ライフサイエンスコーパス: integrase inhibitor

1 ds for the development of a new class of HIV integrase inhibitor.

2 n between boceprevir and raltegravir, an HIV integrase inhibitor.

3 ter molecule could open a route to new HIV-1 integrase inhibitors.

4 and offer new catechol isosteres for use in integrase inhibitors.

5 h the identification and characterization of integrase inhibitors.

6 rmation which may guide the future design of integrase inhibitors.

7 oumermycin monomeric derivatives were active integrase inhibitors.

8 cleoside reverse transcriptase inhibitors or integrase inhibitors.

9 rus harboring resistance to first-generation integrase inhibitors.

10 dapivirine, rilpivirine, maraviroc, and new integrase inhibitors.

11 IN119 is under selection by HLA alleles and integrase inhibitors.

12 ted PI monotherapies and future options with integrase inhibitors.

13 the viral genome after intensification with integrase inhibitors.

14 viral DNA processing site for inhibition by integrase inhibitors.

15 as well as for the molecular pharmacology of integrase inhibitors.

16 oward the potential design of improved HIV-1 integrase inhibitors.

17 ymmetric total synthesis of the potent HIV-1 integrase inhibitor 5 is described.

18 Similarly, raltegravir, a pharmacologic integrase inhibitor, abolished HIV-1-induced cell killin

19 These studies demonstrate integrase inhibitor activity in vivo and suggest that ce

20 The potency of integrase inhibitors against 3'-processing and their abi

21 The potency of an allosteric integrase inhibitor, ALLINI-2, for rendering produced vi

22 Allosteric integrase inhibitors (ALLINIs) affect multiple viral pro

23 inding to the viral RNA genome by allosteric integrase inhibitors (ALLINIs) or through mutations with

24 protease and integrase, and the most potent integrase inhibitors also inhibited HIV protease.

25 avir has been shown to be non-inferior to an integrase inhibitor and superior to a non-nucleoside rev

26 bitors and drugs in novel classes, including integrase inhibitors and CCR5 antagonists.

27 reen a library of chemicals related to known integrase inhibitors and found a new compound, quinaliza

28 cell depletion, raising the possibility that integrase inhibitors and interventions directed towards

29 that is applicable to a wide range of potent integrase inhibitors and is consistent with the availabl

30 In 2007, raltegravir became the first integrase inhibitor approved for use in the treatment of

31 zyl-4-hydroxy-1,5-naphthyridin-2(1H)-one HIV-integrase inhibitors are disclosed.

32 Integrase inhibitors are emerging anti-human immunodefic

33 Human immunodeficiency virus type 1 (HIV-1) integrase inhibitors are in clinical trials, and raltegr

34 e between pre- and post-integration latency, integrase inhibitors are routinely used, preventing nove

35 The first integrase inhibitors are undergoing clinical trial, but

36 leoside reverse transcriptase inhibitors and integrase inhibitors are used to treat infection with HI

37 C as a single tablet and represent the first integrase inhibitor based complete FDC regimen.

38 The findings support guidelines recommending integrase inhibitor based regimens in first-line antiret

39 nhibitor-based, 100% (95% CI, 91%-100%); and integrase inhibitor based, 95% (95% CI, 83%-99.4%).

40 A total of 56/86 (65%) initiated an integrase inhibitor-based regimen and 30/86 (35%) a prot

41 nd chronic HIV infection, in particular when integrase inhibitor-based regimens were used.

42 would be the only single-tablet, once-daily, integrase-inhibitor-based regimen for initial treatment

43 s given, EVG/COBI/FTC/TDF would be the first integrase-inhibitor-based regimen given once daily and t

44 progress toward a clinically effective HIV-1 integrase inhibitor can at least in part be attributed t

45 rystal structure studies illustrate specific integrase-inhibitor contacts that prevent cross-linking

46 For this purpose, we used a known HIV-1 integrase inhibitor containing aryl di-O-acetyl groups (

47 that the rapid decay observed in patients on integrase-inhibitor-containing regimens is not necessari

48 The HIV integrase inhibitor d[G(3)(TG(3))(3)] forms an extremely

49 e promising lead compounds for further HIV-1 integrase inhibitor development.

50 n the plasma drug concentration of the viral integrase inhibitor dolutegravir.

51 human immunodeficiency virus type-1 (HIV-1) integrase inhibitors dolutegravir (S/GSK1349572) (3) and

52 The integrase inhibitor elvitegravir (EVG) has been co-formu

53 ty of the human immunodeficiency virus (HIV) integrase inhibitor elvitegravir to comparator ritonavir

54 e CYP3A without anti-HIV activity) and a new integrase inhibitor, elvitegravir (EVG).

55 In addition, the approval of the second integrase inhibitor, elvitegravir, and a novel pharmacoe

56 appears to be a more favorable effect of the integrase inhibitor EVG over efavirenz on immune activat

57 Additionally, in integrase inhibitor-experienced patients, only R263K and

58 macophore of aryl beta-diketo acids (DKA) as integrase inhibitors, fails in certain cases of highly e

59 need to accelerate the study and approval of integrase inhibitors for use in young children.

60 very of 10 novel, structurally diverse HIV-1 integrase inhibitors, four of which have an IC50 value l

61 linking assays to probe the binding sites of integrase inhibitors from different chemical families an

62 d virological failure with resistance in the integrase inhibitor group compared with three participan

63 252 (87%) women in the integrase inhibitor group had plasma HIV-1 RNA less than

64 of adverse events compared with five in the integrase inhibitor group.

