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1 barrier to resistance are used (lamivudine, adefovir).
2 turning to baseline after discontinuation of adefovir.
3 ht loss (P<.001) were associated with use of adefovir.
4 associated with resistance to foscarnet and adefovir.
5 confirmed using an OAT1-specific substrate, adefovir.
6 fovir may be a more promising alternative to adefovir.
7 with pegylated interferon alfa (Peg-IFN) and adefovir.
8 tions conveying resistance to lamivudine and adefovir.
9 n effort to improve the therapeutic index of adefovir, 1-aryl-1,3-propanyl prodrugs were synthesized
10 compensated CHB (group A) were randomized to adefovir 10 mg daily (n = 46) or placebo (n = 49) for 52
11 fference in de novo rates: LAM 8% (5 of 62), adefovir 15% (5 of 33), tenofovir 0% (0 of 3), entecavir
12 malization at follow-up after treatment with adefovir (2 RCTs; 600 patients) and HBeAg loss with lami
13 ted for 48 weeks with either PEG-alfa-2a and adefovir (ADV) or either drug alone in the Hep-Net-Inter
14 proved for HBV therapy, lamivudine (LVD) and adefovir (ADV), in several ways: ETV is >100-fold more p
16 nged kidneys, compared to placebo treatment, adefovir, an EF inhibitor, decreased urine cAMP levels,
18 (mOat1), originally identified as NKT (e.g. adefovir and cidofovir), two (ddC and ddI) manifested si
19 tical role in the organ-specific toxicity of adefovir and cidofovir, and indicates that CHOh OAT cell
22 ,3-propanyl prodrugs enhance the delivery of adefovir and its metabolites to the liver, with pradefov
24 ss-resistance profiles of these variants for adefovir and lamivudine, two other antiviral agents that
31 P4 is involved in the luminal efflux of both adefovir and tenofovir, but it makes only a limited cont
32 nelfinavir together with delavirdine and/or adefovir and were followed for safety and antiretroviral
33 ucleoside or nucleotide analogs, lamivudine, adefovir, and entecavir, suppress HBV replication and ar
34 is is particularly true for tenofovir (TFV), adefovir, and other antiviral nucleosides that demonstra
35 e, probenecid-sensitive uptake of cidofovir, adefovir, and other nucleoside phosphonate antivirals.
38 ays a role in the etiology of cidofovir- and adefovir-associated nephrotoxicity, we attempted to iden
39 resistant HBV to lamivudine, penciclovir, or adefovir but instead enhanced viral replication efficien
42 the 50% effective concentration (EC(50)) for adefovir compared to the wild-type baseline isolate, whi
45 nhance liver levels of the active metabolite adefovir diphosphate (ADV-DP) and/or decrease kidney exp
46 lovir-associated mutations were sensitive to adefovir diphosphate (ADVDP) in in vitro enzymatic assay
48 s B virus (HBV), the inhibition constants of adefovir diphosphate and lamivudine triphosphate for wil
50 with famciclovir, also remained sensitive to adefovir diphosphate with the inhibition constant increa
51 However, these mutants remained sensitive to adefovir diphosphate with the inhibition constants incre
52 (3TCTP), emtricitabine triphosphate (FTCTP), adefovir diphosphate, penciclovir triphosphate, and lobu
53 A crystal structure of CyaA-calmodulin with adefovir diphosphate, the metabolite of an approved anti
54 ques, only 1 of the 24 subjects who received adefovir dipivoxil (125 mg/day) developed any genotypic
55 eived 48 weeks of TDF 300 mg (HVL n = 82) or adefovir dipivoxil (ADV) 10 mg (HVL n = 47), followed by
58 he efficacy, safety, and pharmacokinetics of adefovir dipivoxil (ADV) in children and adolescents wit
61 n has been reported in patients treated with adefovir dipivoxil (ADV); however, its incidence and cli
63 to receive either a single 120-mg/d dose of adefovir dipivoxil (n = 219) or an indistinguishable pla
65 treatment with lamivudine were randomized to adefovir dipivoxil 10 mg, lamivudine 100 mg, or addition
69 is study assessed the safety and efficacy of adefovir dipivoxil alone and in combination with lamivud
70 ith compensated liver disease, indicate that adefovir dipivoxil alone or in combination with ongoing
74 s enrolled in a phase I/II clinical trial of adefovir dipivoxil demonstrated that the K70E RT mutatio
75 B-infected patients treated daily with 30 mg adefovir dipivoxil for 12 weeks displayed a median 4.1-l
76 % of patients who entered clinical trials of adefovir dipivoxil for the treatment of lamivudine-resis
80 ment-related adverse effects associated with adefovir dipivoxil in this setting were primarily mild t
85 /mL in the adefovir dipivoxil/lamivudine and adefovir dipivoxil monotherapy groups, respectively (P <
88 randomly assigned in a 2:1 ratio to receive adefovir dipivoxil or placebo as a once-daily oral dose
95 evaluated the efficacy and safety of adding adefovir dipivoxil to lamivudine in 135 patients with ch
