ライフサイエンスコーパス: saquinavir

1 eptibility only to lopinavir, darunavir, and saquinavir.

2 recursor is more responsive to inhibition by saquinavir.

3 aller effects occur among those treated with saquinavir.

4 uded zidovudine, didanosine, nevirapine, and saquinavir.

5 easured by PCR), and resistance mutations to saquinavir.

6 ovudine-nevirapine, and stavudine-zidovudine-saquinavir.

7 T80V and T80N had decreased the affinity for saquinavir.

8 iptase inhibitors and the protease inhibitor saquinavir.

9 o current protease inhibitors, Indinavir and Saquinavir.

10 rotease inhibitors indinavir, ritonavir, and saquinavir.

11 ibitors, including ritonavir, indinavir, and saquinavir.

12 RRs (95% CIs) for other drugs were: soft-gel saquinavir, 0.54 (0.07-3.97); nelfinavir, 2.44 (1.68-3.5

13 ion were randomly assigned to receive either saquinavir (1800 mg per day) plus both zidovudine (600 m

14 %, p = 0.001), indinavir (34.6%, p = 0.001), saquinavir (24.3%, p = 0.001), or ritonavir (18%, p < 0.

15 1/106-4:27 clone with the protease inhibitor saquinavir (250 nM) completely inhibited TNF-alpha-induc

16 were: indinavir, 1.75 (0.82-3.73); hard-gel saquinavir, 3.48 (0.36-33.37); nelfinavir, 2.64 (1.37-5.

17 .9%), nelfinavir (5.9%; 95% CI, 1.2%-16.2%), saquinavir (5.9%; 95% CI, 0.15%-28.7%), and indinavir(6.

18 Subjects received nelfinavir, saquinavir, abacavir, and either another nucleoside anal

19 nked clinically to osteopenia, ritonavir and saquinavir, abrogate a physiological block to RANKL acti

20 ata indicated that the HIV PIs lopinavir and saquinavir affect preerythrocytic-stage parasite develop

21 Therapy with high-dose saquinavir alone or in combination with other antiretrov

22 Whereas saquinavir also competitively inhibits UGT activity, thi

23 However, saquinavir, amprenavir, and indinavir blood levels are i

24 We studied the safety and efficacy of saquinavir, an HIV-protease inhibitor, given with one or

25 tidrug-resistant isolate, the combination of saquinavir and indinavir demonstrated antagonism at all

26 ombinations of the HIV-1 protease inhibitors saquinavir and indinavir was determined.

27 pogenesis of hMSCs was strongly inhibited by saquinavir and NFV (>50%, p < 0.001) and moderately inhi

28 Finally, the HIV protease inhibitors saquinavir and ritonavir were potent inhibitors of trans

29 the three-drug combination than with either saquinavir and zidovudine (P=0.017) or zalcitabine and z

30 valuated (nelfinavir, ritonavir, amprenavir, saquinavir, and indinavir), only nelfinavir both effecti

31 proved HIV-1 protease inhibitors, ritonavir, saquinavir, and indinavir, are very effective in inhibit

32 udy, we found that PIs, including ritonavir, saquinavir, and indinavir, inhibited the growth of DU145

33 mprenavir, nelfinavir, indinavir, ritonavir, saquinavir, and lopinavir, including amino acid substitu

34 Indinavir, ritonavir, saquinavir, and nelfinavir inhibit the A and C subtype p

35 he protease inhibitors indinavir, ritonavir, saquinavir, and nelfinavir to the wild-type HIV-1 protea

36 s well as the protease inhibitors indinavir, saquinavir, and nelfinavir.

37 Zidovudine, lamivudine, saquinavir, and nevirapine were used at IC(90)s, IC(99)s

38 e binding affinity of indinavir, nelfinavir, saquinavir, and ritonavir by factors of 4000, 3300, 5800

39 ies, suggesting that resistance mutations to saquinavir appear within close temporal proximity in lym

40 tionships among characteristics of patients, saquinavir area under the curve (AUC) and trough concent

41 f phenotypic susceptibility to indinavir and saquinavir at baseline were significantly associated wit

42 sence or absence of a resistance mutation to saquinavir at codons 48 or 90 of the HIV-1 protease gene

43 a regimen of tenofovir disoproxil fumarate, saquinavir, atazanavir, and an integrase inhibitor start

44 Higher saquinavir AUC and C(min) values were associated with a

45 licit solvent over a time scale of 24 ns for saquinavir bound to the wildtype, G48V, L90M and G48V/L9

