ライフサイエンスコーパス: rimonabant

1 -alpha (MK886) or cannabinoid CB1 receptors (rimonabant).

2 co-administration of the CB1 inverse agonist rimonabant.

3 sts tested as well as by the inverse agonist rimonabant.

4 ranges, and both effects were attenuated by rimonabant.

5 s high and displaceable by pretreatment with rimonabant.

6 pensable for the acute hypophagic effects of rimonabant.

7 out mice and after subchronic treatment with rimonabant.

8 itro, similar to the CB1 receptor antagonist rimonabant.

9 tries about suicide in individuals receiving rimonabant.

10 cross the accumbens and were not affected by rimonabant.

11 late membrane remodeling like LPI, AM251, or rimonabant.

12 ns of behaving rats treated with intravenous rimonabant (0.3 mg/kg) or vehicle, followed by methamphe

13 Administration of rimonabant (1 mg/kg, intravenously) also blocked the spe

14 of the cannabinoid CB1 receptor antagonists rimonabant (1 microg; 1 microl) or AM251 (1 microg; 1 mi

15 Finally, the cannabinoid-1 antagonist rimonabant (1 muM) inhibited DGL-alpha-induced neuritoge

16 der baseline and pretreatment conditions (3, rimonabant, 10 mg/kg, iv) and quantified at later times

17 negative affective states in humans (FG7142, rimonabant, 13-cis retinoic acid).

18 istration of the cannabinoid inverse agonist rimonabant (150 mug/kg, i.v).

19 ase were randomly assigned to receive either rimonabant 20 mg (n=9381) or matching placebo (n=9314).

20 r large trials, after one year of treatment, rimonabant 20 mg led to greater weight loss and reductio

21 etary counseling, were randomized to receive rimonabant (20 mg daily) or matching placebo, and underw

22 Pretreatment with intra-RM rimonabant (20 microg) antagonized the antinociception p

23 -1 I.P.).However, CB1 receptor antagonism by rimonabant (4.6mg kg-1 I.P.) or SLV319 (15mg kg-1 I.P.)b

24 Pretreatment with rimonabant (50 microg, ivt) produced a statistically sig

25 s of intracerebral (i.c.) microinjections of rimonabant (a CB(1) receptor inverse agonist) were studi

26 are uniformly inhibited by administration of rimonabant, a cannabinoid receptor (CB1) antagonist, sug

27 Rimonabant, a selective cannabinoid-1 receptor blocker,

28 Rimonabant administration robustly reduced breakpoints i

29 Peripheral treatment with CB1 antagonist (Rimonabant) also reduced food intake and body weight but

30 The anti-obesity medication rimonabant, an antagonist of cannabinoid type-1 (CB(1))

31 administering a receptor-saturating dose of rimonabant, an inverse agonist at the CB(1) receptor.

32 ive antagonists of CB1 have largely targeted rimonabant, an inverse agonist of CB1.

33 milar to the CB1R antagonist/inverse agonist rimonabant, analogues 27 and 30 decrease oral alcohol se

34 Both rimonabant and 14g, a potent brain penetrant CB1 recepto

35 occurred in 364 (3.9%) patients assigned to rimonabant and 375 (4.0%) assigned to placebo (hazard ra

36 However, both rimonabant and AM4113 reduced cue-induced reinstatement

37 Both rimonabant and AM4113 reduced two effects of nicotine an

38 monkeys by the CB1-receptor inverse agonist rimonabant and by the recently developed CB1-receptor ne

39 A) pathway, inhibited by the CB1R antagonist rimonabant and Gi uncoupler pertussis toxin, and absent

40 nger adenylyl cyclase activation compared to rimonabant and it is a better enhancer of insulin secret

41 receptor GPR55 responded strongly to AM251, rimonabant, and lysophosphatidylinositol but only very w

42 Rimonabant appears to have a favorable safety and tolera

43 s were compared in reversed-phase HPLC using rimonabant as an analyte.

44 1997), orlistat (FDA approved in 1999), and rimonabant (available in Europe and given FDA approvable

45 Rimonabant blocked LPS hypothermia when administered I.C

46 also blocked by the CB1 receptor antagonist rimonabant, but this is thought to represent an effect o

47 ity for the inverse agonist JD-5037 than for rimonabant compared to CB1 full length.

