ライフサイエンスコーパス: naltrexone

1 in reuptake inhibitors, N-acetylcysteine, or naltrexone).

2 hin 2 to 3 days on rechallenge with low-dose naltrexone.

3 llowing treatment with the opioid antagonist naltrexone.

4 arding drugs, and this effect was blocked by naltrexone.

5 medication adherence and a second dose of XR-naltrexone.

6 toxification, followed by an injection of XR-naltrexone.

7 ng was inhibited by the mu-opiate antagonist naltrexone.

8 ized, placebo-controlled laboratory trial of naltrexone.

9 macological chaperone, the opioid antagonist naltrexone.

10 r agonist SKF 38393 or the opioid antagonist naltrexone.

11 endent attenuation of ethanol consumption by naltrexone.

12 with official prescribing information for XR-naltrexone.

13 (CD-1) mouse strains previously tested with naltrexone.

14 rior administration of the opioid antagonist naltrexone.

15 ntal medication options of buprenorphine and naltrexone.

16 ving buprenorphine and 604 (10.8%) receiving naltrexone.

17 nt opioid detoxification for induction to XR-naltrexone.

18 itiating adults with opioid dependence to XR-naltrexone.

19 n are associated with a positive response to naltrexone.

20 ith alcohol dependence who are responsive to naltrexone.

21 ted rats with Alzet minipumps delivering (+)-naltrexone (0, 7.5, 15, 30 mg/kg/day, subcutaneous) for

22 vehicle, SCH23390 (50-1600 nmol/kg, ip) and naltrexone (0.001-5 mg/kg, sc).

23 The influence of pretreatment with either naltrexone (0.1-1-3 mg/kg) or GSK1521498 (0.1-1-3 mg/kg)

24 igned to (1) prolonged exposure therapy plus naltrexone (100 mg/d), (2) prolonged exposure therapy pl

25 pill placebo, (3) supportive counseling plus naltrexone (100 mg/d), or (4) supportive counseling plus

26 eatment with sertraline (200 mg/day [N=40]), naltrexone (100 mg/day [N=49]), the combination of sertr

27 Furthermore, chronic delivery of (+)-naltrexone (15 or 30 mg/kg/day) or acute systemic inject

28 lets (also known as NB32), sustained-release naltrexone 16 mg per day plus sustained-release bupropio

29 0.0001 vs placebo) and 186 (39%) assigned to naltrexone 16 mg plus bupropion (p<0.0001 vs placebo).

30 (p<0.0001 vs placebo) and -5.0% (0.3) in the naltrexone 16 mg plus bupropion group (p<0.0001 vs place

31 mg plus bupropion, 171 participants [29.8%]; naltrexone 16 mg plus bupropion, 155 [27.2%]; placebo, 3

32 ent (naltrexone 32 mg plus bupropion, n=583; naltrexone 16 mg plus bupropion, n=578; placebo, n=581).

33 either the competitive mu-opioid antagonist naltrexone (25 mg) or a placebo in a randomized double-b

34 Low-dose naltrexone, 3 mg nightly, titrated to 4.5 mg nightly in

35 Oral naltrexone (30 mg/kg, bid) for 14 days also reduced etha

36 hours/day, 9 days), chronic delivery of (+)-naltrexone (30 mg/kg/day) during the withdrawal phase ha

37 n a 1:1:1 ratio to receive sustained-release naltrexone 32 mg per day plus sustained-release bupropio

38 or more compared with 226 (48%) assigned to naltrexone 32 mg plus bupropion (p<0.0001 vs placebo) an

39 .3) in the placebo group, -6.1% (0.3) in the naltrexone 32 mg plus bupropion group (p<0.0001 vs place

40 ssigned to combination treatment was nausea (naltrexone 32 mg plus bupropion, 171 participants [29.8%

41 ed and randomised to double-blind treatment (naltrexone 32 mg plus bupropion, n=583; naltrexone 16 mg

42 re randomized to receive placebo (n=4454) or naltrexone, 32 mg/d, and bupropion, 360 mg/d (n=4456).

