ライフサイエンスコーパス: buprenorphine

1 lation after CCL2 treatment was inhibited by buprenorphine.

2 ization, suggesting a mechanism of action of buprenorphine.

3 the hyperalgesia elicited by ultra-low-dose buprenorphine.

4 ritonavir or fosamprenavir-ritonavir but not buprenorphine.

5 renavir-ritonavir induced glucuronidation of buprenorphine.

6 brain slices to characterize the actions of buprenorphine.

7 oid agonist therapy (OAT) with methadone and buprenorphine.

8 r time when treated with methadone than with buprenorphine.

9 lity disorder did not affect the response to buprenorphine.

10 All animals received buprenorphine (0.05 mg/kg, SC) and imipenem/cilastatin (

11 In contrast, a 15,000-fold lower dose of buprenorphine (0.1 mug.kg(-1)), which caused thermal and

12 atment with sublingual tablets consisting of buprenorphine (16 mg) in combination with naloxone (4 mg

13 ompared levomethadyl acetate (75 to 115 mg), buprenorphine (16 to 32 mg), and high-dose (60 to 100 mg

14 ine (8 [22.2%]), tramadol ER (7 [19.4%]), or buprenorphine (3 [9.7%]) groups did not differ significa

15 ed concentrations of the inactive metabolite buprenorphine-3-glucuronide suggested that darunavir-rit

16 ity of 35 with levomethadyl acetate, 34 with buprenorphine, 38 with high-dose methadone, and 53 with

17 o 396 for buprenorphine, 472 to 400 for [2H4]buprenorphine, 414 to 101 for norbuprenorphine, 423 to 1

18 ing of the transitions of m/z 468 to 396 for buprenorphine, 472 to 400 for [2H4]buprenorphine, 414 to

19 assess the feasibility of discontinuing the buprenorphine 72 h before surgery.

20 norbuprenorphine is a high efficacy agonist, buprenorphine a low efficacy agonist, and diprenorphine

21 Buprenorphine, a partial mu-opioid agonist, is an altern

22 his study examined drug interactions between buprenorphine, a partial opioid agonist used for opioid

23 ver a 192-h period, morphine, etorphine, and buprenorphine administered before elicitation of CHS on

24 tors failed to exhibit antinociception after buprenorphine administration.

25 Treatment with buprenorphine after the onset of infection also arrested

26 (16 mg) in combination with naloxone (4 mg), buprenorphine alone (16 mg), or placebo given daily for

27 uprenorphine and naloxone in combination and buprenorphine alone are safe and reduce the use of opiat

28 uprenorphine and naloxone in combination and buprenorphine alone were found to have greater efficacy

29 bjects receiving a sublingual tablet of 8 mg buprenorphine and 2 mg naloxone, buprenorphine and norbu

30 89.2%) of medication-treated youth receiving buprenorphine and 604 (10.8%) receiving naltrexone.

31 rding to treatment group (with 58 exposed to buprenorphine and 73 exposed to methadone) showed that t

32 ustments are not likely to be necessary when buprenorphine and darunavir-ritonavir or fosamprenavir-r

33 g residues W293(6.48) and N150(3.35), whilst buprenorphine and diprenorphine did not.

34 ervations show the unique characteristics of buprenorphine and further demonstrate the range of agoni

35 The pharmacokinetics of buprenorphine and its metabolites and symptoms of opioid

36 Although buprenorphine and methadone are both effective treatment

37 n this period, but little difference between buprenorphine and methadone was noted thereafter or for

38 osing, randomized, controlled study in which buprenorphine and methadone were compared for use in the

39 Opioid-based analgesics such as buprenorphine and morphine also have immunomodulatory pr

40 ever, here we show that mice pretreated with buprenorphine and morphine do not die from clostridial m

41 cyclase by the low-efficacy partial agonists buprenorphine and nalbuphine was increased in cells expr

42 s who participated in an open-label study of buprenorphine and naloxone (at daily doses of up to 24 m

43 tion with a sublingual-tablet formulation of buprenorphine and naloxone has been proposed, but its ef

44 ble-blind trial was terminated early because buprenorphine and naloxone in combination and buprenorph

45 Buprenorphine and naloxone in combination and buprenorph

46 fy time trends and disparities in receipt of buprenorphine and naltrexone among youth with OUD in the

47 In this first national study of buprenorphine and naltrexone receipt among youth, dispen

48 ver, for these outcomes, differences between buprenorphine and naltrexone were not significant.

