ライフサイエンスコーパス: saquinavir

1 aller effects occur among those treated with saquinavir.

2 uded zidovudine, didanosine, nevirapine, and saquinavir.

3 recursor is more responsive to inhibition by saquinavir.

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

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

6 T80V and T80N had decreased the affinity for saquinavir.

7 eptibility only to lopinavir, darunavir, and 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 tic HIV-infected H9 cells in the presence of saquinavir, after which the activation process of HIV-sp

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

23 Whereas saquinavir also competitively inhibits UGT activity, thi

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

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

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

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

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

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

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

31 lidomide), (b) a bRo5 orally available drug (Saquinavir), and (c) a polar PROTAC (CMP 98) to focus on

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

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

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

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

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

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

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

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

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

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

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

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

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

45 e foam cells with ritonavir, nelfinavir, and saquinavir at least doubled cholestryl ester accumulatio

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

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

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

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

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

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

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

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

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

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

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

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

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

59 Both atazanavir and saquinavir exhibited a remarkable synergistic activity w

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

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

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

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

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

65 Lopinavir and saquinavir have gametocytocidal and transmission blockin

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

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

68 Patients received saquinavir in combination with either ritonavir or nelfi

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

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

71 two HIV protease inhibitors, atazanavir and saquinavir, in combination with posaconazole exhibited p

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

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

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

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

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

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

78 Saquinavir is a potent antiviral agent that has a favora

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

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

81 zidovudine, lamivudine-stavudine, lamivudine-saquinavir, lamivudine-nevirapine, stavudine-zidovudine,

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

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

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

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

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

87 37%, and 42% loss of activity for indinavir, saquinavir, nelfinavir, ritonavir, and amprenavir, respe

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

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

90 (2.25 mg per day) or zidovudine plus either saquinavir or zalcitabine.

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

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

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

94 The atazanavir/posaconazole and saquinavir/posaconazole combinations significantly reduc

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

115 333 was an open-label trial of a switch from saquinavir (SQV) hard capsules (SQVhc) to indinavir (IDV

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

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

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

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

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

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

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

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

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

125 Saquinavir therapy resulted in a reduction in HIV RNA le

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

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

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

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

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

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

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

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

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

135 mmonly used ARTs (ritonavir, nelfinavir, and saquinavir) were found altering the activity of AR-RGN,

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

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

138 Patients received saquinavir with ritonavir or nelfinavir together with de

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

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

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