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1 iple mutant (V32I/I47V/V82I) in complex with amprenavir.
2 R that constitute points of interaction with amprenavir.
3 chemically related to the clinical inhibitor amprenavir.
4 ied the N88S mutation were hypersensitive to amprenavir.
5 has been studied with the clinical inhibitor amprenavir (1) and two potent antiviral investigational
6  and >/=5000 HIV RNA copies/mL were assigned amprenavir (1200 mg) alone or with zidovudine (300 mg) p
7              Female mice given ritonavir and amprenavir (23 and 10 microg/mouse/day, respectively) de
8          In the present study, we identified amprenavir, a widely used HIV PI, as a potent PXR-select
9 twice per day (n = 157); in combination with amprenavir, abacavir, efavirenz, and adefovir dipivoxil.
10                                              Amprenavir (Agenerase, 141-W94, VX-478) is a human immun
11                                              Amprenavir alone suppressed HIV-1 RNA levels to <400 cop
12                     Thirty men, 19 receiving amprenavir and 11 receiving amprenavir, zidovudine, and
13 ype HIV-1 and HIV-2 proteases complexed with amprenavir and darunavir to models of the PRDelta4 enzym
14  of HIV-1 and HIV-2 proteases complexed with amprenavir and darunavir.
15                                              Amprenavir and indinavir did not affect adipogenesis or
16 ivariate models, except for small effects of amprenavir and lopinavir.
17  the greatest for ritonavir, nelfinavir, and amprenavir and lowest for indinavir.
18 ation calorimetry of 40 nM for 3, 178 nM for amprenavir, and 960 nM for 2.
19                         However, saquinavir, amprenavir, and indinavir blood levels are increased sub
20 ndinavir, nelfinavir, saquinavir, ritonavir, amprenavir, and lopinavir.
21 loney murine leukemia virus was inhibited by amprenavir, and the Envs were solubilized in Triton X-10
22 e I50V substitution is often associated with amprenavir (APV) and darunavir (DRV) resistance, while t
23                       The protease inhibitor amprenavir (APV) generates a signature set of HIV type 1
24 n of zidovudine (ZDV), lamivudine (3TC), and amprenavir (APV), given alone and in combination with th
25               Although chemically similar to amprenavir (APV), the potency of TMC114 is substantially
26 concentrations of atazanavir, lopinavir, and amprenavir (APV).
27 inavir, ritonavir, indinavir, nelfinavir, or amprenavir at concentrations >200-fold the IC(50)s for W
28   In this study, most subjects who had taken amprenavir-based regimens and who changed to a 4-drug re
29            Subjects who had previously taken amprenavir combination therapy were more likely to exper
30 XN structure of the wild-type HIV-1 protease-amprenavir complex suggests that the three mutations do
31 subjects were enrolled and were changed from amprenavir-containing regimens to the 4-drug regimen.
32 on data to Morrison's equation, Ki values of amprenavir, darunavir, and tipranavir were determined to
33             In contrast, lopinavir (LPV) and amprenavir did not increase osteoclast activity.
34                                              Amprenavir efficiently activated PXR and induced PXR tar
35 150 mg lamivudine, each given twice daily in amprenavir-experienced subjects.
36 rotease inhibitors (PIs) administered and on amprenavir/fosamprenavir treatment.
37 f the protease in complex with clinical drug amprenavir has been determined at 2.0 A resolution.
38  infected antiretrovirally treated patients, amprenavir HS has been associated with the mutation N88S
39 presence of the N88S mutation and associated amprenavir hypersensitivity may be useful in predicting
40 irmed the causal role of N88S in determining amprenavir hypersensitivity.
41  occurring in some of these subjects induces amprenavir hypersusceptibility and a reduction of fitnes
42 ut changing Gag-processing efficiency, while amprenavir hypersusceptibility was further diminished.
43 n addition, these mutations partially ablate amprenavir hypersusceptibility.
44   The Kd value for the competitive inhibitor amprenavir increased 12-fold over this concentration ran
45 /I84V/L90M, G48V, and L90M with three drugs, amprenavir, indinavir, and saquinavir, yield good agreem
46 atment with lopinavir and ritonavir, but not amprenavir, induced ER stress, as indicated by a decreas
47                   The HIV protease inhibitor amprenavir inhibits calpain activity and is also effecti
48                                              Amprenavir is a human immunodeficiency virus (HIV) prote
49                        One potential use for amprenavir is as salvage therapy for patients for whom t
50 nts selected against the following four PIs: amprenavir, JE-2147, KNI-272, and UIC-94003.
51                                              Amprenavir lacks interactions due to PR20 mutations in t
52                                  Three drugs-amprenavir, levomefolic acid, and calcipotriol-were pred
53                   For three P-gp substrates (amprenavir, loperamide, and quinidine), we have successf
54                                              Amprenavir-mediated PXR activation stimulated the expres
55 e virologic failure than those who had taken amprenavir monotherapy (odds ratio, 7.7; P=.0012).
56 nterim review resulted in termination of the amprenavir monotherapy arm.
57 evels of HIV RNA significantly more than did amprenavir monotherapy.
58 e subsequently tested and three of the five (amprenavir, nelfinavir, and saquinavir but not ritonavir
59            The HIV protease inhibitors (HPI) amprenavir, nelfinavir, and saquinavir have previously b
60 ons associated with high-level resistance to amprenavir, nelfinavir, indinavir, ritonavir, saquinavir
61         We evaluated the cross-resistance to amprenavir of viruses that evolved during treatment with
62               In addition, in vivo, doses of amprenavir or nelfinavir comparable with the therapeutic
63 combined dual-PI arms was higher than in the amprenavir-plus-placebo arm (35% [112/324] vs 23% [36/15
64 I50V revealed specific resistance to ATV and amprenavir, respectively, with no evidence of cross-resi
65 avir, saquinavir, nelfinavir, ritonavir, and amprenavir, respectively.
66 indinavir-ritonavir and, to a lesser extent, amprenavir-ritonavir may be effective for many patients
67  predicting an improved clinical response to amprenavir salvage therapy.
68               We applied this strategy to an Amprenavir sample incubated with human liver microsomes.
69 ng the PIs evaluated (nelfinavir, ritonavir, amprenavir, saquinavir, and indinavir), only nelfinavir
70 lysis with ritonavir, indinavir, nelfinavir, amprenavir, saquinavir, lopinavir, and atazanavir reveal
71                These models suggest that the amprenavir sensitivity of PRDelta4 is attributable to st
72                       Short-term exposure to amprenavir significantly increased plasma total choleste
73 t model, where, in the absence of androgens, amprenavir significantly reduces tumor growth.
74 G, and produced the virus in the presence of amprenavir to also inhibit the R-peptide cleavage.
75          In the current work, the binding of amprenavir to both of the wild-type and the drug-resista
76                          These indinavir and amprenavir troughs exceed IC(95) for most protease inhib
77 rate constant for association of enzyme with amprenavir was independent of NaCl concentration, wherea
78 only used HIV PIs (lopinavir, ritonavir, and amprenavir) were used; their effects on ER stress activa
79 ion for darunavir and the chemically related amprenavir, while saquinavir showed competitive inhibiti
80 a calculations to analyze the association of amprenavir with HIV protease.
81                               Treatment with amprenavir, zidovudine, and lamivudine together reduced
82 en, 19 receiving amprenavir and 11 receiving amprenavir, zidovudine, and lamivudine, donated blood an