49 the more experimental medication options of buprenorphine and naltrexone.

50 let of 8 mg buprenorphine and 2 mg naloxone, buprenorphine and norbuprenorphine were detected for up

51 ged from 2.2 to 2.8 and 1.5 to 2.4 ng/ml for buprenorphine and norbuprenorphine, respectively (i.e.,

52 bstinence during weeks 5-6 were continued on buprenorphine and randomly assigned to receive clonidine

53 option for expanding treatment is the use of buprenorphine and the buprenorphine-naloxone combination

54 tinent (p=0.0007), with all results best for buprenorphine and worst for placebo.

55 luoroethyl-diprenorphine, [(18)F]fluoroethyl-buprenorphine, and [(18)F]fluoroethyl-phenethyl-orvinol

56 n of a mu- and kappa-opioid partial agonist, buprenorphine, and a mu-opioid antagonist, samidorphan,

57 ntrinsic agonist efficacy, norbuprenorphine, buprenorphine, and diprenorphine.

58 We compared the efficacy of naltrexone, buprenorphine, and no additional treatment, in patients

59 ntagonist diprenorphine, the partial agonist buprenorphine, and the full agonist phenethyl-orvinol.

60 stants were obtained for morphine, naloxone, buprenorphine, and zidovudine, and the results were conf

61 y related drug group (oripavine derivatives [buprenorphine] and natural opium alkaloids).

62 Methadone and buprenorphine are currently the most common pharmacologi

63 Our findings underscore the use of buprenorphine as a therapeutic for neuroinflammation as

64 and safety of very low dosages of sublingual buprenorphine as a time-limited treatment for severe sui

65 These results are consistent with the use of buprenorphine as an acceptable treatment for opioid depe

66 ontrolled trial of ultra-low-dose sublingual buprenorphine as an adjunctive treatment.

67 ioid-dependent pregnant women have suggested buprenorphine as an alternative treatment to methadone d

68 dissemination of maintenance treatment with buprenorphine as an effective public-health approach to

69 Compared with participants in the buprenorphine-assisted detoxification condition, partici

70 Buprenorphine-assisted detoxification included a 7-day b

71 imens, naltrexone-assisted detoxification or buprenorphine-assisted detoxification, followed by an in

72 , including interdisciplinary pain programs, buprenorphine-assisted dose reduction, and behavioral in

73 opioid agonist treatments (eg, methadone vs buprenorphine) associated with differences in efficacy f

74 ns that lead to P-glycoprotein inhibition in buprenorphine-associated fatalities and respiratory depr

75 ttributed to the partial agonist activity of buprenorphine at opioid receptors.

76 ly reversible opioid antagonists naloxone or buprenorphine before norBNI responded strongly in the ta

77 ceptor transmembrane domains showed that the buprenorphine-bound receptor occupied a distinct set of

78 entified potential antidepressant effects of buprenorphine (BPN), a drug with high affinity for mu op

79 Methadone (MET) and buprenorphine (BUP) are widely prescribed for opiate mai

80 combination of a mu-opioid partial agonist, buprenorphine (BUP), and a potent mu-opioid antagonist,

81 Here we demonstrate that buprenorphine, but not morphine, activates mitogen-activ

82 is hypothesis, the antinociceptive effect of buprenorphine, but not morphine, was markedly enhanced i

83 Acute application of buprenorphine caused a hyperpolarization that was preven

84 8 opioid-dependent patients at an outpatient buprenorphine clinic.

