ライフサイエンスコーパス: cannabidiol

1 ition of resurgent and persistent current by cannabidiol.

2 mphasis on Delta(9)-tetrahydrocannabinol and cannabidiol.

3 a(2+) store-dependent component sensitive to cannabidiol.

4 these parameters following administration of cannabidiol.

5 2-arachidonoylglycerol, methanandamide, and cannabidiol.

6 ne, is blocked by SR141716A (1 microM) or by cannabidiol (10 microM).

7 Hypotension by Abn-cbd is also inhibited by cannabidiol (20 microgram/g), which does not influence a

8 eded by the ingestion of Delta9-THC (10 mg), cannabidiol (600 mg), or placebo in a double-blind, rand

9 deletion of GPR55 or by the GPR55 antagonist cannabidiol, a constituent of Cannabis sativa.

10 Glutamate toxicity was reduced by both cannabidiol, a nonpsychoactive constituent of marijuana,

11 The cannabinoid analog abnormal cannabidiol [abn-cbd; (-)-4-(3-3,4-trans-p-menthadien-[1

12 The cannabinoid analog "abnormal cannabidiol" (abn-cbd) causes endothelium-dependent vaso

13 Here we show that "abnormal cannabidiol" (Abn-cbd) is a neurobehaviorally inactive c

14 g approximately 40 fold more potent than (+)-cannabidiol; abnormal-cannabidiol is a full agonist.

15 her, the results from this study reveal that cannabidiol, acting through CB2 and regulation of Nox4 a

16 of GPR18, including anandamide and abnormal cannabidiol, also failed to induce inhibition of calcium

17 The cannabidiol analog O-1918 does not bind to CB(1) or CB(2

18 This potentiation was abolished by the cannabidiol analog O-1918 or by pertussis toxin but was

19 patients who became seizure-free was 5% with cannabidiol and 0% with placebo (P=0.08).

20 in convulsive-seizure frequency was 43% with cannabidiol and 27% with placebo (odds ratio, 2.00; 95%

21 pophilic fraction containing 0.2 and 2.2g of cannabidiol and cannabidiolic acid per 100g of threshing

22 f urinary Delta9-tetrahydrocannabinol (THC), cannabidiol and cannabinol, and two major metabolites of

23 certain plant-derived cannabinoids, such as cannabidiol and Delta9-tetrahydrocannabivarin, which are

24 ve peaks as high as 74%, as was the case for cannabidiol and interference #1 at 70 mus gate pulse wid

25 of substituted phenols were used to prepare cannabidiol and linderatin derivatives, and their struct

26 The neuroprotective actions of cannabidiol and other cannabinoids were examined in rat

27 binoid levels by use of the phytocannabinoid cannabidiol and selective fatty acid amide hydrolase inh

28 Cannabidiol and THC also were shown to prevent hydropero

29 The neuroprotection observed with cannabidiol and THC was unaffected by cannabinoid recept

30 to establish the safety and tolerability of cannabidiol and the primary efficacy endpoint was median

31 These findings suggest that Abn-cbd and cannabidiol are a selective agonist and antagonist, resp

32 roposed, and the antipsychotic properties of cannabidiol are currently being investigated in humans.

33 ying neurons, we propose that cannabinol and cannabidiol are promising nonpsychotropic therapeutics t

34 es per month decreased from 12.4 to 5.9 with cannabidiol, as compared with a decrease from 14.9 to 14

35 Patients were given oral cannabidiol at 2-5 mg/kg per day, up-titrated until into

36 Interestingly, we found that cannabidiol can preferentially target resurgent sodium c

37 binoids Delta(9)-tetrahydrocannabinol (THC), cannabidiol, cannabichromene, and cannabinol is presente

38 aration of seven cannabinoids (cannabigerol, cannabidiol, cannabinol, delta-9-tetrahydrocannabinol, d

39 Furthermore, the abnormal-cannabidiol (CBD) analog trans-4-[3-methyl-6-(1-methylet

40 Cannabidiol (CBD) and (9)-tetrahydrocannabinol (THC) hav

41 -2 and CP55,940), and two phytocannabinoids (cannabidiol (CBD) and Delta(9)-tetrahydrocannabinol (THC

42 inoids delta9-tetrahydrocannabinol (THC) and cannabidiol (CBD) both have immunosuppressive effects; a

43 Here we show that cannabidiol (CBD) effectively reduced seizures and autis

44 ch in both animals and humans indicates that cannabidiol (CBD) has antipsychotic properties.

