alpha-bungarotoxin binding sites were

31 Cytisine and 5-halogenated cytisines had moderate effica

32 The pharmacokinetic characteristics of [(3)H]cytisine and [(125)I]alpha-bungarotoxin binding in the f

33 These results indicate that [(3)H]cytisine and [(125)I]alpha-bungarotoxin identify distinc

34 adiography, we examined the binding of [(3)H]cytisine and [(125)I]alpha-bungarotoxin in the laminated

35 sitive to the beta4-containing nAChR agonist cytisine and antagonist mecamylamine (MEC).

36 Cytisine and DMPP seemed to be partial agonists.

37 Cytisine and lobeline serve as full agonists at alpha4be

38 Cytisine and nicotine bound to specific sites in homogen

39 Binding of tritiated cytisine and nicotine to cell homogenates revealed the p

40 rchloroepibatidine, [3H](-)-nicotine and [3H]cytisine and that of nAChR densities determined in postm

41 y-metanicotine (TC-2559), cytisine, and 3-Br-cytisine and the antagonists dihydro-beta-erythroidine a

42 alpha4beta2* nAChR partial agonist and like cytisine and varenicline has antidepressant-like effects

43 Here we present the co-crystal structures of cytisine and varenicline in complex with Aplysia califor

44 essation therapy (nicotine, varenicline, and cytisine) and by sazetidine.

45 +/-)-epibatidine, 2S-(-)-nicotine, 7R,9S-(-)-cytisine, and 1,1-dimethyl-4-phenylpiperazinium in a cel

46 ses to the agonists acetylcholine, nicotine, cytisine, and 1,1-dimethyl-4-phenylpiperazinium, suggest

47 eptors from SH-SY5Y cells for acetylcholine, cytisine, and 1,1-dimethyl-4-phenylpiperazinium.

48 oline, 24 nM for (+)-epibatidine, 6.6 microM cytisine, and 15 microM 1,1-dimethyl-4-phenylpiperaziniu

49 trast, inhibition experiments with nicotine, cytisine, and 3-(2(S)-azetidinylmethoxy)pyridine-2HCl (A

50 (A-85380), 5-ethoxy-metanicotine (TC-2559), cytisine, and 3-Br-cytisine and the antagonists dihydro-

51 riatum have similar affinities for nicotine, cytisine, and A85380, that alpha-conotoxin MII discrimin

52 cacy for 1,1-dimethyl-4-phenyl-piperazinium, cytisine, and suberyldicholine; competitive antagonism b

53 ies investigated the effects of varenicline, cytisine, and the cytisine-derivative 3-(pyridin-3'-yl)-

54 es the decay kinetics ("desensitization") of cytisine- and nicotine-evoked currents (pK(a) approximat

55 with a rank order of epibatidine >> A85380 > cytisine approximately 1,1-dimethyl-4-phenyl-piperaziniu

56 The novel compound NS3861 and cytisine are agonists of nicotinic acetylcholine recepto

57 ne receptor (nAChR) agonists varenicline and cytisine are widely used as smoking cessation treatments

58 is study assessed the efficacy and safety of cytisine as compared with placebo.

59 The lower price of cytisine as compared with that of other pharmacotherapie

60 ine (IC50, 1.3 microM), but had no effect on cytisine binding at a concentration of 30 microM.

61 ine and nicotine (IC50, 2.5 nM), and reduced cytisine binding in a competitive manner (Ki 20 nM).

62 Similarly, 3H-cytisine binding in cortex of SAM-R/1 mice was higher at

63 the optic nerve for 6 weeks decreased [(3)H]cytisine binding in layers 8/9 by 70+/-1%, whereas 6-mon

64 le to published values for the high affinity cytisine binding site in rat brain (alpha4beta2), demons

65 id not seem to influence the number of [(3)H]cytisine binding sites across mouse strains.

