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1 lity disorder did not affect the response to buprenorphine.
2 lation after CCL2 treatment was inhibited by buprenorphine.
3 ization, suggesting a mechanism of action of buprenorphine.
4 the hyperalgesia elicited by ultra-low-dose buprenorphine.
5 ritonavir or fosamprenavir-ritonavir but not buprenorphine.
6 renavir-ritonavir induced glucuronidation of buprenorphine.
7 brain slices to characterize the actions of buprenorphine.
8 ication for opioid use disorder will soon be buprenorphine.
9 ects of BU08028 (0.001-0.01 mg/kg, i.m.) and buprenorphine (0.003-0.056 mg/kg, i.m.), the drugs were
11 In contrast, a 15,000-fold lower dose of buprenorphine (0.1 mug.kg(-1)), which caused thermal and
12 ine (8 [22.2%]), tramadol ER (7 [19.4%]), or buprenorphine (3 [9.7%]) groups did not differ significa
13 ed concentrations of the inactive metabolite buprenorphine-3-glucuronide suggested that darunavir-rit
15 norbuprenorphine is a high efficacy agonist, buprenorphine a low efficacy agonist, and diprenorphine
16 r OUD are methadone (a full opioid agonist), buprenorphine (a partial agonist), and naltrexone (an op
18 his study examined drug interactions between buprenorphine, a partial opioid agonist used for opioid
19 bers did not offer new appointments or rapid buprenorphine access to callers reporting active heroin
22 (MOP) receptor agonist buprenorphine and the buprenorphine analog (2S)-2-[(5R,6R,7R,14S)-N-cyclopropy
24 rding to treatment group (with 58 exposed to buprenorphine and 73 exposed to methadone) showed that t
25 files to characterize changes in coverage of buprenorphine and buprenorphine-naloxone for opioid use
26 ustments are not likely to be necessary when buprenorphine and darunavir-ritonavir or fosamprenavir-r
28 ervations show the unique characteristics of buprenorphine and further demonstrate the range of agoni
31 n this period, but little difference between buprenorphine and methadone was noted thereafter or for
32 osing, randomized, controlled study in which buprenorphine and methadone were compared for use in the
34 ever, here we show that mice pretreated with buprenorphine and morphine do not die from clostridial m
35 fy time trends and disparities in receipt of buprenorphine and naltrexone among youth with OUD in the
40 bstinence during weeks 5-6 were continued on buprenorphine and randomly assigned to receive clonidine
41 the mu opioid peptide (MOP) receptor agonist buprenorphine and the buprenorphine analog (2S)-2-[(5R,6
43 ists, (eg, methadone), partial agonists (eg, buprenorphine), and alpha2-adrenergic receptor agonists
44 luoroethyl-diprenorphine, [(18)F]fluoroethyl-buprenorphine, and [(18)F]fluoroethyl-phenethyl-orvinol
45 n of a mu- and kappa-opioid partial agonist, buprenorphine, and a mu-opioid antagonist, samidorphan,
47 pioid use disorder, which include methadone, buprenorphine, and extended-release naltrexone, signific
49 s with opioid use disorder from methadone to buprenorphine, and tapering opioids in patients with chr
50 ntagonist diprenorphine, the partial agonist buprenorphine, and the full agonist phenethyl-orvinol.