43 ent (BOLD) fMRI sessions following 3 days of naltrexone (50 mg) and matched time for placebo.

44 The study drug was naltrexone (50 mg) given once daily or corresponding pla

45 one A118G G (Asp) allele, were randomized to naltrexone (50 mg) or placebo for 16 weeks and administe

46 ; RD -0.09; 95% CI, -0.13 to -0.04) for oral naltrexone (50 mg/d).

47 RD, -0.05; 95% CI, -0.10 to -0.002) for oral naltrexone (50 mg/d).

48 urse of naltrexone alone (50 mg/day [N=50]), naltrexone (50 mg/day) with gabapentin (up to 1,200 mg/d

49 cannabis smokers were randomized to receive naltrexone (50 mg: n=18 M and 5 F) or placebo (0 mg; n=2

50 assessed acamprosate (27 studies, n = 7519), naltrexone (53 studies, n = 9140), or both.

51 ore likely to be successfully inducted to XR-naltrexone (56.1% compared with 32.7%) and to receive th

52 14-O-Cinnamoyl esters of naltrexone (6) were synthesized and evaluated in isolate

53 -54.2%] for prolonged exposure therapy plus naltrexone; -63.9% [95% CI, -73.9% to -53.8%] for prolon

54 If treated with MM alone and naltrexone, 87.1% of Asp40 carriers had a good clinical

55 rmined the effect of the TLR4 antagonist (+)-naltrexone (a mu-opioid receptor inactive isomer) on the

56 Extended-release naltrexone, a sustained-release monthly injectable formu

57 avy drinking (median delay=98 days) than the naltrexone (abstinence rate: 21.3%; delay=29 days), sert

58 Focusing only on effectiveness, MM-naltrexone-acamprosate therapy is not significantly bett

59 considering cost and cost-effectiveness, MM-naltrexone-acamprosate therapy may be a better choice, d

60 (+)-Naltrexone acts as a Toll-like receptor 4 (TLR4) antagon

61 id not improve learning, which suggests that naltrexone acts via inhibition of endogenous MOR action

62 The results showed that naltrexone administration reduced cue-reactivity in sens

63 ce were tested in a water maze after chronic naltrexone administration.

64 ere randomly assigned to a 16-week course of naltrexone alone (50 mg/day [N=50]), naltrexone (50 mg/d

65 of naltrexone and gabapentin was better than naltrexone alone and/or placebo during the early drinkin

66 o naltrexone improved drinking outcomes over naltrexone alone during the first 6 weeks after cessatio

67 d had fewer drinks per drinking day than the naltrexone-alone group and the placebo group.

68 eep was associated with more drinking in the naltrexone-alone group but not in the naltrexone-gabapen

69 a longer interval to heavy drinking than the naltrexone-alone group, which had an interval similar to

70 roup; had fewer heavy drinking days than the naltrexone-alone group, which in turn had more than the

71 norphine followed by ascending doses of oral naltrexone along with clonidine and other adjunctive med

72 Naltrexone also weakened the associations between subjec

73 disparities in receipt of buprenorphine and naltrexone among youth with OUD in the United States.

74 Naltrexone, an efficacious medication for alcohol depend

75 Naltrexone, an opioid antagonist, has been shown to modu

76 igned and synthesized compounds based on (+)-naltrexone and (+)-noroxymorphone and evaluated their TL

77 rticipants were assigned to extended-release naltrexone and 155 to usual treatment.

78 ividuals were randomized to extended-release naltrexone and 79 to buprenorphine-naloxone; 105 (66.0%)

79 apy ($671 per patient), and MM plus combined naltrexone and acamprosate therapy ($1003 per patient).

80 Combination treatment with sustained-release naltrexone and bupropion was developed to produce comple

81 l trial evaluated whether the combination of naltrexone and gabapentin was better than naltrexone alo

82 Naltrexone and GSK1521498 dose-dependently reduced both

83 procedure was used to compare the effects of naltrexone and GSK1521498, a novel selective mu-opioid r

84 er delineate the biobehavioral mechanisms of naltrexone and its pharmacogenetics.

