ライフサイエンスコーパス: darunavir

1 z, lopinavir plus ritonavir, atazanavir, and darunavir).

2 nd 242 assigned to receive ritonavir-boosted darunavir).

3 contacts with PR than the bis-THF moiety of darunavir.

4 bserved for atazanavir and lopinavir but not darunavir.

5 binding affinity of 41 +/- 1 nM measured for darunavir.

6 lutegravir was superior to ritonavir-boosted darunavir.

7 in lipids observed with either atazanavir or darunavir.

8 se rate than is once-daily ritonavir-boosted darunavir.

9 tively, at the C4 position of the bis-THF of darunavir.

10 IV-2 proteases complexed with amprenavir and darunavir.

11 protease inhibitors, such as atazanavir and darunavir.

12 actions with the protein backbone similar to darunavir (1) or inhibitor 2.

13 eive either dolutegravir 50 mg once daily or darunavir 800 mg plus ritonavir 100 mg once daily, with

14 omly assigned (1:1) to dolutegravir 50 mg or darunavir 800 mg plus ritonavir 100 mg, with investigato

15 consisted of a fixed-dose tablet containing darunavir 800 mg, cobicistat 150 mg, emtricitabine 200 m

16 All subjects received darunavir 800 mg, ritonavir 100 mg, and emtricitabine 20

17 NRS143) assessing the efficacy and safety of darunavir (800 mg once per day) and ritonavir (100 mg on

18 ); we recommended ritonavir (100 mg)-boosted darunavir (800 mg) once daily or ritonavir (100 mg)-boos

19 00 mg/d; raltegravir, 400 mg twice daily; or darunavir, 800 mg/d, with ritonavir, 100 mg/d, plus comb

20 Darunavir, a potent antiviral drug, showed an unusual se

21 ver, drugs aliskiren (a renin inhibitor) and darunavir (an HIV-1 PR inhibitor) showed high affinity f

22 A series of darunavir analogues featuring a substituted bis-THF ring

23 h 400 mg raltegravir twice daily plus 800 mg darunavir and 100 mg ritonavir once daily (NtRTI-sparing

24 xed-dose combination once daily, plus 800 mg darunavir and 100 mg ritonavir once daily (standard regi

25 nt with the observed second binding site for darunavir and helps to explain its antiviral potency.

26 ., 5 pM to 40 nM) in the binding affinity of darunavir and saquinavir to mature multidrug resistant p

27 ong nine clinical protease inhibitors (PIs), darunavir and saquinavir were the most effective in inhi

28 ype competitive-uncompetitive inhibition for darunavir and the chemically related amprenavir, while s

29 ciency virus type 1) protease (PR) inhibitor darunavir and the chemically related GRL98065 and GRL065

30 served, all 45 sequences were susceptible to darunavir and tipranavir, whereas 47% showed resistance

31 Twice-daily darunavir, once-daily darunavir, and efavirenz had the highest CSF 95% inhibit

32 The HIV-1 PIs assessed included atazanavir, darunavir, and lopinavir (administered with ritonavir).

33 lly useful susceptibility only to lopinavir, darunavir, and saquinavir.

34 orrison's equation, Ki values of amprenavir, darunavir, and tipranavir were determined to be 135, 10,

35 However, all HIV-PIs, including darunavir, are generally administered with ritonavir, an

36 69 ng/mL and 74 ng/mL in the atazanavir and darunavir arms, respectively) and were not associated wi

37 rs, currently receiving boosted lopinavir or darunavir as monotherapy (n = 67) or triple antiretrovir

38 isolate showed low-level cross-resistance to darunavir, atazanavir, lopinavir, and saquinavir, but no

39 how the safety and efficacy of single-tablet darunavir, cobicistat, emtricitabine, and tenofovir alaf

40 y of switching to a single-tablet regimen of darunavir, cobicistat, emtricitabine, and tenofovir alaf

41 observed in the hydrophobic contacts for the darunavir complexes, in agreement with relative inhibiti

42 lative to wild type enzyme than reported for darunavir complexes.