55 and safety of very low dosages of sublingual buprenorphine as a time-limited treatment for severe sui
56 These results are consistent with the use of buprenorphine as an acceptable treatment for opioid depe
58 ioid-dependent pregnant women have suggested buprenorphine as an alternative treatment to methadone d
61 imens, naltrexone-assisted detoxification or buprenorphine-assisted detoxification, followed by an in
62 , including interdisciplinary pain programs, buprenorphine-assisted dose reduction, and behavioral in
63 opioid agonist treatments (eg, methadone vs buprenorphine) associated with differences in efficacy f
64 ns that lead to P-glycoprotein inhibition in buprenorphine-associated fatalities and respiratory depr
65 ceptor transmembrane domains showed that the buprenorphine-bound receptor occupied a distinct set of
66 entified potential antidepressant effects of buprenorphine (BPN), a drug with high affinity for mu op
68 combination of a mu-opioid partial agonist, buprenorphine (BUP), and a potent mu-opioid antagonist,
69 d use disorder that enhances the benefits of buprenorphine by delivering sustained, optimal exposure,
72 y Behavior study demonstrates high uptake of buprenorphine collocated with HCV treatment, and it show
73 ded adults (18-64 years of age) who received buprenorphine continuously for >=180 days by cohorts ret
75 ial agonist, subsaturating concentrations of buprenorphine decreased the [Met](5)enkephalin (ME)-indu
78 the ability of a novel, weekly, subcutaneous buprenorphine depot formulation, CAM2038, to block eupho
79 ific to C. perfringens-mediated myonecrosis; buprenorphine did not protect against disease caused by
80 implants compared with continued sublingual buprenorphine did not result in an inferior likelihood o
81 service use and overdose were high following buprenorphine discontinuation irrespective of treatment
85 is shown that a phenyl ring analogue (1d) of buprenorphine displays the desired profile in vitro with
86 e naltrexone, in conjunction with single-day buprenorphine dosing and adjunctive nonopioid medication
89 n lasted 7 days and included a single day of buprenorphine followed by ascending doses of oral naltre
91 Outpatients were prescribed daily sublingual buprenorphine for 6 months or more, were abstinent while
93 nt while taking 8 mg/d or less of sublingual buprenorphine for 90 days or longer, and were determined
94 ysician assistants with waivers to prescribe buprenorphine for treating opioid use disorder and assoc
95 acy and safety of longer-term treatment with buprenorphine for young individuals with opioid dependen
98 Seventy-eight percent of patients in the buprenorphine group (89 of 114 [95% CI, 70%-85%]) vs 37%
101 and from stabilization to post taper in the buprenorphine group (stabilization mean, 0.46 [SE, .05]
102 n adverse events: 61 patients (56.5%) in the buprenorphine group and 29 (52.7%) in the placebo group.
103 administered in 5 of 33 infants (15%) in the buprenorphine group and in 7 of 30 infants (23%) in the
106 norphine(>/= 1 mg/kg) and to a lesser extent buprenorphine (>/= 10 mg/kg) were responsible for dose-d
108 ared to methadone-treated subjects, those on buprenorphine had significantly lower rates of metabolic
109 ered oxycodone, fentanyl, or heroin, but not buprenorphine had similar profiles of escalation and inc
111 rm opioid agonist therapy with methadone and buprenorphine have great efficacy for OUD treatment and
112 rats were injected with either the analgesic buprenorphine-HCl or saline every 12 hrs; injections wer
113 uration, but the group that was treated with buprenorphine-HCl showed no significant difference compa
115 plants or sublingual placebo plus four 80-mg buprenorphine hydrochloride implants (expected efficacy,
116 oxification) from opioids using clonidine or buprenorphine hydrochloride is a widely used treatment.
117 ase naltrexone will be as effective as daily buprenorphine hydrochloride with naloxone hydrochloride
118 erse events occurred in 48.3% and 23% of the buprenorphine implant group and in 52.8% and 13.5% of pa
120 naloxone tablets, patients received either 4 buprenorphine implants (80 mg per implant) or 4 placebo
122 One hundred eight were randomized to receive buprenorphine implants and 55 to receive placebo implant
123 Over 6 months, 72 of 84 (85.7%) receiving buprenorphine implants and 64 of 89 (71.9%) receiving su
125 dose of sublingual buprenorphine, the use of buprenorphine implants compared with continued sublingua
126 g persons with opioid dependence, the use of buprenorphine implants compared with placebo resulted in
127 l of 71 of 108 patients (65.7%) who received buprenorphine implants completed the study vs 17 of 55 (
129 uprenorphine with placebo implants and 87 to buprenorphine implants with sublingual placebo; 165 of 1
130 ly a handful of EECA countries (methadone or buprenorphine in five countries and needle and syringe p
131 lower than that of cocaine, remifentanil, or buprenorphine in monkeys responding under a progressive-
134 ials of naloxone, naltrexone, nalmefene, and buprenorphine in patients with schizophrenia to determin
135 CAM2038 produces a rapid initial rise of buprenorphine in plasma with maximum concentration aroun
136 f-administration of oxycodone, fentanyl, and buprenorphine in rats allowed long access sessions (12 h
137 e effective than clonidine and comparable to buprenorphine in reducing opioid withdrawal symptoms dur
139 ent article describes aryl ring analogues of buprenorphine in which the standard C20-methyl group has
141 ian wait time from first contact to possible buprenorphine induction was 8 days (IQR, 4 to 15 days) f
142 ify additional potential mechanisms by which buprenorphine inhibits CCL2-induced monocyte migration,
150 ioid agonist therapies such as methadone and buprenorphine is available in prisons in only a handful
151 adverse events compared with other opioids, buprenorphine is considered a safe option for pain and s
155 000, referred to as BUP-XR (extended-release buprenorphine), is a subcutaneously injected, monthly bu
156 o an interest in developing compounds with a buprenorphine-like pharmacological profile but with lowe
158 ts and 64 of 89 (71.9%) receiving sublingual buprenorphine maintained opioid abstinence (hazard ratio
159 nd adverse effects were compared between the buprenorphine-maintained participants and an equal numbe
160 agonist therapy (OAT), such as methadone or buprenorphine maintenance therapy, to optimise HIV outco
168 at understanding the distinctive features of buprenorphine metabolic effects vis-a-vis those of metha
169 ared 4 MOUD treatment strategies: methadone, buprenorphine, methadone taper for detoxification, and n
170 Maintenance treatment with opioid agonists (buprenorphine, methadone) is effective for opioid addict
171 clonidine (n = 36), tramadol ER (n = 36), or buprenorphine (n = 31) was then instituted, and patients
172 the Sweet Taste Test (STT) were measured in buprenorphine- (n = 26) or methadone (n = 32)- treated s
173 the barriers encountered by patients seeking buprenorphine-naloxone ("buprenorphine") treatment.