85 Similarly, both naltrexone and nalmefene were more effective in suppress

86 For naltrexone and nalmefene, NNHs for withdrawal from trial

87 Differences between naltrexone and placebo were not significant for any outc

88 A critical difference between naltrexone and risperidone loaded microspheres is their

89 Both naltrexone and SKF 38393 were found to attenuate oversha

90 Ondansetron by itself was similar to naltrexone and the combination in the overall analysis b

91 ations of medications (i.e., acamprosate and naltrexone) and behavioral interventions (i.e., medical

92 ed the classical opioid receptor antagonist, naltrexone, and in mu-opioid receptor knockout mice, sup

93 es better TLR-4 antagonist activity than (+)-naltrexone, and the ratio of its cell viability IC50, a

94 d by observed capsule administration, plasma naltrexone, and urinary riboflavin.

95 7% to -61.2%] for supportive counseling plus naltrexone; and -61.0% [95% CI, -68.9% to -53.0%] for su

96 The opioid antagonists naloxone/naltrexone are involved in improving learning and memory

97 patients (2 in the placebo arm and 2 in the naltrexone arm) stopped medication therapy because of ad

98 The success of these cases suggests low-dose naltrexone as a novel therapy for Hailey-Hailey disease.

99 The results provide evidence for naltrexone as the first pharmacotherapy to reduce postsm

100 e intoxication, and lower alcohol craving on naltrexone, as compared to placebo, and to Asn40 homozyg

101 alcohol use among nonsmokers did not vary by naltrexone assignment.

102 Naltrexone-assisted detoxification lasted 7 days and inc

103 e of two outpatient detoxification regimens, naltrexone-assisted detoxification or buprenorphine-assi

104 fication condition, participants assigned to naltrexone-assisted detoxification were significantly mo

105 n treatment, opioid abstinent, and receiving naltrexone at the end of the study).

106 )) induces similar conformational changes as naltrexone at the Galphai-betagamma interface, whereas i

107 -D-Trp-Orn-Thr-Pen-Thr-NH(2)), naloxone, and naltrexone behave like partial agonists.

108 The administration of the opioid antagonist naltrexone blocked placebo analgesia and also resulted i

109 raglutide (OR, 2.95; 95% CrI, 2.11-4.23) and naltrexone-bupropion (OR, 2.64; 95% CrI, 2.10-3.35) were

110 95% CrI, 4.16-7.78; SUCRA, 0.83), 55% taking naltrexone-bupropion (OR, 3.96; 95% CrI, 3.03-5.11; SUCR

111 placebo group and 90 patients (2.0%) in the naltrexone-bupropion group (HR, 0.88; adjusted 99.7% CI,

112 Adverse effects were more common in the naltrexone-bupropion group, including gastrointestinal e

113 r limit of the 95% CI of the HR for MACE for naltrexone-bupropion treatment, compared with placebo, d

114 lutide, 5.3 kg (95% CrI, -6.06 to -4.52 kg); naltrexone-bupropion, 5.0 kg (95% CrI, -5.94 to -3.96 kg

115 eight or obese adults, orlistat, lorcaserin, naltrexone-bupropion, phentermine-topiramate, and liragl

116 in 59 placebo-treated patients (1.3%) and 35 naltrexone-bupropion-treated patients (0.8%; HR, 0.59; 9

117 d in the USA or European Union are orlistat, naltrexone/bupropion, and liraglutide; in the USA, lorca

118 Liraglutide, naltrexone/bupropion, and phentermine/topiramate are new

119 greater reduction in activation who received naltrexone, but not placebo, experienced the least heavy

120 ndent patients receiving the sertraline plus naltrexone combination achieved abstinence from alcohol,

121 The sertraline plus naltrexone combination produced a higher alcohol abstine

122 s significantly lower for women treated with naltrexone compared with placebo (6 months, 3.3 vs. 5.5

123 d by pretreatment with the opioid antagonist naltrexone, confirming the opioid nature of these respon

124 in rats trained under the opioid antagonist naltrexone, consistent with an opioid-mediated negative

125 week-long delay before administration of XR-naltrexone, consistent with official prescribing informa

126 phase, participants received 4.5 mg of oral naltrexone daily.