43 We found that darunavir does not inhibit the biochemical activity of Z

44 aily, lopinavir (LPV) 400 mg twice daily, or darunavir (DRV) 600 mg twice daily, each with ritonavir

45 Elvitegravir (EVG), RPV, and darunavir (DRV) concentrations were quantified by the li

46 Darunavir (DRV) inhibits the replication of most existin

47 Darunavir (DRV) is the most potent of these inhibitors,

48 trols, coadministration of OBV/PTV/r + DSV + darunavir (DRV) lowered DRV trough concentration (Ctroug

49 s often associated with amprenavir (APV) and darunavir (DRV) resistance, while the I50L substitution

50 Importantly, darunavir (DRV) was >1,000 times less active against a h

51 tion), PR(I54V), and PR(I54M) complexed with darunavir (DRV) were determined at resolutions of 1.05-1

52 crystal structures of PR(D25N) complexed to darunavir (DRV), a potent clinical inhibitor, or a non-h

53 the HIV-1 PR inhibitors lopinavir (LPV) and darunavir (DRV), as well as to the broad-based inhibitor

54 re against the PR inhibitor lopinavir (LPV), darunavir (DRV), or TL-3.

55 5-7 degrees C in the presence of inhibitors darunavir (DRV), saquinavir (SQV), and lopinavir (LPV),

56 it also has weaker affinity for both NFV and darunavir (DRV).

57 en associated with reduced susceptibility to darunavir (DRV).

58 TI-R virus, they change to ritonavir-boosted darunavir (DRV/r)-based ART.

59 74.7%; 95% CI, 41.4%-100%; TDF+FTC+ boosted darunavir [DRV/r], 93.9%; 95% CI, 90.2%-97.7%) and lowes

60 bi), rilpivirine (RPV), or ritonavir-boosted darunavir (DRVrtv).

61 scontinuation of atazanavir, raltegravir, or darunavir for toxicity.

62 nd 164 (68%) of 242 in the ritonavir-boosted darunavir group had HIV-1 RNA less than 50 copies per mL

63 The chemically related darunavir had similar relative inhibition, except for PR

64 Overall, inhibitor 3 compares favorably with darunavir in affinity for PR20 and shows promise for fur

65 he two new compounds are more effective than darunavir in inhibiting mature PR20 and show promise for

66 hether a new and chemically distinct HIV-PI, darunavir, inhibits ZMPSTE24.

67 This property of darunavir is potentially attractive.

68 TMC114 (darunavir) is a promising clinical inhibitor of HIV-1 pr

69 the hydroxy group of the bound clinical drug darunavir, located in the catalytic site of enzyme HIV-1

70 suggests that canagliflozin, aliskiren, and darunavir may induce profound effects toward dual HIV-1

71 ions, and the mutation profiles suggest that darunavir might be the drug of choice for third-line reg

72 rate than did those taking ritonavir-boosted darunavir once daily, with similar tolerability.

73 Twice-daily darunavir, once-daily darunavir, and efavirenz had the h

74 ilpivirine) or a boosted protease inhibitor (darunavir or atazanavir).

75 previr had no clinically relevant effects on darunavir or tenofovir PK (15% and 22% AUC increase, res

76 ir-boosted protease inhibitor (atazanavir or darunavir), or an integrase strand transfer inhibitor (r

77 andomized to ritonavir-boosted atazanavir or darunavir, or raltegravir-based cART.

78 Patients being treated with darunavir, or who had homozygous familial hypercholester

79 r dolutegravir (four [2%] patients) than for darunavir plus ritonavir (ten [4%] patients) and contrib

80 diarrhoea (dolutegravir 41 [17%] patients vs darunavir plus ritonavir 70 [29%] patients), nausea (39

81 the dolutegravir group and 13 (four) in the darunavir plus ritonavir group discontinued because of a

82 he dolutegravir group vs 57/242 [24%] in the darunavir plus ritonavir group), nausea (31/242 [13%] vs

83 olutegravir and 200 (83%) patients receiving darunavir plus ritonavir had HIV-1 RNA of less than 50 c

84 In FLAMINGO, we compared dolutegravir with darunavir plus ritonavir in individuals naive for antire

85 aily dolutegravir was superior to once-daily darunavir plus ritonavir.

86 vourably in efficacy and safety to a boosted darunavir regimen with nucleoside reverse transcriptase

87 %) had previous virological failure on a non-darunavir regimen.