46 ree of the five (amprenavir, nelfinavir, and saquinavir but not ritonavir or indinavir) inhibited Akt

47 nce to darunavir, atazanavir, lopinavir, and saquinavir, but not other PIs, and contained a single R4

48 tic precursor to the HIV-protease inhibitor, saquinavir, by formation of an NHS ester followed by acy

49 d that lopinavir, nelfinavir, ritonavir, and saquinavir caused dose-dependent block of HERG channels

50 HIV) RNA levels, and resistance mutations to saquinavir (codons 48 and 90) and zidovudine (codon 215)

51 IV-1 protease variants were estimated in the saquinavir concentration range of 0-10(-7) M.

52 of the protease species is driven by in vivo saquinavir concentration, which appears to be in the ran

53 ties of the four protease species at certain saquinavir concentrations appear to correlate with the p

54 usually initially selected by nelfinavir and saquinavir, D30N and L90M, respectively, impair fitness.

55 th ongoing infection, the protease inhibitor saquinavir efficiently suppresses NL4-R3A replication.

56 Indinavir and saquinavir exhibited slight anti-P. carinii activity at

57 at nelfinavir may have limited utility after saquinavir failure, particularly without potent concomit

58 ctivity of the HIV-1 protease inhibitor (PI) saquinavir for both P-gp (rho = 0.75; P = 0.0019) and CX

59 In addition, saquinavir had a strong inhibitory effect on the T-cell

60 ed the two-drug combination (zidovudine plus saquinavir) had only codon 48 mutations, 45.8% had only

61 Lopinavir and saquinavir have gametocytocidal and transmission blockin

62 inhibitors (HPI) amprenavir, nelfinavir, and saquinavir have previously been shown to sensitize tumor

63 he approval of the first protease inhibitor (saquinavir, Hoffman La-Roche, 1995) and two decades sinc

64 Patients received saquinavir in combination with either ritonavir or nelfi

65 an be attributed to higher concentrations of saquinavir in females than in males.

66 haracteristics of indinavir, nelfinavir, and saquinavir in vitro using the model P-glycoprotein expre

67 old to >100-fold) to zidovudine, lamivudine, saquinavir, indinavir, and nelfinavir and lower-level re

68 The inhibitors included saquinavir, indinavir, nelfinavir, 141W94, ritonavir (al

69 to atazanavir, and >60% showed resistance to saquinavir, indinavir, nelfinavir, and fosamprenavir.

70 with a viral load below 200 copies/mL in the saquinavir, indinavir, nelfinavir, and placebo arms were

71 e) of the other four currently approved PRIs-saquinavir, indinavir, ritonavir, and nelfinavir-has fai

72 e better predictors of response than was the saquinavir inhibitory quotient.

73 Saquinavir is a potent antiviral agent that has a favora

74 e envelope fusion dependent, as T20, but not saquinavir, is capable of reducing thymocyte apoptosis.

75 Saquinavir, KNI-272, and ritonavir inhibited the replica

76 zidovudine, lamivudine-stavudine, lamivudine-saquinavir, lamivudine-nevirapine, stavudine-zidovudine,

77 stavudine-nevirapine, lamivudine-zidovudine-saquinavir, lamivudine-zidovudine-stavudine, stavudine-z

78 itonavir, indinavir, nelfinavir, amprenavir, saquinavir, lopinavir, and atazanavir revealed that the

79 The 4 PIs available are saquinavir mesylate, ritonavir, indinavir sulfate, and n

80 en HIV-positive patients receiving high-dose saquinavir monotherapy (3600 or 7200 mg/day) underwent 1

81 omized assignment (per prior PI exposure) to saquinavir (n = 116); indinavir (n = 69); nelfinavir (n

82 37%, and 42% loss of activity for indinavir, saquinavir, nelfinavir, ritonavir, and amprenavir, respe

83 eloped the V82A mutation either on continued saquinavir or after a switch to nelfinavir or indinavir.

84 sistant HIV-1 (RF) in the presence of either saquinavir or SC52151, which represented sequential drug

85 (2.25 mg per day) or zidovudine plus either saquinavir or zalcitabine.

86 han did treatment with zidovudine and either saquinavir or zalcitabine.

87 w that other protease inhibitors are weaker (saquinavir) or unable to activate SXR (nelfinavir, indin

88 Monotherapy with 3600 mg or 7200 mg of saquinavir per day, in six divided doses, for 24 weeks.

89 The low-dose saquinavir regimen (3600 mg/d) resulted in a maximal mea

90 The high-dose saquinavir regimen (7200 mg/d) produced a mean maximal d

91 tional genotypic changes, including the L90M saquinavir resistance mutation, and decreased phenotypic

92 eceiving the high-dose regimen developed key saquinavir resistance mutations.