127 show for the first time that maintenance on naltrexone decreased cannabis self-administration and ra

128 rations of 14-heteroaromatically substituted naltrexone derivatives were designed, synthesized, and e

129 +naltrexone; paroxetine+placebo; desipramine+naltrexone; desipramine+placebo.

130 Pretreatments with (+)-naloxone or (+)-naltrexone did not attenuate, and under certain conditio

131 he MOR knockout and GluA1-S845A mutant mice, naltrexone did not improve learning, which suggests that

132 However, naltrexone did not show evidence of efficacy in this pop

133 , the TLR4 antagonists, (+)-naloxone and (+)-naltrexone, did not specifically block neurochemical or

134 nol consumption sessions during adulthood, a naltrexone dose-response challenge (0-0.4 mg/kg) was ini

135 % CI, 0.41-1.18; P = .17), with a very small naltrexone effect in the Asp40 group (odds ratio, 1.10;

136 In vitro prolonged naloxone/naltrexone exposure significantly increased synaptic and

137 yohimbine and mu-opioid receptor antagonist naltrexone failed to alter the stimulus effects of CR405

138 atory studies have shown that the effects of naltrexone for alcoholism may be moderated by the Asn40A

139 fferences were found between acamprosate and naltrexone for controlling alcohol consumption.

140 mechanism and to define the role of low-dose naltrexone for treatment of Hailey-Hailey disease.

141 -analyses of trials comparing acamprosate to naltrexone found no statistically significant difference

142 During the first 6 weeks, the naltrexone-gabapentin group had a longer interval to hea

143 in the naltrexone-alone group but not in the naltrexone-gabapentin group, while a history of alcohol

144 l was associated with better response in the naltrexone-gabapentin group.

145 e no overdose events in the extended-release naltrexone group and seven in the usual-treatment group

146 those in the prolonged exposure therapy plus naltrexone group had the smallest increases.

147 improvement item, 56% of the patients in the naltrexone group showed much or very much improvement, c

148 Retention in the extended-release naltrexone group was noninferior to the buprenorphine-na

149 inistering active cannabis compared with the naltrexone group.

150 ther illicit opioids in the extended-release naltrexone group.

151 e, participants assigned to extended-release naltrexone had a longer median time to relapse than did

152 effects, but G-allele carriers who received naltrexone had an accelerated return to heavy drinking a

153 However, smokers who received naltrexone had better drinking outcomes than smokers who

154 Naltrexone had intrinsic effects: decreasing ratings of

155 However, those who received naltrexone had lower percentages of days drinking than t

156 ary evidence continues to show that low-dose naltrexone has a specific and clinically beneficial impa

157 The opioid antagonist naltrexone has shown promise to reduce weight gain durin

158 cts were treated for 16 weeks with 100 mg of naltrexone hydrochloride (234 Asn40 homozygotes and 67 w

159 Each patient was treated with low-dose naltrexone hydrochloride at a dosage of 1.5 to 3.0 mg pe

160 To date, extended-release naltrexone hydrochloride has not previously been compare

161 To assess low-dose naltrexone hydrochloride in the treatment of recalcitran

162 ntification of moderators of the response to naltrexone hydrochloride treatment for alcohol dependenc

163 -naloxone, 4 to 24 mg/d, or extended-release naltrexone hydrochloride, 380 mg, administered intramusc

164 Interventions: Oral naltrexone hydrochloride, 50 mg/d, or daily placebo with

165 dividuals are reward drinkers and respond to naltrexone if their reward score was higher than their r

166 ments, we found that acute injections of (+)-naltrexone immediately before withdrawal day 13 extincti

167 ion rate was 52% for patients who received a naltrexone implant and 28% for those who received a plac

168 The authors assessed the effectiveness of a naltrexone implant in the treatment of coexisting heroin

169 died the overall real-world effectiveness of naltrexone implant in this patient population.

