ライフサイエンスコーパス: SR141716A

1 ophenyl)-4-methyl-1H-pyrazol e-3-carboxamide(SR141716A).

2 ophenyl)-4-methyl-1H-pyrazole -3-carboxamide(SR141716A).

3 yl-1H-p yrazole-3-carboxamide hydrochloride (SR141716A).

4 the CB(1) cannabinoid antagonist rimonabant (SR141716A).

5 h is elevated by the CB1 receptor antagonist SR141716A.

6 ion that is reversed by the CB(1) antagonist SR141716A.

7 effects were blocked by co-administration of SR141716A.

8 d by the CB1 cannabinoid receptor antagonist SR141716A.

9 ffect that was dose-dependent and blocked by SR141716A.

10 treatment with SR1444528 and GW6471, but not SR141716A.

11 mulations, we determined the binding mode of SR141716A.

12 reatment of DIO mice with the CB1 antagonist SR141716A.

13 the affinity change for the inverse agonist SR141716A.

14 DSI was blocked by the antagonist, SR141716A.

15 n diacetate, and this effect was reversed by SR141716A.

16 ker picrotoxin, but not by pretreatment with SR141716A.

17 the cannabinoid receptor 1 (CB1) antagonist SR141716A.

18 nd the CB1 (cannabinoid) receptor antagonist SR141716A.

19 for anandamide from WIN55,212-2, as well as SR141716A.

20 of which ethanol preference is unaffected by SR141716A.

21 to reduce the central activity observed with SR141716A.

22 On the day of the experiment, rats received SR141716A (0, 1 or 3 mg/kg, i.p.) 15 min prior to behavi

23 t was blocked by the CB1 receptor antagonist SR141716A (1 microM) but not by the opioid antagonist na

24 nitroprusside, or capsaicine, is blocked by SR141716A (1 microM) or by cannabidiol (10 microM).

25 by the cannabinoid CB(1) receptor antagonist SR141716A (1 microM), although at higher concentrations

26 ophenyl)-4-methyl-1H-pyrazole-3-carboxamide (SR141716A; 1) was the lead compound for initiating studi

27 FD) for 12 weeks and then treated daily with SR141716A (10 mg/kg) for 4 weeks while continuing HFD.

28 The cannabinoid CB1 receptor antagonist SR141716A (10 microM) also attenuated endothelium-depend

29 cipient rat with the CB1 receptor antagonist SR141716A (3 mg/kg i.v.), which also inhibits the hypote

30 versed by co-infusion of the CB1R antagonist SR141716A (30 microM), which alone had no effect up to t

31 with a cannabinoid CB1 receptor antagonist, SR141716A (5 mg/kg, i.p.), or dopamine D2 receptor antag

32 ation of the cannabinoid receptor antagonist SR141716A (5 microg).

33 ed negative binding cooperativity with [(3)H]SR141716A [5-(4-chlorophenyl)-1-(2,4-dichloro-phenyl)-4-

34 55,212-2 (5 microg, selective CB1 agonist), SR141716A (50 microg, competitive CB1 antagonist), both

35 es in intact goldfish retinas, we found that SR141716A (a CB(1) receptor antagonist) application alon

36 Of these, (-)-Delta8-THC and SR141716A, a biarylpyrazole CB1 antagonist, were found t

37 dependent and abolished by pretreatment with SR141716A, a CB(1) receptor antagonist.

38 hancement of outflow facility was blocked by SR141716A, a CB1 antagonist, and was partially blocked b

39 al at 16 hr and abolished in the presence of SR141716A, a selective CB(1) receptor antagonist.

40 M of noladin ether was completely blocked by SR141716A, a selective CB1 antagonist.

41 These adverse effects were reversed by SR141716A, a specific CB1-R antagonist.

42 In membrane assays versus [3H]SR141716A, a two-site model was indicated for the C-2 H/

43 econd study was to assess the effects of the SR141716A administration on food-maintained responding a

44 These data suggest that the effects of SR141716A administration shift in the tolerant animal an

45 In CB(1)(-/-) membranes, SR141716A affected both basal and anandamide- or WIN5521

46 constructed that combined the evaluation of SR141716A affinity at WT CB1 and K3.28A with an evaluati

47 ion, inhibits binding of the antagonist drug SR141716A (also known as Rimonabant or Accomplia), but d

48 Although SR141716A, also known as rimonabant, has been withdrawn

49 ceptor inverse agonists/antagonists, such as SR141716A, AM251, and AM281, were reported to activate G

50 unaffected by 43Gap 27 peptide, 18alpha-GA, SR141716A, AM404 and indomethacin and their genesis rema

51 he wild-type CB1 and K3.28A affinities of an SR141716A analog, 5-(4-chlorophenyl)-3-[(E)-2-cyclohexyl

52 raction occurs between the C3 substituent of SR141716A and K3.28 in WT CB1.