85 Sixty-one percent of participants in the buprenorphine condition and 5% of those in the clonidine

86 Those in the buprenorphine condition generally reported more positive

87 ial agonist, subsaturating concentrations of buprenorphine decreased the [Met](5)enkephalin (ME)-indu

88 Buprenorphine decreases the formation of membrane projec

89 We show that buprenorphine decreases these phosphorylations in CCL2-t

90 the ability of a novel, weekly, subcutaneous buprenorphine depot formulation, CAM2038, to block eupho

91 ific to C. perfringens-mediated myonecrosis; buprenorphine did not protect against disease caused by

92 implants compared with continued sublingual buprenorphine did not result in an inferior likelihood o

93 is shown that a phenyl ring analogue (1d) of buprenorphine displays the desired profile in vitro with

94 e naltrexone, in conjunction with single-day buprenorphine dosing and adjunctive nonopioid medication

95 However, in human and animal studies, buprenorphine exhibited ceiling respiratory effects, whe

96 nd to evaluate correlations, if any, between buprenorphine exposure and neonatal outcomes.

97 cific method can be used to monitor in utero buprenorphine exposure and to evaluate correlations, if

98 n lasted 7 days and included a single day of buprenorphine followed by ascending doses of oral naltre

99 Treatment of animals with buprenorphine for 1 week resulted in the inhibition of t

100 Outpatients were prescribed daily sublingual buprenorphine for 6 months or more, were abstinent while

101 nt while taking 8 mg/d or less of sublingual buprenorphine for 90 days or longer, and were determined

102 acy and safety of longer-term treatment with buprenorphine for young individuals with opioid dependen

103 reated with opioids (morphine, methadone, or buprenorphine) for up to 6 days.

104 ne group (18%) and 28 of the 86 women in the buprenorphine group (33%).

105 Seventy-eight percent of patients in the buprenorphine group (89 of 114 [95% CI, 70%-85%]) vs 37%

106 Eleven percent of patients in the buprenorphine group (95% CI, 6%-19%) used inpatient addi

107 on group, and 57.6% (95% CI, 47%-68%) in the buprenorphine group (P = .17).

108 and from stabilization to post taper in the buprenorphine group (stabilization mean, 0.46 [SE, .05]

109 n adverse events: 61 patients (56.5%) in the buprenorphine group and 29 (52.7%) in the placebo group.

110 administered in 5 of 33 infants (15%) in the buprenorphine group and in 7 of 30 infants (23%) in the

111 The buprenorphine group reduced the number of days of illici

112 For those in the buprenorphine group, a significantly higher percentage o

113 and 13.5% of participants in the sublingual buprenorphine group, respectively.

114 es was greater in the combined-treatment and buprenorphine groups (17.8 percent and 20.7 percent, res

115 norphine(>/= 1 mg/kg) and to a lesser extent buprenorphine (>/= 10 mg/kg) were responsible for dose-d

116 Patients who initiated with buprenorphine had reduced all-cause and drug-related mor

117 ered oxycodone, fentanyl, or heroin, but not buprenorphine had similar profiles of escalation and inc

118 Recently, buprenorphine has been shown to activate opioid receptor

119 Although buprenorphine has been shown to interact with multiple o

120 rats were injected with either the analgesic buprenorphine-HCl or saline every 12 hrs; injections wer

121 uration, but the group that was treated with buprenorphine-HCl showed no significant difference compa

122 and without pre-treatment with the analgesic buprenorphine-HCl.

123 sipramine hydrochloride (0 or 150 mg/d) plus buprenorphine hydrochloride (12 mg/d) or methadone hydro

124 plants or sublingual placebo plus four 80-mg buprenorphine hydrochloride implants (expected efficacy,

125 oxification) from opioids using clonidine or buprenorphine hydrochloride is a widely used treatment.