170 Naltrexone implants resulted in higher retention in the

171 The addition of gabapentin to naltrexone improved drinking outcomes over naltrexone al

172 ward thresholds were unchanged by alcohol or naltrexone in 118AA mice.

173 following mu-opioid receptor blockade using naltrexone in 119 of these subjects unmasked a greater t

174 d is associated with an improved response to naltrexone in alcohol dependence.

175 been proposed that therapeutic responses to naltrexone in alcoholism are moderated by variation at t

176 , double-blind, placebo-controlled trials of naltrexone in nicotine dependence.

177 ression (sertraline) and alcohol dependence (naltrexone) in treating patients with both disorders.

178 fety, efficacy, and tolerability of low-dose naltrexone, in conjunction with single-day buprenorphine

179 fMRI analyses tested naltrexone-induced differences in BOLD activation and fu

180 es revealed that the greatest sensitivity to naltrexone-induced inhibition of sucrose (10%) intake wa

181 /J strains displayed far less sensitivity to naltrexone-induced inhibition of sucrose intake.

182 ent, concomitant medication utilization, and naltrexone induction.

183 The possible mechanism may involve low-dose naltrexone influencing opioid or toll-like receptor sign

184 Retention and naltrexone ingestion also were superior in the 4-week vs

185 negative for illicit opioid use, retention, naltrexone ingestion, and favorable treatment response (

186 Naltrexone initiation was voluntary and the percentage o

187 rats, and injection of the opioid antagonist naltrexone into the VTA disrupts the onset of maternal b

188 To determine whether low-dose naltrexone is an effective treatment for Hailey-Hailey d

189 lin) and a low dose of the opioid antagonist naltrexone (LDN) on expression of myelin oligodendrocyte

190 ment with 4.5mg nightly naltrexone (low-dose naltrexone, LDN) on self-reported quality of life of MS

191 y of 8 weeks of treatment with 4.5mg nightly naltrexone (low-dose naltrexone, LDN) on self-reported q

192 uprenorphine stabilization, brief taper, and naltrexone maintenance for treatment of PO dependence.

193 ay respond positively to a 4-week taper plus naltrexone maintenance intervention.

194 laboratory study, we assessed the effects of naltrexone maintenance on the reinforcing, subjective, p

195 methamphetamine addiction and suggests that naltrexone may be reducing drug cue salience by decreasi

196 Low-dose naltrexone may represent a low-cost and low-risk alterna

197 For injectable naltrexone, meta-analyses found no association with retu

198 itro release characteristics of the prepared naltrexone microspheres and the reference-listed drug (V

199 antly, predicting the in vivo performance of naltrexone microspheres in the investigated animal model

200 ed with the in vitro release profiles of the naltrexone microspheres obtained using USP apparatus 4.

201 The pharmacokinetics of the naltrexone microspheres were investigated using a rabbit

202 e compositionally equivalent formulations of naltrexone microspheres with different release character

203 These results suggest that naltrexone might be particularly beneficial for improvin

204 njections of 10mg/kg OGF (MOG+OGF), 0.1mg/kg naltrexone (MOG+LDN), or saline (MOG+Vehicle) at the tim

205 f the endogenous mu-opioid receptor (MOR) by naltrexone, MOR knockout, and GluA1-S845A mutant (in whi

206 [N=49]), the combination of sertraline plus naltrexone (N=42), or double placebo (N=39) while receiv

207 gene (OPRM1), A118G (Asn40Asp), may moderate naltrexone (NTX) effects in alcohol dependence.

208 Naltrexone (NTX) is an opioid receptor antagonist with d

209 l studies suggest that the opioid antagonist naltrexone (NTX) is effective in reducing the abuse liab

210 A single eye drop of 10(-5) M naltrexone (NTX), 10(-5) M [Met(5)]-enkephalin, or steri

211 ia was reinstated by the MOR inverse agonist naltrexone (NTX), but not by its neutral antagonist 6bet

212 ct might be blocked by the opioid antagonist naltrexone (NTX).