65 thesis of a complex chiral atropisomeric HIV integrase inhibitor has been accomplished.

66 human immunodeficiency virus type 1 (HIV-1) integrase inhibitor, has limited cross-resistance to ral

67 Previous screens for integrase inhibitors have assayed inhibition of reaction

68 The structures of a large number of HIV-1 integrase inhibitors have in common two aryl units separ

69 leoside reverse transcriptase inhibitors and integrase inhibitors have slopes of approximately 1, cha

70 TIs (NNRTIs), protease inhibitors (PIs), and integrase inhibitors (IIs) did not affect HK2, except fo

71 linical demonstration of the activity of any integrase inhibitor in subjects with HIV-1 resistant to

72 However, there are currently no integrase inhibitors in clinical use for AIDS.

73 automated LC-MS/MS methods to quantify five integrase inhibitors in plasma with the limits of quanti

74 cleotide (e.g., human immunodeficiency virus integrase) inhibitors, in applications such as antisense

75 (DTG), a human immunodeficiency virus (HIV) integrase inhibitor (INI), would be efficacious in INI-r

76 Two-metal binding HIV-1 integrase inhibitors (INIs) are potent inhibitors of HIV

77 This proposed binding mechanism for integrase inhibitors involves interaction with a specifi

78 genotypes exclude testing for resistance to integrase inhibitors ("IR testing"), although this class

79 deficiency virus (HIV) treatments containing integrase inhibitors is unknown.

80 ncy levels described in models that only use integrase inhibitors may be overestimated.

81 AG1/2 and integrase and suggest that certain integrase inhibitors may have the potential to interfere

82 results further indicate that resistance to integrase inhibitors may include both integrase and LTR

83 tiretroviral drugs under study, particularly integrase inhibitors, may prove useful in treatment-naiv

84 Integrase-inhibitor-naive patients with HIV resistant to

85 ble long-term efficacy and safety profile in integrase-inhibitor-naive patients with triple-class res

86 curcumin analog with the recently described integrase inhibitor NSC 158393 resulted in integrase inh

87 HIV-1 integrase, we sought to determine how integrase inhibitors of the diketo acid type would affec

88 Integrase inhibitors of the strand transfer reaction rem

89 ction analysis to investigate the effects of integrase inhibitors on each step in the reaction.

90 trate this by comparing the effect of RT and integrase inhibitors on viral dynamics.

91 For integrase inhibitors, only IC(50) is affected.

92 cells infected either in the presence of an integrase inhibitor or with an integrase-deficient virus

93 It is unclear whether the integrase inhibitor raltegravir (RAL) reduces inflammati

94 148R(H)(K) that reduce susceptibility to the integrase inhibitor raltegravir have been identified in

95 Recent clinical trials of the integrase inhibitor raltegravir have demonstrated more r

96 y acquired significant resistance to APV, an integrase inhibitor raltegravir, and a GRL-09510 congene

97 itors zidovudine (AZT) and tenofovir and the integrase inhibitor raltegravir.

98 virine, ritonavir-boosted lopinavir, and the integrase inhibitors raltegravir and elvitegravir.

99 289 were randomly assigned to receive the integrase inhibitor regimen and 286 to receive the prote

100 the safety and efficacy of the single tablet integrase inhibitor regimen containing elvitegravir, cob

101 citabine, and tenofovir disoproxil fumarate (integrase inhibitor regimen) or ritonavir-boosted atazan

102 Data on integrase inhibitor resistance come primarily from clini

103 When present in certain combinations, some integrase inhibitor resistance mutations increased resis

104 ever, 25 out of 41 mutations associated with integrase inhibitor resistance were present.

105 Based upon a class of known HIV-1 integrase inhibitors, several pharmacophore models were

106 Cross-linking interference by eight integrase inhibitors shows that the most potent cross-li

107 on data derived from a large number of HIV-1 integrase inhibitors, similar structural features can be

108 xil fumarate, saquinavir, atazanavir, and an integrase inhibitor starting at 12 days after inoculatio

109 ed to integrase, which is also the target of integrase inhibitors such as raltegravir.

110 It has been shown that L-731988, a potent integrase inhibitor, targets a conformation of the integ

111 for T30695, which is the most potent of the integrase inhibitors that have been identified thus far.

112 Among all the HIV-1 integrase inhibitors, the beta-diketo acids (DKAs) repre

113 evel replication of HIV-1 in the presence of integrase inhibitor therapy.

114 significantly shorter in those receiving an integrase inhibitor- versus a protease inhibitor-based r

115 ase inhibitors, 7 protease inhibitors, and 1 integrase inhibitor was achieved in 0.25 g of meconium.

116 human immunodeficiency virus type 1 (HIV-1) integrase inhibitor, was evaluated for distribution and

117 avir (S/GSK1349572), a once-daily, unboosted integrase inhibitor, was recently approved in the United

118 New integrase inhibitors were also identified.

119 uctural leads for the development of new HIV integrase inhibitors which do not rely on this potential

120 rk has resulted in the identification of new integrase inhibitors which may be regarded as bis-caffeo

121 ence of reverse-transcriptase inhibitors and integrase inhibitors, which allows for the specific isol

122 nhibitors were quinolone antibiotics and HIV integrase inhibitors, which share common structural feat

123 Compound 8g was also the most potent integrase inhibitor with an IC50 value of 26 nM.

124 tructural basis and rationale for developing integrase inhibitors with the potential for unique and n

125 leoside reverse transcriptase inhibitors and integrase inhibitors (without cobicistat).