45 Cannabidiol (CBD) is a natural nonpsychotropic cannabino

46 Cannabidiol (CBD) is a non-psychoactive component of mar

47 rahydroxycannabinol (THC) or nonpsychotropic cannabidiol (CBD) is via the attenuation of this formati

48 Delta(9)-Tetrahydrocannabinol (THC) and cannabidiol (CBD) occur naturally in marijuana (Cannabis

49 s study, we have investigated the effects of cannabidiol (CBD) on myocardial dysfunction, inflammatio

50 paration comprising equal amounts of THC and cannabidiol (CBD)) to mice bearing BRAF wild-type melano

51 Cannabidiol (CBD), a constituent of cannabis with few ps

52 t systemic and intrathecal administration of cannabidiol (CBD), a major nonpsychoactive component of

53 Here, we examined the effects of cannabidiol (CBD), a nonpsychoactive constituent of cann

54 Cannabidiol (CBD), a nonpsychotropic, nontoxic compound

55 55,940, Delta(9)-tetrahydrocannabinol (THC), cannabidiol (CBD), and THC+CBD (1:1), and compared betwe

56 etrahydrocannabinol (THC), cannabinol (CBN), cannabidiol (CBD), and the metabolites 11-nor-9-carboxy-

57 100 additional phytocannabinoids, including cannabidiol (CBD), cannabidivarin (CBDV), Delta(9)-tetra

58 The cannabis-derived phytochemical, cannabidiol (CBD), has been shown to have pharmacotherap

59 pic phytocannabinoid of Cannabis sativa, (-)-cannabidiol (CBD), on human sebaceous gland function and

60 lta-9-tetrahydrocannabinol (delta-9-THC) and cannabidiol (CBD), the two major derivatives of cannabis

61 ve effects of a nonpsychotropic cannabinoid, cannabidiol (CBD), were examined in streptozotocin-induc

62 phytochemical component of marijuana called cannabidiol (CBD), which possesses promising therapeutic

63 ding Delta(9)-tetrahydrocannabinol (THC) and cannabidiol (CBD).

64 t is the primary nonpsychoactive constituent cannabidiol (CBD).

65 ease of the potentially therapeutic compound cannabidiol (CBD).

66 as demonstrated using 11 drugs (amphetamine, cannabidiol, cocaine, codeine, heroine, methamphetamine,

67 The cannabidiol content has decreased on average from ~.28%

68 potential protection from harmful effects by cannabidiol continues to increase but is not definitive.

69 These findings suggest that cannabidiol could be exerting its anticonvulsant effects

70 on (SPME) is applied to the determination of cannabidiol, delta 8-tetrahydrocannabinol (delta 8-THC),

71 A catalytic hydrogenation of cannabidiol derivatives known as phenylcyclohexenes was

72 We also demonstrated that cannabidiol evoked a concentration-dependent release of

73 Moreover, the cannabidiol-evoked CGRP release depended on extracellula

74 repetitive stimulation studies, to show that cannabidiol-evoked CGRP release is mediated, at least in

75 that TRPV2 may comprise a mechanism whereby cannabidiol exerts its clinically beneficial effects in

76 Finally, cannabidiol exposure led to a decrease in the levels of

77 It is noteworthy that cannabidiol exposure led to an increase in reactive oxyg

78 From a mechanistic standpoint, cannabidiol exposure resulted in activation of caspase-8

79 We studied cannabidiol for the treatment of drug-resistant seizures

80 he ratio of Delta(9)-tetrahydrocannabinol to cannabidiol from 14 times in 1995 to ~80 times in 2014.