53 ced morphologic changes were also blocked by SR141716A and PD98059.

54 2 receptors, notably the CB1 receptor, using SR141716A and SR144528 indicate that the endogenous cann

55 ocked by the cannabinoid receptor antagonist SR141716A and the Gi/Go protein inhibitor pertussis toxi

56 M was examined with CB1 receptor antagonist, SR141716A and these studies indicated that CP55,940 stim

57 The binding of SR141716A and WIN55,212-2 were found to be affected by t

58 romatic microdomain as the binding region of SR141716A and WIN55,212-2, but not of anandamide.

59 [3H]SR141716A and WIN55,212-2-stimulated [35S]GTPgammaS bind

60 ied C386 residue with the piperidine ring of SR141716A and/or disruption of an aromatic microdomain i

61 yl-1H-p yrazole-3-carboximide hydrochloride (SR141716A) and guanosine 5'-O-(3-[35S]thio)triphosphate

62 yl)-4-methyl-1H- pyrazole-3-carboxamide ([3H]SR141716A) and the cannabinoid agonist [3H](-)-cis-3-[2-

63 (3)H-SR141716A), and did not alter endocannabinoid metabolism

64 d by coincubation with the CB(1) antagonist, SR141716A, and was absent in nontransfected human embryo

65 Conversely, SR141716A application alone at night or SR141716A applic

66 ely, SR141716A application alone at night or SR141716A application in the day following 30-min spiper

67 yl-1H-p yrazole-3-carboximide hydrochloride (SR141716A) before measuring neurogenesis with BrdU.

68 ates the perturbation of TM2 that attenuates SR141716A binding indirectly.

69 nor binding pocket formed by TM2/TM3/TM7 for SR141716A binding, which complements the major binding p

70 SR141716A binds selectively to the brain cannabinoid (CB

71 p42/44 MAP kinase, whereas pretreatment with SR141716A blocked the p42/44 MAP kinase-activating effec

72 th our previously determined binding site of SR141716A but extends extracellularly.

73 on in normal rats, which can be prevented by SR141716A but not by inhibition of nitric oxide synthase

74 observed in the presence of WIN 55,212-2 and SR141716A but not CP55,940 and anandamide.

75 fect reversed by the CB1 receptor antagonist SR141716A but not mimicked by the vanilloid receptor ago

76 ndamide-induced vasodilation is inhibited by SR141716A, but other potent CB1 receptor agonists, such

77 gnenolone but not lipoxin A4 displaced [(3)H]SR141716A, but there was no functional interaction betwe

78 for CB1 R due to a hydrogen bond between the SR141716A C3 substituent and K3.28(192), a residue avail

79 the hypothesis that hydrogen bonding of the SR141716A C3 substituent with K3.28 is responsible for i

80 utation at residue 3.28(192) (i.e., K3.28A), SR141716A competitively antagonizes the effects of WIN55

81 phenyl)-4-methyl-1H- pyrazole-3-carboxamide (SR141716A) competitively antagonizes the Ca(2+) current

82 Simulation of the F174(2.61)A mutant CB1-SR141716A complex demonstrates the perturbation of TM2 t

83 We found from the simulation of the CB1-SR141716A complex that SR141716A projects toward TM5 to

84 increase in affinity for the inverse agonist SR141716A, consistent with a shift away from an enhanced

85 lative to the wild type that is inhibited by SR141716A, consistent with receptor-mediated Gs precoupl

86 Last, SR141716A did not affect social play after infusion into

87 The CB1 antagonist, SR141716A, differentially blocks Delta(9)-THC versus AEA

88 ms similar interactions with the receptor as SR141716A does, the benzhydryl piperazine scaffold is st

89 The acute administration of SR141716A dose-dependently decreased rates of responding

90 rt that a selective CB1 receptor antagonist, SR141716A, elicits an increase in blood pressure in rats

91 pretreatment with the cannabinoid antagonist SR141716A enhanced the stimulation of motor behavior eli

92 These results suggest SR141716A exerts inverse agonist activity through the st

93 erative to understand the mechanism by which SR141716A exerts its inverse agonist activity.

94 The cannabinoid receptor antagonist, SR141716A, failed to block the response.

95 noid agonist [3H]CP 55,940 or antagonist [3H]SR141716A, for which rank order differences in affinity

96 s with the selective CB1 receptor antagonist SR141716A have implicated peripherally located CB1 recep

97 LDK1229 exhibits efficacy comparable with SR141716A in antagonizing the basal G protein coupling a

98 .28 is involved in a strong interaction with SR141716A in WT CB1, but does not interact with VCHSR.