126 ase naltrexone will be as effective as daily buprenorphine hydrochloride with naloxone hydrochloride

127 erse events occurred in 48.3% and 23% of the buprenorphine implant group and in 52.8% and 13.5% of pa

128 The buprenorphine implant group had significantly more urine

129 naloxone tablets, patients received either 4 buprenorphine implants (80 mg per implant) or 4 placebo

130 Those who received buprenorphine implants also had fewer clinician-rated (P

131 One hundred eight were randomized to receive buprenorphine implants and 55 to receive placebo implant

132 Over 6 months, 72 of 84 (85.7%) receiving buprenorphine implants and 64 of 89 (71.9%) receiving su

133 Eighty-one of 84 (96.4%) receiving buprenorphine implants and 78 of 89 (87.6%) receiving su

134 dose of sublingual buprenorphine, the use of buprenorphine implants compared with continued sublingua

135 g persons with opioid dependence, the use of buprenorphine implants compared with placebo resulted in

136 l of 71 of 108 patients (65.7%) who received buprenorphine implants completed the study vs 17 of 55 (

137 Patients with buprenorphine implants had a mean percentage of urine sa

138 uprenorphine with placebo implants and 87 to buprenorphine implants with sublingual placebo; 165 of 1

139 ly a handful of EECA countries (methadone or buprenorphine in five countries and needle and syringe p

140 indicate that the antinociceptive effect of buprenorphine in mice is micro-opioid receptor-mediated

141 lower than that of cocaine, remifentanil, or buprenorphine in monkeys responding under a progressive-

142 ittle is known about the synaptic effects of buprenorphine in nociceptive pathways.

143 spiratory depression have been attributed to buprenorphine in opioid abusers.

144 CAM2038 produces a rapid initial rise of buprenorphine in plasma with maximum concentration aroun

145 f-administration of oxycodone, fentanyl, and buprenorphine in rats allowed long access sessions (12 h

146 e effective than clonidine and comparable to buprenorphine in reducing opioid withdrawal symptoms dur

147 nal age or older and exposed to methadone or buprenorphine in utero .

148 ent article describes aryl ring analogues of buprenorphine in which the standard C20-methyl group has

149 st, enhanced the antinociceptive efficacy of buprenorphine in wild-type mice but not in mice lacking

150 tors by substitute drugs (e.g. methadone and buprenorphine) in opiate addicts.

151 Dose-response curves for buprenorphine-induced antinociception display ceiling ef

152 ated the bell-shaped dose-response curve for buprenorphine-induced antinociception in wild-type mice.

153 tinociception, we tested the hypothesis that buprenorphine-induced antinociception might be compromis

154 for a modulatory role for ORL-1 receptors in buprenorphine-induced antinociception was that coadminis

155 The ultra-low-dose buprenorphine-induced synaptic facilitation was mediated

156 ify additional potential mechanisms by which buprenorphine inhibits CCL2-induced monocyte migration,

157 Patients who received ultra-low-dose buprenorphine (initial dosage, 0.1 mg once or twice dail

158 Methadone and buprenorphine initially abolished these changes uniforml

159 Buprenorphine is a mixed opioid receptor agonist-antagon

160 Buprenorphine is a partial opioid agonist that can be pr

161 Buprenorphine is a successful analgesic and treatment fo

162 Buprenorphine is a weak partial agonist at mu-opioid rec

163 Buprenorphine is an efficacious, widely used treatment f

164 ioid agonist therapies such as methadone and buprenorphine is available in prisons in only a handful

165 adverse events compared with other opioids, buprenorphine is considered a safe option for pain and s

166 If buprenorphine is continued during the perioperative peri

167 Buprenorphine is emerging as the drug of choice for main

168 Buprenorphine is used to treat opiate addiction.

169 r determination of the antiabuse medication, buprenorphine, its primary metabolite, norbuprenorphine,

170 o an interest in developing compounds with a buprenorphine-like pharmacological profile but with lowe

171 We propose that buprenorphine limits CCL2-mediated monocyte transmigrati

172 ts and 64 of 89 (71.9%) receiving sublingual buprenorphine maintained opioid abstinence (hazard ratio

173 nd adverse effects were compared between the buprenorphine-maintained participants and an equal numbe

174 Prenatal buprenorphine maintenance treatment (BMT) versus methado

175 icacy of adding a behavioral intervention to buprenorphine maintenance treatment.