175 R-NTX), an opioid antagonist, and sublingual buprenorphine-naloxone (BUP-NX), a partial opioid agonis
177 ize changes in coverage of buprenorphine and buprenorphine-naloxone for opioid use disorder in 2007,
178 ease naltrexone group was noninferior to the buprenorphine-naloxone group (difference, -0.1; with 95%
179 weeks 1 through 12, patients in the 12-week buprenorphine-naloxone group reported less opioid use (c
180 ended-release naltrexone was as effective as buprenorphine-naloxone in maintaining short-term abstine
182 -release naltrexone showed noninferiority to buprenorphine-naloxone on group proportion of total numb
184 dence interval [CI] = 47%-75%) vs 58 12-week buprenorphine-naloxone patients (26%; 95% CI = 14%-38%).
185 Brief treatment (phase 1) included 2-week buprenorphine-naloxone stabilization, 2-week taper, and
186 rmes) and BUP-NX was daily self-administered buprenorphine-naloxone sublingual film (Suboxone; Indivi
189 Success rates 8 weeks after completing the buprenorphine-naloxone taper (phase 2, week 24) dropped
190 ase 2 outcomes were more common while taking buprenorphine-naloxone than 8 weeks after taper (49.2% [
191 to-pay threshold of $100 000 per QALY showed buprenorphine-naloxone to be preferable to extended-rele
192 ccessful outcomes in phase 2 during extended buprenorphine-naloxone treatment (week 12), with no diff
194 patients entered phase 2: extended (12-week) buprenorphine-naloxone treatment, 4-week taper, and 8-we
195 are most likely to reduce opioid use during buprenorphine-naloxone treatment; if tapered off bupreno
197 he availability of opioid agonist treatment (buprenorphine-naloxone) and nonpharmacologic therapies (
198 altrexone), agonist-antagonist combinations (buprenorphine-naloxone), or neither agonists nor antagon
199 omization to either daily oral flexible dose buprenorphine-naloxone, 4 to 24 mg/d, or extended-releas
200 enorphine-naloxone treatment; if tapered off buprenorphine-naloxone, even after 12 weeks of treatment
201 or excess were compared in opioid-dependent, buprenorphine-naloxone-maintained, human immunodeficienc
204 zed to extended-release naltrexone and 79 to buprenorphine-naloxone; 105 (66.0%) completed the trial.