66 s ca.50 pM affinity for rat brain [(3)H]-(-)-cytisine binding sites and 163% efficacy compared to nic

67 horbol-12-myristate-13-acetate increased [3H]cytisine binding sites and nAChR function and enhanced t

68 secutive coronal sections the density of [3H]cytisine binding sites was decreased in pre-hypertensive

69 ecutive coronal sections, the density of [3H]cytisine binding sites was decreased in SHR by up to 25%

70 The increase in [3H]cytisine binding sites was initiated by low concentratio

71 However, the number of [(3)H]cytisine binding sites was not correlated with nicotine-

72 isplayed moderate to high affinity for [(3)H]cytisine binding sites, while three (17b, 18b,c) and six

73 within each strain with the number of [(3)H]cytisine binding sites.

74 vatives were measured by inhibition of [(3)H]cytisine binding to rat brain tissue.

75 [(3)H]Cytisine binding was significantly higher in the tecta o

76 cotine-stimulated (86)Rb(+) efflux and [(3)H]cytisine binding were found to vary across brain regions

77 cotine-stimulated (86)Rb(+) efflux and [(3)H]cytisine binding, both of which seem to measure the nico

78 Nicotine fully blocked cytisine binding, but cytisine only partially blocked ni

79 nicotine was a full competitive inhibitor of cytisine binding.

80 These data indicate that cytisine binds only to surface receptors on intact cells

81 N in the brain was evaluated in baseline and cytisine-blocking studies of 4 male Papio anubis baboons

82 Varenicline and cytisine, but not 3-pyr-Cyt, diminished the nicotine wit

83 Acetylcholine, (-)-nicotine, cytisine, carbachol, and (+/-)-epibatidine all stimulate

84 -dimethyl-4-phenylpiperzinium iodide (DMPP), cytisine (CYT) and epibatidine (EPI) were investigated o

85 [(3)H]Cytisine demonstrated high specific binding in adult fro

86 The dose-dependent blocking experiments with cytisine demonstrated that (18)F-AZAN binds specifically

87 he effects of varenicline, cytisine, and the cytisine-derivative 3-(pyridin-3'-yl)-cytisine (3-pyr-Cy

88 The cytisine-derivative 3-pyr-Cyt is a very weak alpha4beta2

89 is and pharmacological properties of several cytisine derivatives.

90 e = 3-(azetidinylmethoxy)pyridine (A-85380), cytisine, dimethylphenylpiperazinium (DMPP).

91 these studies indicate that varenicline and cytisine diminish the dysphoric-like state associated wi

92 Application of agonists (nicotine, cytisine, epibatidine) activated a large (100-200 pA/pF)

93 randomly assigned in a 1:1 ratio to receive cytisine for 25 days or nicotine-replacement therapy for

94 The effectiveness of cytisine for continuous abstinence was superior to that

95 The apparent affinity of cytisine for surface receptors (K(d)=0.8 nM) was not sig

96 ver 6 months occurred more frequently in the cytisine group (288 events among 204 participants) than

97 events were reported more frequently in the cytisine group (difference, 5.7 percentage points; 95% C

98 abstinence was 8.4% (31 participants) in the cytisine group as compared with 2.4% (9 participants) in

99 e at the 12-month follow-up was 13.2% in the cytisine group versus 7.3% in the placebo group (P=0.01)

100 1-dimethyl-4-phenylpiperazinium>(-)nicotine>cytisine>carbamylch oli ne> /=d-tubocurarine).

101 In contrast, cytisine had no effect on DMV neurones previously expose

102 Cytisine and 5-halogenated cytisines had moderate efficacy at LS receptors but had

103 w nicotinic ligand based on the structure of cytisine, has recently been approved by the U.S. Food an

104 fluoxetine and the nicotinic partial agonist cytisine have synergistic effects in a mouse model of an

105 Rapid application of nicotine and cytisine indicated EC50 values of congruent with22 and c

106 The blocking of nAChRs with cytisine is dose-dependent and it showed that (18)F-AZAN

107 the United States for smoking cessation and cytisine is used in Eastern European countries.