176 rences in therapeutic efficacy compared with buprenorphine maintenance treatment.

177 icacy of adding a behavioral intervention to buprenorphine maintenance treatment.

178 in women than in men, particularly those on buprenorphine maintenance.

179 ans aim for in terms of treatment outcome in buprenorphine maintenance?

180 Buprenorphine may be more effective than morphine for th

181 Our study revealed that buprenorphine mediates its modulatory effects on transmi

182 ble for both in vivo and in vitro studies of buprenorphine metabolism to norbuprenorphine.

183 , 2C19, 2D6, and 2E1 may also be involved in buprenorphine metabolism to other products.

184 clonidine (n = 36), tramadol ER (n = 36), or buprenorphine (n = 31) was then instituted, and patients

185 ling and maintenance with naltrexone (n=43), buprenorphine (n=44), or placebo (n=39).

186 Buprenorphine-naloxone (BUP) is an effective treatment o

187 R-NTX), an opioid antagonist, and sublingual buprenorphine-naloxone (BUP-NX), a partial opioid agonis

188 Strategies to improve buprenorphine-naloxone adherence are needed.

189 reatment is the use of buprenorphine and the buprenorphine-naloxone combination.

190 ease naltrexone group was noninferior to the buprenorphine-naloxone group (difference, -0.1; with 95%

191 weeks 1 through 12, patients in the 12-week buprenorphine-naloxone group reported less opioid use (c

192 Patients in the 12-week buprenorphine-naloxone group were prescribed up to 24 mg

193 Continuing treatment with buprenorphine-naloxone improved outcome compared with sh

194 ended-release naltrexone was as effective as buprenorphine-naloxone in maintaining short-term abstine

195 Among patients receiving buprenorphine-naloxone in primary care for opioid depend

196 -release naltrexone showed noninferiority to buprenorphine-naloxone on group proportion of total numb

197 21 years who were randomized to 12 weeks of buprenorphine-naloxone or a 14-day taper (detox).

198 esults (54%; 95% CI = 38%-70%) vs 52 12-week buprenorphine-naloxone patients (23%; 95% CI = 11%-35%).

199 dence interval [CI] = 47%-75%) vs 58 12-week buprenorphine-naloxone patients (26%; 95% CI = 14%-38%).

200 esults (51%; 95% CI = 35%-67%) vs 49 12-week buprenorphine-naloxone patients (43%; 95% CI = 29%-57%).

201 %) remained in treatment vs 52 of 74 12-week buprenorphine-naloxone patients (70%; chi(2)(1) = 32.90,

202 Brief treatment (phase 1) included 2-week buprenorphine-naloxone stabilization, 2-week taper, and

203 rmes) and BUP-NX was daily self-administered buprenorphine-naloxone sublingual film (Suboxone; Indivi

204 After induction with sublingual buprenorphine-naloxone tablets, patients received either

205 Success rates 8 weeks after completing the buprenorphine-naloxone taper (phase 2, week 24) dropped

206 ase 2 outcomes were more common while taking buprenorphine-naloxone than 8 weeks after taper (49.2% [

207 ccessful outcomes in phase 2 during extended buprenorphine-naloxone treatment (week 12), with no diff

208 tablished for the primary care, office-based buprenorphine-naloxone treatment of opioid dependence.

209 Adherence to buprenorphine-naloxone treatment varied; increased adher

210 if a threshold for rescue use of sublingual buprenorphine-naloxone treatment was exceeded.