48 ke the case with improgan, pretreatment with rimonabant completely blocked CP-55,940 hypothermia.

49 Pretreatment with rimonabant completely blocked the antinociceptive effect

50 Moreover, rimonabant decreased LFP gamma power at 80 Hz (high gamm

51 ive placebo or continued to receive the same rimonabant dose while the placebo group continued to rec

52 placebo, 5 mg/d of rimonabant, or 20 mg/d of rimonabant for 1 year.

53 With rimonabant, gastrointestinal (3038 [33%] vs 2084 [22%]),

54 tric adverse effects were more common in the rimonabant group (43.4% vs 28.4%, P < .001).

55 Four patients in the rimonabant group and one in the placebo group committed

56 ompared with the placebo group, the 20 mg of rimonabant group produced greater mean (SEM) reductions

57 Patients who were switched from the 20 mg of rimonabant group to the placebo group during year 2 expe

58 rse event was nausea (11.2% for the 20 mg of rimonabant group vs 5.8% for the placebo group).

59 ebo group, 620 (51%) patients in the 5 mg of rimonabant group, and 673 (55%) patients in the 20 mg of

60 roup, and 673 (55%) patients in the 20 mg of rimonabant group.

61 However, intra-RM pretreatment with rimonabant had no effect on antinociceptive responses fo

62 s an agent with a novel mechanism of action, rimonabant has a potential to be a useful adjunct to lif

63 Although SR141716A, also known as rimonabant, has been withdrawn from the market due to se

64 ion which is blocked by the CB(1) antagonist rimonabant, implying a cannabinoid mechanism of action.

65 cell lines and attenuated inverse agonism by rimonabant in CB1-HEK cells.

66 ed and compared for the determination of the rimonabant in mouse plasma samples at the low nanograms

67 was reversed by the CB1 receptor antagonist rimonabant in naive rats but not in CFA-treated rats.

68 Finally, the effects of microinfusion of rimonabant in the CeA on anxiety-like behavior, and food

69 ht into the neurobiological effectiveness of rimonabant in treating addictive disorders.

70 8, an analog of the selective CB1 antagonist rimonabant, in vivo as a potential CB1 radioligand for P

71 Consistently, we found that rimonabant increases gastrointestinal metabolism via inc

72 n in the nucleus tractus solitarii abolished rimonabant-induced hypophagia.

73 e with the centrally and peripherally acting rimonabant induces weight loss and improves glucose home

74 cal injection of the CB1 receptor antagonist rimonabant into the rostral ventromedial medulla blocked

75 f the CB(1)-cannabinoid receptor antagonist, rimonabant, into the duodenum markedly reduced fat sham

76 Rimonabant is a first selective blocker of the cannabino

77 Therapy with rimonabant is also associated with favorable changes in

78 t versus human CB1R, whereas the affinity of rimonabant is comparable for all three CB1Rs.

79 Determining whether rimonabant is useful in management of coronary disease w

80 hile those who continued to receive 20 mg of rimonabant maintained their weight loss and favorable ch

81 The activation of GPR55 by rimonabant may be responsible for some of the off-target

82 Finally, rimonabant, microinfused directly into the CeA, precipit

83 id CB(1) receptor inverse agonist/antagonist rimonabant [N-piperidino-5-(4-chlorophenyl)-1-(2,4-dichl

84 In contrast, neither rimonabant nor AM4113 modified cocaine-reinforced or foo

85 The effects of systemic administration of rimonabant on anxiety-like behavior, food intake, body w

86 ment, the study failed to show an effect for rimonabant on disease progression for the primary end po

87 inistration of the CB1 antagonist SR141716A (Rimonabant) on cocaine self-administration (0.5 mg/kg/in

88 the antagonist drug SR141716A (also known as Rimonabant or Accomplia), but does not affect the bindin

89 Treatment with the CB1 antagonists rimonabant or AM281 markedly improved cardiac dysfunctio

90 ithdrawal was blocked by the CB1R antagonist rimonabant or the genetic deletion of CB1R in forebrain

91 ere randomized to receive placebo, 5 mg/d of rimonabant, or 20 mg/d of rimonabant for 1 year.

92 multicenter trial, treatment with 20 mg/d of rimonabant plus diet for 2 years promoted modest but sus

93 Systemic administration of rimonabant precipitated anxiety-like behavior and anorex

94 The CB1 antagonist rimonabant precipitated withdrawal in mice treated chron

95 dose CP55,940 did not produce hypothermia or rimonabant-precipitated withdrawal in CB1KO mice.