205 signed to treatment with either methadone or buprenorphine/naloxone (Suboxone) over a 24-week open-la
206 d Nor-BNI, we demonstrate that the effect of buprenorphine on CCL2 signaling is opioid receptor media
207 monstrate dose-dependent, bimodal effects of buprenorphine on transmission at C-fiber synapses in rat
208 Outpatients (N=182) maintained on daily buprenorphine or methadone provided self-reports of stre
212 ing care models include pharmacotherapy with buprenorphine or naltrexone, provider and community educ
215 use were randomly assigned to receive either buprenorphine or placebo (in a 2:1 ratio), in addition t
217 We then implanted osmotic pumps containing buprenorphine or TRV130 (0, 3, 6, or 9 mg/kg/day) and pe
218 ased by incubation with the alkaloid agonist buprenorphine or with either naltrexone or naloxone, str
219 nalysis, use of MOUD maintenance with either buprenorphine (OR = 0.38; 95% CI, .17-.85) or methadone
222 ipants were randomized to receive sublingual buprenorphine plus 4 placebo implants or sublingual plac
224 fit from adding a behavioral intervention to buprenorphine plus medical management, and four studies
225 tment centers only and that do not encompass buprenorphine prescribed in ambulatory care settings, pr
228 dministration temporarily relaxed outpatient buprenorphine prescribing regulations in March 2020 in r
230 Rates of new appointments offered, whether buprenorphine prescription was possible at the first vis
231 on database to compare between the number of buprenorphine prescriptions filled and the number of US
232 opioid agonist therapies (eg, methadone and buprenorphine) prevents blood-borne infections via reduc
233 ncreased caudate/putamen metabolism, whereas buprenorphine produced increased ventral striatum and mo
234 rt D plans requiring prior authorization for buprenorphine products before and after a 2017 FDA rquir
235 -XR safety profile was consistent with other buprenorphine products for treatment of opioid use disor
237 nalgesically active dose of 1500 mug.kg(-1), buprenorphine reduced the strength of spinal C-fiber syn
238 pioid substitution therapy with methadone or buprenorphine reduces mortality risk, especially for dru
240 ycoprotein inhibitor, significantly enhanced buprenorphine-related effects on TI (p < .01) and TE (p
243 -glycoprotein plays a key-protective role in buprenorphine-related respiratory effects, by allowing n
246 stinence syndrome, treatment with sublingual buprenorphine resulted in a shorter duration of treatmen
249 ceive adjunctive treatment with 2 mg/2 mg of buprenorphine/samidorphan (the 2/2 dosage group), 8 mg/8
250 dorphan (the 2/2 dosage group), 8 mg/8 mg of buprenorphine/samidorphan (the 8/8 dosage group), or pla
253 irst 4 weeks of opioid substitution therapy, buprenorphine seemed to reduce mortality in this period,
257 gorous experimental evaluation of outpatient buprenorphine stabilization, brief taper, and naltrexone
258 ine-assisted detoxification included a 7-day buprenorphine taper followed by a week-long delay before
259 7.4; post-taper mean, 2.8; P = .03), but not buprenorphine (taper mean, 6.4; post-taper mean, 7.4).
261 of treatment was significantly shorter with buprenorphine than with morphine (15 days vs. 28 days),
263 abstinence with a stable dose of sublingual buprenorphine, the use of buprenorphine implants compare
266 ality difference was noted for switches from buprenorphine to methadone or for switches to either med
268 creased cingulate cortex metabolism, whereas buprenorphine-treated females showed decreased metabolis
269 Wales, Australia, who started a methadone or buprenorphine treatment episode from Aug 1, 2001, to Dec
273 atient parenteral antimicrobial therapy with buprenorphine treatment had similar clinical and drug us
276 ounseling is a required part of office-based buprenorphine treatment of opioid use disorders, the nat
278 is, there is an urgent need for expansion of buprenorphine treatment research to provide critical inf
279 mong opioid-dependent patients, ED-initiated buprenorphine treatment vs brief intervention and referr
280 earch to date shows the successful impact of buprenorphine treatment, including the pharmacogenomics
285 t-term use of very low dosages of sublingual buprenorphine was associated with decreased suicidal ide
286 d more than 10-fold, from 3.0% in 2002 (when buprenorphine was introduced) to 31.8% in 2009, but decl
288 minated after 22 months of enrolment because buprenorphine was shown to have greater efficacy in an i
289 determination of clenbuterol, fentanyl, and buprenorphine was successfully achieved in human urine.
290 related opioids (morphine-6-glucuronide and buprenorphine) was blocked by JNK inhibition, but not by
291 Recently, norbuprenorphine, in contrast to buprenorphine, was shown in vitro to be a substrate of h
292 wn mu-opioid receptor (MOR) partial agonist, buprenorphine, was structurally elaborated to include an
294 oid substitution treatment with methadone or buprenorphine were 0.93 (0.76-1.10) and 1.79 (1.47-2.10)
295 ng chronic treatment, effects of BU08028 and buprenorphine were maintained for several weeks without
296 ts and 78 of 89 (87.6%) receiving sublingual buprenorphine were responders, an 8.8% difference (1-sid
298 g the risk for misuse and diversion of daily buprenorphine while retaining its therapeutic benefits.
299 g that displays a similar binding profile to buprenorphine with improved affinity and efficacy at NOP
300 9% female), 90 were randomized to sublingual buprenorphine with placebo implants and 87 to buprenorph