213 with GSK1521498 (0.1, 1, and 3 mg/kg; IP) or naltrexone (NTX, 0.1, 1, and 3 mg/kg; SC).

214 ntrolled, three-period crossover design with naltrexone (NTX; 25 mg OD for 2 days, then 50 mg OD for

215 dently blocked by pretreatment with general (naltrexone: NTX), mu (beta-funaltrexamine: BFNA), kappa

216 Effects of naltrexone on alcohol reward were examined using intracr

217 ical trial, we tested the impact of low-dose naltrexone on daily self-reported pain.

218 domized clinical trial tested the effects of naltrexone on drinking and alcohol cue-elicited brain ac

219 The SL phenotype moderated the effect of naltrexone on heavy drinking (6.1 fewer heavy drinking d

220 A nonsignificant effect of naltrexone on heavy drinking was noted (4.8 fewer heavy

221 We investigated the effect of naloxone/naltrexone on hippocampal alpha-amino-3-hydroxy-5-methyl

222 The beneficial effect of naltrexone on spatial learning and memory under normal c

223 eport the assessment of (+)-naloxone and (+)-naltrexone on the acute dopaminergic effects of cocaine

224 The goal was to examine effects of naltrexone on weight gain over long-term follow-up in me

225 stigated the effects of opioid blockade, via naltrexone, on functional magnetic resonance imaging (fM

226 agonized by the opioid receptor antagonists (naltrexone or Cys2, Tyr3, Arg5, Pen7-amide).

227 Effects of naltrexone or nalmefene on alcohol intake were examined

228 lkaloid agonist buprenorphine or with either naltrexone or naloxone, structurally related MOR antagon

229 After taking naltrexone or placebo, participants completed an intrave

230 rticipants were randomly assigned to receive naltrexone or placebo.

231 conditions to one of four groups: paroxetine+naltrexone; paroxetine+placebo; desipramine+naltrexone;

232 The objective of this study is to test the naltrexone pharmacogenetic effects of the Asn40Asp SNP i

233 much-needed extension of previous studies of naltrexone pharmacogenetics to individuals of Asian desc

234 A sustained-release combination of naltrexone plus bupropion could be a useful therapeutic

235 and dry mouth were also more frequent in the naltrexone plus bupropion groups than in the placebo gro

236 tion of around 1 mm Hg below baseline in the naltrexone plus bupropion groups.

237 nclude pharmacotherapy with buprenorphine or naltrexone, provider and community education, coordinati

238 is first national study of buprenorphine and naltrexone receipt among youth, dispensing increased ove

239 amine D1-like (SCH23390) and general opioid (naltrexone) receptor antagonism to alter intake of fat e

240 Naltrexone reduced alcohol craving relative to placebo,

241 Furthermore, naltrexone reduced feelings of warmth and increased vaso

242 Naltrexone reduces drinking among individuals with alcoh

243 These data replicate previous findings that naltrexone reduces heavy drinking and reward-related bra

244 To measure naloxone/naltrexone-regulated AMPAR trafficking, pHluorin-GluA1 i

245 Naltrexone, relative to placebo, significantly reduced a

246 n (FDA)-approved alcoholism pharmacotherapy, naltrexone, relative to placebo.

247 Discontinuation of low-dose naltrexone resulted in flaring of symptoms, which cleare

248 ver, controllable stimulation, combined with naltrexone, reverses the capsaicin-induced deficit.

249 their cannabis use are warranted to evaluate naltrexone's efficacy as a treatment for cannabis use di

250 At this concentration, naltrexone selectively suppressed alcohol intake in 118G

251 expressing Galphao RGSi subunits exhibited a naltrexone-sensitive enhancement of baseline latency in

252 Treatment with extended-release naltrexone showed noninferiority to buprenorphine-naloxo

253 d day of acquisition, which is the time when naltrexone significantly improved learning.