96 -dose CP55,940 also produced hypothermia and rimonabant-precipitated withdrawal in WT, but not CB1KO,

97 satory mechanism to dampen anxiety, and (ii) rimonabant precipitates a negative emotional state by bl

98 We investigated whether rimonabant precipitates a negative emotional state in ra

99 Rimonabant produced persistent blockade of 2-AG self-adm

100 L/6 mice with the CB(1) receptor antagonist, rimonabant, produced a reduction of both D(2) and D(4) d

101 ing analogues of the CB1 receptor antagonist Rimonabant(R), CB2 receptor agonists, and Cannabis sativ

102 Compounds with TPSAs higher than that for rimonabant (rimonabant TPSA = 50) and excellent function

103 Since rimonabant's withdrawal, several groups are pursuing per

104 Rimonabant seems to be well tolerated, with a primary si

105 Similar studies with improgan demonstrated rimonabant-sensitive sites within the dorsal and ventrol

106 ocking studies suggested that taranabant and rimonabant shared the same general binding area of CB1R

107 on, combination treatment with FGFR4 ASO and rimonabant showed additive reduction in BW and adiposity

108 At the same dose, rimonabant significantly increased cigarette smoking qui

109 nnabinoid receptor-1 (CB1) by the antagonist rimonabant (SR141716) has been associated with activatio

110 (1) cannabinoid receptor (CB(1) receptor) by rimonabant (SR141716) reduces self-administration of alc

111 th the cannabinoid CB(1) receptor antagonist rimonabant (SR141716).

112 tion of CB1 inverse agonists, represented by rimonabant (SR141716A), otenabant, and taranabant, are c

113 revented by the CB(1) cannabinoid antagonist rimonabant (SR141716A).

114 rse cannabinoid receptor 1 agonist SR141716 (Rimonabant) suggesting that the anti-inflammatory effect

115 Similarly to rimonabant, systemic administration of the peripherally

116 Similar to rimonabant, taranabant interacted with a cluster of arom

117 rectic effects similar to the CB1 antagonist rimonabant that once was marketed for the treatment of o

118 tem (CNS) related side effects observed with rimonabant, the first clinically approved CB1 inverse ag

119 In contrast to rimonabant,the I.C.V. administration of AEA (50 mug) enh

120 ptimized to reduce lipophilicity compared to rimonabant to achieve peripherally active molecules with

121 entricularly with ghrelin and CB1 antagonist rimonabant to study tissue AMPK activity and gene expres

122 with TPSAs higher than that for rimonabant (rimonabant TPSA = 50) and excellent functional activity

123 Rimonabant-treated patients had a larger reduction in bo

124 Rimonabant-treated patients had greater decreases in hig

125 Rimonabant-treated patients were rerandomized to receive

126 n CB1-KO mice and by intracerebroventricular rimonabant treatment, suggesting that central CB1 recept

127 In the rimonabant vs placebo groups, high-density lipoprotein c

128 In the rimonabant vs placebo groups, imputing results based on

129 In the rimonabant vs placebo groups, PAV (95% confidence interv

130 The blockade of LPS hypothermia by I.C.V. rimonabant was associated with suppression of the circul

131 The effect of rimonabant was further studied.

132 Rimonabant was generally well tolerated; the most common

133 th S(7.39)383 but not with K(3.28)192, while rimonabant was hydrogen-bonded with K(3.28)192 but not w

134 e notable distinction between taranabant and rimonabant was that taranabant was hydrogen-bonded with

135 clinically approved CB1 receptor antagonist, rimonabant, was withdrawn because of adverse central ner

136 ing the cannabinoid receptor inverse agonist rimonabant were successful in producing modest weight lo

137 r data demonstrate that AM251 and SR141716A (rimonabant), which are cannabinoid antagonists, and the

138 with an intracerebroventricular infusion of rimonabant while assessing glucose fluxes during a clamp

139 lment December 2004-December 2005) comparing rimonabant with placebo in 839 patients at 112 centers i

140 ute injection of the CB1 receptor antagonist rimonabant with the use of conditional CB1-knockout mice

141 We assessed whether rimonabant would improve major vascular event-free survi