211 patients entered phase 2: extended (12-week) buprenorphine-naloxone treatment, 4-week taper, and 8-we

212 are most likely to reduce opioid use during buprenorphine-naloxone treatment; if tapered off bupreno

213 omization to either daily oral flexible dose buprenorphine-naloxone, 4 to 24 mg/d, or extended-releas

214 enorphine-naloxone treatment; if tapered off buprenorphine-naloxone, even after 12 weeks of treatment

215 or excess were compared in opioid-dependent, buprenorphine-naloxone-maintained, human immunodeficienc

216 s opioid dependence counseling; all received buprenorphine-naloxone.

217 ith lower phase 2 success rates while taking buprenorphine-naloxone.

218 new practice of office-based treatment with buprenorphine-naloxone.

219 zed to extended-release naltrexone and 79 to buprenorphine-naloxone; 105 (66.0%) completed the trial.

220 signed to treatment with either methadone or buprenorphine/naloxone (Suboxone) over a 24-week open-la

221 NA-expressed P450s were incubated with 21 nM buprenorphine, norbuprenorphine formation was detected f

222 ss spectrometry method for quantification of buprenorphine, norbuprenorphine, and glucuronidated conj

223 d Nor-BNI, we demonstrate that the effect of buprenorphine on CCL2 signaling is opioid receptor media

224 monstrate dose-dependent, bimodal effects of buprenorphine on transmission at C-fiber synapses in rat

225 on-assisted withdrawal treatment with either buprenorphine or clonidine.

226 Outpatients (N=182) maintained on daily buprenorphine or methadone provided self-reports of stre

227 , such as medication-assisted treatment with buprenorphine or methadone.

228 Dispensing of a medication (buprenorphine or naltrexone) within 6 months of first re

229 ing care models include pharmacotherapy with buprenorphine or naltrexone, provider and community educ

230 inence syndrome to receive either sublingual buprenorphine or oral morphine.

231 There were no significant changes in buprenorphine or PI plasma levels and no significant cha

232 use were randomly assigned to receive either buprenorphine or placebo (in a 2:1 ratio), in addition t

233 ased by incubation with the alkaloid agonist buprenorphine or with either naltrexone or naloxone, str

234 Buprenorphine participants (28 [90.3%]) were significant

235 ipants were randomized to receive sublingual buprenorphine plus 4 placebo implants or sublingual plac

236 ch design affected the results of studies of buprenorphine plus behavioral treatment?

237 fit from adding a behavioral intervention to buprenorphine plus medical management, and four studies

238 ncreased the least rapidly when treated with buprenorphine plus placebo, while cocaine abstinence was

239 opioid agonist therapies (eg, methadone and buprenorphine) prevents blood-borne infections via reduc

240 ncreased caudate/putamen metabolism, whereas buprenorphine produced increased ventral striatum and mo

241 nalgesically active dose of 1500 mug.kg(-1), buprenorphine reduced the strength of spinal C-fiber syn

242 pioid substitution therapy with methadone or buprenorphine reduces mortality risk, especially for dru

243 We show that buprenorphine reduces the chemotactic phenotype of monoc

244 ycoprotein inhibitor, significantly enhanced buprenorphine-related effects on TI (p < .01) and TE (p

245 In P-glycoprotein-knockout mice, buprenorphine-related effects on VE (p < .01), TE (p < .

246 vivo and study its role in the modulation of buprenorphine-related respiratory effects in mice.

247 -glycoprotein plays a key-protective role in buprenorphine-related respiratory effects, by allowing n

248 phine withdrawal and subsequent methadone or buprenorphine replacement.

249 stinence syndrome, treatment with sublingual buprenorphine resulted in a shorter duration of treatmen

250 ceive adjunctive treatment with 2 mg/2 mg of buprenorphine/samidorphan (the 2/2 dosage group), 8 mg/8

251 dorphan (the 2/2 dosage group), 8 mg/8 mg of buprenorphine/samidorphan (the 8/8 dosage group), or pla

252 The buprenorphine/samidorphan combination is a novel and pro

253 Overall, the buprenorphine/samidorphan combinations were well tolerat

254 irst 4 weeks of opioid substitution therapy, buprenorphine seemed to reduce mortality in this period,

255 When possible, patients maintained on buprenorphine should be evaluated preoperatively to asse

256 predictor of treatment response, followed by buprenorphine stabilization dose.

