ライフサイエンスコーパス: naltrexone

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

2 mography (PET) as a predictor of response to naltrexone.

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

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

5 after 1 week of supervised 100 mg daily oral naltrexone.

6 with official prescribing information for XR-naltrexone.

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

8 nt opioid detoxification for induction to XR-naltrexone.

9 itiating adults with opioid dependence to XR-naltrexone.

10 n are associated with a positive response to naltrexone.

11 ith alcohol dependence who are responsive to naltrexone.

12 llowing treatment with the opioid antagonist naltrexone.

13 agonist therapy, and 13 trials (n = 1718) of naltrexone.

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

15 after the larger MCAM dose and <1 day after naltrexone.

16 herapy to support treatment and adherence to naltrexone.

17 Buprenorphine-naloxone and extended-release naltrexone.

18 n emotional attribution, and were blunted by naltrexone.

19 oid withdrawal and were transitioned to oral naltrexone.

20 ological variables affecting the efficacy of naltrexone.

21 ification before initiating extended-release naltrexone.

22 at 6 months compared with those taking oral naltrexone.

23 receptor (KOR) in the therapeutic effect of naltrexone.

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

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

26 .32 mg/kg) or the opioid receptor antagonist naltrexone (0.001-0.032 mg/kg) was injected prior to tes

27 For comparison, continuous 7-day naltrexone (0.01-0.1 mg/kg/h) and 7-day clonidine (3.2-1

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

29 1.0 mg/kg, i.m.), whereas the MOP antagonist naltrexone (1.7-5.6 mg/kg, i.m.) decreased both ethanol

30 gms (ADPs) separated by a week of open-label naltrexone (100 mg daily).

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

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

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

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

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

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

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

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

39 The first dose of XR-naltrexone (380 mg) was administered prior to discharge,

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

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

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

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

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

45 dose of 20 mg/day) enhances the efficacy of naltrexone (50 mg/day) in reducing alcohol drinking and

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

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

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

49 -54.2%] for prolonged exposure therapy plus naltrexone; -63.9% [95% CI, -73.9% to -53.8%] for prolon

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

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

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

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

54 Long-acting injection naltrexone (XR-naltrexone), administered monthly, circumvents the need

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

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

57 (heroin, prescription opioids), antagonists (naltrexone), agonist-antagonist combinations (buprenorph

58 id antagonist naltrexone, when compared with naltrexone alone, would have a greater influence on alco

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

60 Naltrexone also weakened the associations between subjec

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

62 ist), buprenorphine (a partial agonist), and naltrexone (an opioid antagonist).

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

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

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

66 l by the pan-opioid antagonists naloxone and naltrexone and evidence for a therapeutic benefit in sch

67 Naltrexone and GSK1521498 dose-dependently reduced both

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

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

70 For naltrexone and nalmefene, NNHs for withdrawal from trial

71 In the 12 participants who completed naltrexone and placebo conditions, naltrexone attenuated

72 l naltrexone placebo (implant group) or oral naltrexone and placebo implant (oral group).

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

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

75 the classic mu opioid antagonists, naloxone, naltrexone, and nalmefene.

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

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

78 7% to -61.2%] for supportive counseling plus naltrexone; and -61.0% [95% CI, -68.9% to -53.0%] for su

79 New forms of the opioid receptor antagonist naltrexone are also being studied.

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

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

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

83 ne-naloxone is preferred to extended-release naltrexone as first-line treatment when both options are

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

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

86 Naltrexone-assisted detoxification lasted 7 days and inc

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

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

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

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

91 completed naltrexone and placebo conditions, naltrexone attenuated the antisuicidality effects of ket

92 f our recent clinical trial, we test whether naltrexone attenuates antisuicidality effects of ketamin

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

94 These results confirm that naltrexone binds at the KOR site and suggest that KOR oc

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

96 We recently reported that naltrexone blocks antidepressant effects of ketamine in

97 Naltrexone blocks the effects of opioid agonists.

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

99 95% CrI, 4.16-7.78; SUCRA, 0.83), 55% taking naltrexone-bupropion (OR, 3.96; 95% CrI, 3.03-5.11; SUCR

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

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

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

103 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

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

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

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

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

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

109 mu and KOR could explain why lower doses of naltrexone can have greater clinical efficacy.

110 whether a small-molecule TLR4 inhibitor, (+)-naltrexone, can mitigate adverse PAF-induced effects.

111 These results support the use of XR-naltrexone combined with behavioral therapy as an effect

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

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

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

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

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

117 Following acute injection, MCAM and naltrexone decreased fentanyl self-administration on the

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

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

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

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

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

123 oid receptors with systemically-administered naltrexone does not abolish the antinociception evoked b

124 e deaths occurred 9-10 months after the last naltrexone dose.

125 % CI, 0.41-1.18; P = .17), with a very small naltrexone effect in the Asp40 group (odds ratio, 1.10;

126 understanding of the neurobiology underlying naltrexone effects could optimize treatments.

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

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

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

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

131 buprenorphine-naloxone with extended-release naltrexone for treating opioid use disorder.

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

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

134 retained in treatment for 6 months in the XR-naltrexone group (16 of 28 patients, 57.1%) than in the

135 (16 of 28 patients, 57.1%) than in the oral naltrexone group (nine of 32 patients, 28.1%) (hazard ra

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

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

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

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

140 inistering active cannabis compared with the naltrexone group.