105 placebo-controlled, dose-escalation study of adefovir dipivoxil, an oral prodrug of adefovir, was con
106 (PMEApp), the active cellular metabolite of adefovir dipivoxil, inhibits the adenylyl cyclase activi
107 d adults evaluated once-daily treatment with adefovir dipivoxil, lamivudine, didanosine, and efaviren
108 ipients of adefovir dipivoxil/lamivudine and adefovir dipivoxil, respectively, compared with 1 of 19
114 ith -2.45 and -2.46 log(10) copies/mL in the adefovir dipivoxil/lamivudine and adefovir dipivoxil mon
115 of 19 (53%) and 9 of 18 (47%) recipients of adefovir dipivoxil/lamivudine and adefovir dipivoxil, re
116 ree patients receiving adefovir dipivoxil or adefovir dipivoxil/lamivudine and none receiving lamivud
117 d -4.04 log(10) copies/mL in the lamivudine, adefovir dipivoxil/lamivudine, and adefovir dipivoxil gr
118 el were seen by 4 weeks in all recipients of adefovir dipivoxil; DAVG(16) was -0.07 in the lamivudine
123 s with mutations resistant to lamivudine and adefovir have marked reduction in sensitivity to combina
124 ss the response to indinavir, efavirenz, and adefovir in human immunodeficiency virus (HIV)-infected
125 tribute to the accumulation of cidofovir and adefovir in renal proximal tubules and, thus, play an ac
126 ction of mono- and diphosphorylated forms of adefovir in the kidney between wild-type and Mrp4 knocko
127 on demonstrated their full susceptibility to adefovir in vitro, and HBV with the rtI233V mutation dev
129 drugs (zidovudine, stavudine, tenofovir, and adefovir) increased when M184V was present, whereas susc
132 The affinity of hOAT1 toward cidofovir and adefovir (K(m) = 46 and 30 microM, respectively) was 5-
133 ressed hOATI mediated efficient transport of adefovir (Km, = 23.8 tLM, V, a,, = 46.0 pmol/106 cells m
134 i-drug resistant HBV mutations to lamivudine+adefovir, lamivudine+hepatitis B immunoglobulin (HBIG),
136 observed susceptibility of these mutants to adefovir, lobucavir, and penciclovir in vitro and adefov
137 was unsuccessfully treated with interferon, adefovir monotherapy and adefovir plus entecavir combina
138 n of adefovir and lamivudine is preferred to adefovir monotherapy for lamivudine-refractory hepatitis
141 n monotherapy, 3) lamivudine monotherapy, 4) adefovir monotherapy, or 5) lamivudine with crossover to
143 hts the impact of exposure to lamivudine and adefovir on development of drug resistance and cross-res
144 However, a hybrid salvage strategy reserving adefovir only for lamivudine-associated viral resistance
145 rom patients who had developed resistance to adefovir or lamivudine, as demonstrated by development o
146 ir or nelfinavir, together with delavirdine, adefovir, or both, in indinavir-experienced persons.
150 )adenine (bis-POM PMEA)], an oral prodrug of adefovir (PMEA), is currently in phase III clinical test
153 eously detect the presence of lamivudine and adefovir resistance mutations in clinical samples, has a
156 (in 2 samples) and S202G (in 1 sample), the adefovir-resistance mutation N236T (in 1 sample), and th
157 N236T (in 1 sample), and the lamivudine and adefovir-resistance mutations V173L, L180M, A181T, and M
158 ted excellent anti-HBV activity against both adefovir-resistant and lamivudine-resistant double (rtL1
159 We used UDPS to analyze the dynamics of adefovir-resistant HBV variants in patients with chronic
160 be added to lamivudine to reduce the risk of adefovir-resistant mutations; however, tenofovir may be
162 t before treatment, and that the dynamics of adefovir-resistant populations are much more complex and
165 cidofovir, oral and intraocular ganciclovir, adefovir, respiratory syncytial virus immune globulin, p
168 udine resistant hepatitis B virus infection, adefovir should be added to lamivudine to reduce the ris
169 The long-term studies of lamivudine (and adefovir) show a consistent reduction in the development
170 howed statistically significant increases in adefovir susceptibility of 3- to 4-fold (to near wild ty
171 ients showed no change or minor decreases in adefovir susceptibility, consistent with the durable ant
172 the licensing of lamivudine and subsequently adefovir, the treatment paradigm shifted from 4 to 6 mon
176 otherapy, or 5) lamivudine with crossover to adefovir upon resistance ("adefovir salvage" strategy).
177 n with two other drugs from the same family (adefovir, used to treat hepatitis B, and cidofovir, used
181 dy of adefovir dipivoxil, an oral prodrug of adefovir, was conducted in 36 human immunodeficiency vir
182 substitutions known to confer resistance to adefovir were detected at baseline in most patients.
183 nd cytarabine as well as the phosphonic acid adefovir were shown to cleave following exposure to live
184 sensitivity to combination of lamivudine and adefovir, whereas constructs with mutations resistant to
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