108 gands, determined in competition assays, was cytisine < nicotine < acetylcholine < carbachol < curare

109 2 nAChRs when measured with [3H]epibatidine, cytisine, nicotine, and acetylcholine.

110 Nicotine fully blocked cytisine binding, but cytisine only partially blocked nicotine binding to inta

111 in displacing (+/-)-[3H]epibatidine, (-)-[3H]cytisine or (-)-[3H]nicotine binding to spinal nicotinic

112 Unlike (-)-[3H]cytisine or (-)-[3H]nicotine, (+/-)-[3H]epibatidine reve

113 Acute administration of cytisine or 3-pyr-Cyt did not affect ICSS thresholds.

114 ) and more than twice that measured with [3H]cytisine or [3H](-)nicotine.

115 However, no changes in hippocampal cytisine or alpha-bungarotoxin binding were found.

116 Relative sensitivity to inhibition by cytisine or alpha-bungarotoxin was used to evaluate phar

117 rticipants were randomly assigned to receive cytisine or matching placebo for 25 days; participants i

118 ent therapies or partial nAChR agonists like cytisine or varenicline.

119 -related alterations in either nicotinic (3H-cytisine) or muscarinic (3H-QNB) cholinergic receptor bi

120 e full agonist nicotine, the partial agonist cytisine, or the competitive antagonist dihydro-beta-ery

121 beta4 Gene deletion partially reduced cytisine-resistant and alpha-bungarotoxin-resistant site

122 Comparison of the cytisine-resistant population's distribution with that o

123 inhibition by cytisine were eliminated, and cytisine-resistant sites were reduced.

124 ites with relatively low cytisine affinity ("cytisine-resistant" sites), resolving [(3)H]epibatidine

125 s nicotine and cytisine with high affinity ("cytisine-sensitive" sites).

126 eled epibatidine, (-)-nicotine, lobeline and cytisine significantly inhibited [18F]FPH binding in tha

127 tine-treated and NGF-treated cells; however, cytisine-stimulated [3H]norepinephrine release indicated

128 creased EC(50) values for both nicotine- and cytisine-stimulated alpha-CtxMII-sensitive dopamine rele

129 tentiated the antidepressant-like effects of cytisine, suggesting that this subtype might mediate the

130 essation compounds varenicline (Chantix) and cytisine (Tabex), have been evaluated at both the 2:3 an

131 ations in hydrogen bonding interactions with cytisine that provide a rationalization for the stoichio

132 malaria (mefloquine) and nicotine addiction (cytisine, varenicline).

133 ber of sites for cytisine was increased, and cytisine was able to fully block nicotine binding.

134 Cytisine was about 3 times more potent than ACh (low-con

135 e ligand-binding domain, whereas efficacy of cytisine was additionally affected by the nature of the

136 We investigated whether cytisine was at least as effective as nicotine-replaceme

137 When combined with brief behavioral support, cytisine was found to be superior to nicotine-replacemen

138 was unchanged, while the number of sites for cytisine was increased, and cytisine was able to fully b

139 In this single-center study, cytisine was more effective than placebo for smoking ces

140 In addition, cytisine was more efficacious at the alpha-CtxMII-sensit

141 Cytisine was provided by mail, free of charge, and nicot

142 ed subgroup analysis of the primary outcome, cytisine was superior to nicotine-replacement therapy am

143 agonists (such as epibatidine, anatoxin, or cytisine) was also powerfully antagonized by bisindolylm

144 differential effects of ACh, TC-2559 and 5-I-cytisine we evaluated the effects of long-term exposure

145 for the agonists epibatidine, nicotine, and cytisine were consistent with reported values, indicatin

146 er-affinity sites sensitive to inhibition by cytisine were eliminated, and cytisine-resistant sites w

147 Compared with cytisine, which selectively activates receptors containi

148 The alpha4beta2 receptor bound [3H]cytisine with a Kdapp of 0.74 +/- 0.14 nM.

149 correspond to that which binds nicotine and cytisine with high affinity ("cytisine-sensitive" sites)