254 Relative to placebo, maintenance on naltrexone significantly reduced both active cannabis se

255 Naltrexone significantly, dose-dependently and different

256 wed significantly greater effectiveness than naltrexone, supporting its potential use for promoting a

257 on of baseline pain in those taking low-dose naltrexone than in those taking placebo (28.8% reduction

258 ot significantly lower with extended-release naltrexone than with usual treatment.

259 MM) with placebo ($409 per patient), MM plus naltrexone therapy ($671 per patient), and MM plus combi

260 and the percentage of participants choosing naltrexone therapy within the clonidine (8 [22.2%]), tra

261 r fatigue or sleep problems) during low-dose naltrexone therapy, as contrasted with an 11% response r

262 receive 1-, 2-, or 4-week tapers followed by naltrexone therapy.

263 therapy is not significantly better than MM-naltrexone therapy.

264 at the highest doses of (+)-naloxone and (+)-naltrexone, those doses also attenuated rates of food-ma

265 ecently, the (+)-enantiomers of naloxone and naltrexone, TLR4 antagonists, have been reported to atte

266 s observed for the abilities of SCH23390 and naltrexone to inhibit intralipid intake across strains.

267 Ondansetron, naltrexone, topiramate, and baclofen are examples.

268 Naltrexone-treated wild-type mice had significantly incr

269 The efficacy of naltrexone treatment for pathological gambling has been

270 sm as a biomarker to predict the response to naltrexone treatment of alcohol dependence.

271 ally significant OPRM1 Asp40 allele predicts naltrexone treatment response in alcoholic individuals.

272 f patients with alcohol dependence and PTSD, naltrexone treatment resulted in a decrease in the perce

273 t the Asp40 allele moderates the response to naltrexone treatment.

274 so significantly lower in women treated with naltrexone versus placebo.

275 We found that chronic delivery of (+)-naltrexone via minipumps during the withdrawal phase dec

276 ompared a 24-week course of extended-release naltrexone (Vivitrol) with usual treatment, consisting o

277 e predominantly reward drinkers and received naltrexone vs placebo had an 83% reduction in the likeli

278 The PREDICT study tested acamprosate and naltrexone vs placebo in 426 randomly assigned AD patien

279 , double-blind, randomized clinical trial of naltrexone vs placebo in individuals with alcohol depend

280 Low-dose naltrexone was also associated with improved general sat

281 Extended-release naltrexone was as effective as buprenorphine-naloxone in

282 criminal justice offenders, extended-release naltrexone was associated with a rate of opioid relapse

283 Naltrexone was chosen as the model drug.

284 No effect of naltrexone was found in the latter group.

285 Low-dose naltrexone was rated equally tolerable as placebo, and n

286 In the Asn40 group, the observed effect of naltrexone was similar to that in previous trials (odds

287 effects of medication on drinking, such that naltrexone was superior to placebo only among smokers.

288 Both acamprosate and oral naltrexone were associated with reduction in return to d

289 comes, differences between buprenorphine and naltrexone were not significant.

290 SCH23390 and naltrexone were respectively 13.3-fold and 9.3-fold more

291 s) would have a better treatment response to naltrexone, whereas individuals whose drinking was drive

292 to extended-release injection naltrexone (XR-naltrexone) while preventing relapse.

293 Hailey-Hailey disease treated with low-dose naltrexone who achieved clinical resolution of symptoms.

294 mine whether treatment with extended-release naltrexone will be as effective as daily buprenorphine h

295 Naltrexone with (P = .02) or without (P = .049) ondanset

296 Using naltrexone with individuals who are predominantly reward

297 ing was associated with a strong response to naltrexone, with 17.1 fewer heavy drinking days (Cohen d

298 Dispensing of a medication (buprenorphine or naltrexone) within 6 months of first receiving an OUD di

299 pendent adults to extended-release injection naltrexone (XR-naltrexone) while preventing relapse.

300 Extended-release naltrexone (XR-NTX), an opioid antagonist, and sublingua