257 Following a brief period of buprenorphine stabilization, 70 PO-dependent adults were

258 gorous experimental evaluation of outpatient buprenorphine stabilization, brief taper, and naltrexone

259 ine-assisted detoxification included a 7-day buprenorphine taper followed by a week-long delay before

260 7.4; post-taper mean, 2.8; P = .03), but not buprenorphine (taper mean, 6.4; post-taper mean, 7.4).

261 ested that all-cause mortality was lower for buprenorphine than methadone (1.66, 1.40-1.96).

262 s cocaine abstinence was increased more with buprenorphine than with methadone.

263 of treatment was significantly shorter with buprenorphine than with morphine (15 days vs. 28 days),

264 rials in the context of six questions: 1) Is buprenorphine that effective?

265 Buprenorphine, the partial mu-opioid receptor agonist an

266 abstinence with a stable dose of sublingual buprenorphine, the use of buprenorphine implants compare

267 not different from the acute application of buprenorphine to brain slices.

268 Patients who switched from buprenorphine to methadone during treatment had lower mo

269 ality difference was noted for switches from buprenorphine to methadone or for switches to either med

270 In contrast, in methadone- or buprenorphine-treated animals no respiratory depression

271 creased cingulate cortex metabolism, whereas buprenorphine-treated females showed decreased metabolis

272 Wales, Australia, who started a methadone or buprenorphine treatment episode from Aug 1, 2001, to Dec

273 In the buprenorphine treatment group, however, individuals with

274 the brief intervention group, and 114 to the buprenorphine treatment group.

275 We aimed to test whether buprenorphine treatment has a lower mortality risk than

276 The effectiveness of buprenorphine treatment of opioid dependence is limited

277 ounseling is a required part of office-based buprenorphine treatment of opioid use disorders, the nat

278 mong opioid-dependent patients, ED-initiated buprenorphine treatment vs brief intervention and referr

279 vative strategies for enhancing retention in buprenorphine treatment.

280 of behavioral interventions in office-based buprenorphine treatment.

281 Buprenorphine utilization generally exceeded norbuprenor

282 t-term use of very low dosages of sublingual buprenorphine was associated with decreased suicidal ide

283 Buprenorphine was associated with greater time to first

284 d more than 10-fold, from 3.0% in 2002 (when buprenorphine was introduced) to 31.8% in 2009, but decl

285 The inhibition of desensitization by buprenorphine was not the result of previous desensitiza

286 minated after 22 months of enrolment because buprenorphine was shown to have greater efficacy in an i

287 determination of clenbuterol, fentanyl, and buprenorphine was successfully achieved in human urine.

288 related opioids (morphine-6-glucuronide and buprenorphine) was blocked by JNK inhibition, but not by

289 Recently, norbuprenorphine, in contrast to buprenorphine, was shown in vitro to be a substrate of h

290 wn mu-opioid receptor (MOR) partial agonist, buprenorphine, was structurally elaborated to include an

291 With buprenorphine, we also recorded significantly greater ti

292 ts and 78 of 89 (87.6%) receiving sublingual buprenorphine were responders, an 8.8% difference (1-sid

293 eater percentage of adolescents who received buprenorphine were retained in treatment (72%) relative

294 r time when treated with methadone than with buprenorphine, whereas cocaine abstinence was increased

295 uman liver microsomes incubated with 5-82 nM buprenorphine, which encompasses the therapeutic plasma

296 g the risk for misuse and diversion of daily buprenorphine while retaining its therapeutic benefits.

297 Combining buprenorphine with behavioral interventions is significa

298 g that displays a similar binding profile to buprenorphine with improved affinity and efficacy at NOP

299 9% female), 90 were randomized to sublingual buprenorphine with placebo implants and 87 to buprenorph

300 that the mu-opioids morphine, etorphine, and buprenorphine would produce significant sex differences