99 Systemic SR141716A induced a dramatic dose-dependent decrease in

100 In CB(1)(+/+) membranes, SR141716A inhibited only 84% of anandamide and 67% of WI

101 Similarly, SR141716A inhibits food intake in food-restricted young,

102 of these results, we hypothesize that bound SR141716A inhibits the ability of transmembrane helix 6

103 site of the CB(1) inverse agonist/antagonist SR141716A is within the TMH3-4-5-6 aromatic microdomain

104 dministration of the cannabinoid antagonist, SR141716A, markedly reduces intake of sucrose solutions,

105 Furthermore, SR141716A mimicked the effects of 43Gap 27 peptide in bl

106 were reversed by the cannabinoid antagonist SR141716A (N-piperidino-5-(4-chlorophenyl)-1-(2,4-dichlo

107 ocked by the cannabinoid receptor antagonist SR141716A [N-piperidino-5-(4-chlorophenyl)-1-(2,4-dichlo

108 was blocked by a selective CB1R antagonist [SR141716A, N-(piperidin-1-yl)-5-(4-chlorophenyl)-1-(2,4-

109 several agonists but bound inverse agonists SR141716A, N-(piperidin-1-yl)-5-(4-iodophenyl)-1-(2,4-di

110 Because the effects of SR141716A on behavior are intensified in animals toleran

111 tuent and K3.28(192), a residue available to SR141716A only in R.

112 al hippocampal, but not septal, infusions of SR141716A or AM251 increased hippocampal ACh release.

113 ahippocampal infusion of the CB1R antagonist SR141716A or pertussis toxin blocked the inhibition of h

114 contrast, this latter effect was blocked by SR141716A or pertussis toxin infused, in dual microdialy

115 n was blocked by the CB1 receptor antagonist SR141716A or the D2 antagonist sulpride.

116 inverse agonists, represented by rimonabant (SR141716A), otenabant, and taranabant, are centrally act

117 SR141716A paradoxically increased the number of BrdU-lab

118 eceptors with the antagonist/inverse agonist SR141716A prevented the play-enhancing effects of system

119 not 1 muM cannabinoid receptor 1 antagonist SR141716A, produced a partial antagonism on the PEA-indu

120 simulation of the CB1-SR141716A complex that SR141716A projects toward TM5 to interact tightly with t

121 Finally, intra-NAc infusions of SR141716A reduced cocaine breakpoints selectively in LgA

122 ccumbal administration of the CB1 antagonist SR141716A (Rimonabant) on cocaine self-administration (0

123 Our data demonstrate that AM251 and SR141716A (rimonabant), which are cannabinoid antagonist

124 t does not bind to CB1 receptors, yet causes SR141716A-sensitive hypotension and mesenteric vasodilat

125 ic but not control patients or rats elicited SR141716A-sensitive hypotension in normal recipient rats

126 Action at one such non-CB1, SR141716A-sensitive site, the VR1 vanilloid receptor, wa

127 ocked by the cannabinoid receptor antagonist SR141716A, showing a dependence on CB1 cannabinoid recep

128 sy surrounding the GPR55-mediated actions of SR141716A; some reports indicate the compound to be an a

129 Coinjection of the CB1 antagonist SR141716A (SR) (1.5 micromol/kg) and WIN2 (0.5 micromol/

130 ocked in a concentration-dependent manner by SR141716A, suggesting that the response was regulated th

131 pecific signal using [3H] CP-55,940 and [3H] SR141716A, though the latter exhibited a lower signal to

132 716A to VR1-KO mice, in which the ability of SR141716A to enhance neurogenesis was abolished.

133 Microinjection of SR141716A to GiA reversed this inhibition of responses t

134 the cannabinoid receptor 1 (CB1) antagonist SR141716A to levels observed in their CB1 knockout litte

135 illoid receptor, was tested by administering SR141716A to VR1-KO mice, in which the ability of SR1417

136 rmore, treatment of primary macrophages with SR141716A up-regulated KLF4 and STAT6, reduced secretion

137 t effect, thus suggesting that the action of SR141716A was directly attributable to effects on gap ju

138 To investigate this discrepancy, SR141716A was given to CB1R-KO mice, in which it still s

139 h at higher concentrations (3 and 10 microM) SR141716A was inhibitory.

140 Of these, SR141716A was marketed as a promising anti-obesity drug,

141 The competitive CB1 receptor antagonist SR141716A was used to test the hypothesis that endogenou

142 Next, using the CB(1)-selective antagonist SR141716A, we observed an increase in excitatory, and to

143 -induced cirrhosis was similarly reversed by SR141716A, which also reduced the elevated mesenteric bl

144 ated [35S]GTP gamma S binding was blocked by SR141716A with a decrease (P < 0.05) in the IC50 values

145 nd inhibiting binding of the inverse agonist SR141716A with negative cooperativity, demonstrated via

146 In this binding site, SR141716A would exhibit higher affinity for CB1 R due to