81 cebo (adjusted median difference between the cannabidiol group and the placebo group in change in sei

82 bal Impression of Change scale in 62% of the cannabidiol group as compared with 34% of the placebo gr

83 events that occurred more frequently in the cannabidiol group than in the placebo group included dia

84 were more withdrawals from the trial in the cannabidiol group.

85 In contrast, administration of cannabidiol had no such effect.

86 to target voltage-gated sodium channels and cannabidiol has recently received attention for its pote

87 Furthermore, cannabidiol-induced apoptosis and reactive oxygen specie

88 d more potent than (+)-cannabidiol; abnormal-cannabidiol is a full agonist.

89 The phytocannabinoid (-)-cannabidiol is a partial agonist, being approximately 40

90 Exposure of leukemia cells to cannabidiol led to cannabinoid receptor 2 (CB2)-mediated

91 hondria was further suggested as exposure to cannabidiol led to loss of mitochondrial membrane potent

92 However, there is first evidence that cannabidiol may ameliorate psychotic symptoms with a sup

93 ally occurring, nonpsychotropic cannabinoid, cannabidiol, may be a potentially useful therapeutic age

94 Our findings suggest that cannabidiol might reduce seizure frequency and might hav

95 psychopathological and cognitive effects of cannabidiol, no published data are available.

96 ate our findings, we examined the effects of cannabidiol on endogenous sodium currents from striatal

97 then examined the effects of anandamide and cannabidiol on peak transient and resurgent currents fro

98 effects of the nonpsychoactive cannabinoid, cannabidiol, on the induction of apoptosis in leukemia c

99 of Delta9-tetrahydrocannabinol and 80 mg of cannabidiol) or placebo with standardized psychosocial i

100 nd drug-resistant seizures to receive either cannabidiol oral solution at a dose of 20 mg per kilogra

101 of all types was significantly reduced with cannabidiol (P=0.03), but there was no significant reduc

102 with the pharmacology of the novel "abnormal-cannabidiol" receptor or a related orphan G protein-coup

103 s well as from the WIN and abn-CBD (abnormal-cannabidiol) receptors, two recently identified cannabin

104 Moreover, current clamp recordings show that cannabidiol reduces overall action potential firing of s

105 Among patients with the Dravet syndrome, cannabidiol resulted in a greater reduction in convulsiv

106 gration by antagonizing the CB2 and abnormal-cannabidiol-sensitive receptors, respectively.

107 fect of 2-AG occurs through CB2 and abnormal-cannabidiol-sensitive receptors, with subsequent activat

108 In addition, cannabidiol significantly inhibits the invasion of gliob

109 rthermore, we show that a nontoxic compound, cannabidiol, significantly downregulates Id-1 gene expre

110 Cannabidiol, THC and several synthetic cannabinoids all

111 Cannabidiol, the most abundant nonpsychoactive constitue

112 CP55940, Delta(9)-tetrahydrocannabinol, and cannabidiol, thus suggesting that the phenomenon is not

113 for the therapeutic development of medicinal cannabidiol to address the current opioid abuse crisis.

114 We aimed to establish whether addition of cannabidiol to existing anti-epileptic regimens would be

115 Furthermore, cannabidiol treatment led to a significant decrease in t

116 It is important to note that cannabinol and cannabidiol, two nonpsychotropic ingredients present in

117 ad severe adverse events possibly related to cannabidiol use, the most common of which was status epi

118 Among these, cannabidiol was found to be the most robust and potent (

119 Cannabidiol was more protective against glutamate neurot

120 2 weeks of follow-up after the first dose of cannabidiol were included in the safety and tolerability

121 By contrast, cannabidiol, which is a non-intoxicating and potentially