88 ration of atazanavir (300 mg once daily) and darunavir regimens exhibited no clinically meaningful dr

89 with a history of virological failure on non-darunavir regimens were allowed.

90 e coadministered with morning atazanavir and darunavir regimens.

91 An extremely darunavir-resistant mutant precursor is more responsive

92 ation than raltegravir and ritonavir-boosted darunavir, respectively, primarily because of hyperbilir

93 (TDF/FTC) plus atazanavir-ritonavir (ATV/r), darunavir-ritonavir (DRV/r), or raltegravir (RAL) in ACT

94 ency virus (HIV)-negative volunteers (11 for darunavir-ritonavir and 10 for fosamprenavir-ritonavir)

95 e buprenorphine-3-glucuronide suggested that darunavir-ritonavir and fosamprenavir-ritonavir induced

96 anagement, and the protease inhibitors (PIs) darunavir-ritonavir and fosamprenavir-ritonavir.

97 ikely to be necessary when buprenorphine and darunavir-ritonavir or fosamprenavir-ritonavir are coadm

98 non-opioid-dependent volunteers who received darunavir-ritonavir or fosamprenavir-ritonavir but not b

99 Patients received darunavir-ritonavir, 600/100 mg twice daily, plus an inv

100 udies, healthy adult volunteers received (1) darunavir/ritonavir (800 mg/100 mg once daily) with and

101 < 50 copies/mL during >/=6 months on stable darunavir/ritonavir (800/100 mg once daily) or lopinavir

102 (TDF/FTC) plus atazanavir/ritonavir (ATV/r), darunavir/ritonavir (DRV/r), or RAL.

103 (TDF/FTC) plus atazanavir/ritonavir (ATV/r), darunavir/ritonavir (DRV/r), or raltegravir (RAL).

104 rse transcriptase inhibitors associated with darunavir/ritonavir (n = 12), saquinavir/ritonavir (n =

105 signed to atazanavir/ritonavir 300/100 mg or darunavir/ritonavir 800/100 mg in combination with tenof

106 or 6 months or longer on triple therapy with darunavir/ritonavir and 2 nucleos(t)ides (tenofovir diso

107 Of 46 subjects enrolled, 56% received darunavir/ritonavir and 44% lopinavir/ritonavir.

108 d to continue therapy (n = 128) or switch to darunavir/ritonavir and lamivudine (n = 129).

109 rapeutic noninferiority of dual therapy with darunavir/ritonavir and lamivudine compared to triple th

110 Dual therapy with darunavir/ritonavir and lamivudine demonstrated noninfer

111 more in the atazanavir/ritonavir arm than in darunavir/ritonavir arm.

112 nued atazanavir/ritonavir and 5 discontinued darunavir/ritonavir due to adverse effects.

113 differences between atazanavir/ritonavir and darunavir/ritonavir in efficacy, clinically relevant sid

114 ctions were observed between faldaprevir and darunavir/ritonavir or tenofovir.

115 , 56 (62%) atazanavir/ritonavir and 62 (71%) darunavir/ritonavir patients remained free of treatment

116 d 71 (79%) atazanavir/ritonavir and 75 (85%) darunavir/ritonavir patients remained free of virologica

117 d lamivudine compared to triple therapy with darunavir/ritonavir plus 2 nucleos(t)ides for maintenanc

118 previr and the commonly used antiretrovirals darunavir/ritonavir, efavirenz, and tenofovir to guide t

119 to first-line regimens containing efavirenz, darunavir/ritonavir, or raltegravir regardless of pretre

120 ricitabine plus either atazanavir/ritonavir, darunavir/ritonavir, or raltegravir.

121 l of 53.4% showed intermediate resistance to darunavir/ritonavir, whereas high-level resistance was n

122 des and more total and subcutaneous fat than darunavir/ritonavir.

123 IV-2 proteases complexed with amprenavir and darunavir to models of the PRDelta4 enzyme.

124 efficacy and tolerability, ritonavir-boosted darunavir was superior to ritonavir-boosted atazanavir,

125 containing raltegravir or ritonavir-boosted darunavir was superior to that of the ritonavir-boosted

126 hibitors including the highly important drug darunavir, was achieved via a one-pot procedure using fu

127 Raltegravir and ritonavir-boosted darunavir were equivalent for tolerability, whereas rito