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

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

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

144 Naltrexone had intrinsic effects: decreasing ratings of

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

146 Patients receiving XR-naltrexone had twice the rate of treatment retention at

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

148 he oral formulation of the opioid antagonist naltrexone has shown limited effectiveness for treatment

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

150 nd implant formulations of buprenorphine and naltrexone have been developed to address issues of safe

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

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

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

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

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

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

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

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

159 ned (1:1) them to addiction treatment with a naltrexone implant and oral naltrexone placebo (implant

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

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

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

163 aloxone to be preferable to extended-release naltrexone in 97% of bootstrap replications at 24 weeks

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

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

166 disorder treated with XR-naltrexone or oral naltrexone in combination with behavioral therapy.

167 5 times better TLR4 antagonist activity than naltrexone in microglial BV-2 cell line, whereas (-)-nor

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

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

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

171 ent, concomitant medication utilization, and naltrexone induction.

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

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

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

175 ata demonstrate that the TLR4 antagonist (+)-naltrexone inhibits the inflammatory cascade induced by

176 Naltrexone initiation was voluntary and the percentage o

177 Prior to naltrexone initiation, KOR availability was determined i

178 enabling PLGA microparticles to entrap more naltrexone into the structure.

179 Naltrexone is a nonselective opioid receptor antagonist

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

181 Naltrexone is one of the rare TLR4 antagonists with good

182 We further showed that low-dose naltrexone (LDN) abrogates hyperinsulinemia-mediated SIR

183 Only opioidergic manipulation through naltrexone led to a reduction in positive facial reactio

184 Naltrexone-loaded poly(lactide-co-glycolide) (PLGA) micr

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

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

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

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

189 e KOR site and suggest that KOR occupancy by naltrexone may be related to clinical response.

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

191 upancy of the kappa opioid receptor (KOR) by naltrexone measured with [(11)C]-LY2795050 positron emis

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

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

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

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

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

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

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

199 Slow-release, long-acting, implantable naltrexone might improve these outcomes.

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

201 treatment with oral naltrexone (N=32) or XR-naltrexone (N=28) for 24 weeks.

202 signed (1:1) to continue treatment with oral naltrexone (N=32) or XR-naltrexone (N=28) for 24 weeks.

203 cebo-controlled clinical trials of naloxone, naltrexone, nalmefene, and buprenorphine in patients wit

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

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

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

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

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

209 ational compound that contained 20 mug/ml of naltrexone (NTX).

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

211 rticipants were randomized to receive either naltrexone (NTX; 50 mg/day) + placebo memantine, or NTX

212 Effects of naltrexone on alcohol reward were examined using intracr

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

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

215 Furthermore, the effects of naltrexone on emotional attribution were partially aboli

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

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

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

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

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

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

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

223 Effects of naltrexone or nalmefene on alcohol intake were examined

224 nts with opioid use disorder treated with XR-naltrexone or oral naltrexone in combination with behavi

225 Participants were pretreated with naltrexone or placebo prior to intravenous ketamine in a

226 rticipants were randomly assigned to receive naltrexone or placebo.

227 led, crossover study of one dose of 50 mg of naltrexone, or placebo immediately before completing two

228 ulpride, 50 mg of the opioidergic antagonist naltrexone, or placebo.

229 eochemistry of (+)-1 is derived from the (+)-naltrexone pharmacophore.

230 treatment with a naltrexone implant and oral naltrexone placebo (implant group) or oral naltrexone an

231 Treatment with (+)-naltrexone prevented preterm delivery and alleviated fet

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

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

234 Naltrexone reduced alcohol craving relative to placebo,

235 Furthermore, naltrexone reduced feelings of warmth and increased vaso

236 Naltrexone reduces drinking among individuals with alcoh

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

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

239 Naltrexone, relative to placebo, significantly reduced a

240 ghly reproducible size distribution, DL, and naltrexone release rate.

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

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

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

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

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

246 Long-acting naltrexone showed positive advantage on prevention of pr

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

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

249 thadone, buprenorphine, and extended-release naltrexone, significantly improve opioid use disorder ou

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

251 (+)-Naltrexone suppressed the cPAF-induced expression of inf

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

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

254 implicated in drinking and craving following naltrexone therapy in alcohol use disorder.

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

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

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

258 , p < .0001) during the second ADP following naltrexone therapy.

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

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

261 The efficacy of naltrexone to treat alcohol use disorder (AUD) is modest

262 with opioid use disorder to extended-release naltrexone, transitioning patients with opioid use disor

263 Naltrexone-treated wild-type mice had significantly incr

264 Pups born after cPAF and (+)-naltrexone treatment exhibited comparable rates of postn

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

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

267 ), and corresponding estimate for antagonist naltrexone treatment were 0.26 (0-0.59) and 1.97 (0-5.18

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

269 By linking 2 naltrexone units through a rigid pyrrole spacer, the biv

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

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

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

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

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

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

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

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

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

279 Higher KOR occupancy by naltrexone was associated with higher alcohol craving du

280 Naltrexone was chosen as the model drug.

281 Response to naltrexone was defined as the difference in craving and

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

283 rge, with monthly doses thereafter, and oral naltrexone was given in a 50-mg daily dose.

284 The reduction in drinking after naltrexone was negatively associated with KOR occupancy,

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 king populations, opioid agonist therapy and naltrexone were associated with decreased risk of drug u

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

290 tagonist memantine and the opioid antagonist naltrexone, when compared with naltrexone alone, would h

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 Using naltrexone with individuals who are predominantly reward

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

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

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

299 Long-acting injection naltrexone (XR-naltrexone), administered monthly, circum

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