93 es of the wild-type HIV-1 protease and three saquinavir resistant mutants, G48V, L90M, and G48V/L90M,

94 protease that affects indinavir, nelfinavir, saquinavir, ritonavir, amprenavir, and lopinavir.

95 At various times, the patient received saquinavir, ritonavir, and nelfinavir in conjunction wit

96 four inhibitors in clinical use (indinavir, saquinavir, ritonavir, and nelfinavir) and a second-gene

97 pproved by the Food and Drug Administration (saquinavir, ritonavir, indinavir, and nelfinavir) as AID

98 No inhibition of PERV protease was seen with saquinavir, ritonavir, indinavir, nelfinavir, or amprena

99 tease mutations present at the initiation of saquinavir-ritonavir therapy were the strongest predicto

100 ssociated with darunavir/ritonavir (n = 12), saquinavir/ritonavir (n = 2), and maraviroc (n = 3).

101 .08); indinavir/ritonavir, 0.32 (0.04-2.49); saquinavir/ritonavir, 0.64 (0.23-1.80); nevirapine, 1.65

102 .54); indinavir/ritonavir, 1.96 (1.02-3.77); saquinavir/ritonavir, 1.12 (0.48-2.61); lopinavir/ritona

103 d GIT-27NO or the NO-modified antiviral drug saquinavir (Saq) named Saq-NO on two colon cancer cell l

104 replicative capacity relative to WT, while a saquinavir-selected L90M substitution moderately decreas

105 and the chemically related amprenavir, while saquinavir showed competitive inhibition.

106 equencing results from patients treated with saquinavir showed significant increases in the frequency

107 hard capsules (SQVhc) to indinavir (IDV) or saquinavir soft-gel capsules (SQVsgc) after >48 weeks of

108 I54M) (PR with I54M mutation) complexed with saquinavir (SQV) as well as PR(G48V) (PR with G48V mutat

109 333 was an open-label trial of a switch from saquinavir (SQV) hard capsules (SQVhc) to indinavir (IDV

110 randomized trial comparing 2 formulations of saquinavir (SQV) to indinavir (IDV) in patients with ext

111 the presence of inhibitors darunavir (DRV), saquinavir (SQV), and lopinavir (LPV), relative to that

112 the presence of increasing concentrations of saquinavir (SQV), gave rise to a new variant containing

113 -zidovudine, stavudine-didanosine, stavudine-saquinavir, stavudine-nevirapine, lamivudine-zidovudine-

114 type 1 (HIV-1), to HIV-1 protease inhibitor saquinavir, the catalytic and inhibition properties of t

115 In the case of saquinavir, the fluorescence changes associated with com

116 The HIV PIs lopinavir and saquinavir, the nonnucleoside reverse-transcriptase inhi

117 ients who developed the G48V mutation during saquinavir therapy developed the V82A mutation either on

118 t that mutations selected in vivo by initial saquinavir therapy may provide more cross-resistance to

119 Saquinavir therapy resulted in a reduction in HIV RNA le

120 nM) in the binding affinity of darunavir and saquinavir to mature multidrug resistant proteases relat

121 The value of k(1) for saquinavir was 62 +/- 2 microM(-1) s(-1).

122 Saquinavir was common in all study arms, and the study i

123 the effect of GW0385 on the binding of E to saquinavir was determined.

124 ls and appearance of resistance mutations to saquinavir were determined in simultaneous lymph node an

125 Concentrations of saquinavir were higher when it was combined with ritonav

126 cal protease inhibitors (PIs), darunavir and saquinavir were the most effective in inhibiting wild-ty

127 combination (zidovudine and zalcitabine plus saquinavir) were codon 48 alone in 1.4%, codon 90 alone

128 s associated with BMS-186318 and A-77003 (or saquinavir) were either inactive or had impaired enzyme

129 ls Group study 359 was a controlled study of saquinavir with either ritonavir or nelfinavir, together

130 iency virus (HIV) 1-infected persons in whom saquinavir with multiple nucleoside reverse transcriptas

131 Patients received saquinavir with ritonavir or nelfinavir together with de

132 nking of binding affinities of the inhibitor saquinavir with the wild type (WT) and three resistant m

133 with three drugs, amprenavir, indinavir, and saquinavir, yield good agreements with experiments.

134 Treatment with saquinavir, zalcitabine, and zidovudine was well tolerat