ライフサイエンスコーパス: maraviroc

1 cline partially reversed after discontinuing maraviroc.

2 rminants with the FDA-approved HIV inhibitor Maraviroc.

3 s to VCV and to the licensed CCR5 antagonist maraviroc.

4 ructure of CCR5 receptor cocrystallized with Maraviroc.

5 receptor antagonists, including the HIV drug maraviroc.

6 re administration of the antiretroviral drug maraviroc.

7 s performed in 12 HIV-negative men receiving maraviroc 300 mg twice daily for 8 days.

8 Participants received maraviroc 600 mg twice daily or placebo added to an ART

9 rmuted block randomisation to receive either maraviroc (600 mg twice daily) or placebo in addition to

10 Maraviroc, a CCR5 antagonist antiretroviral drug, might

11 Maraviroc, a CCR5 antagonist, is active against R5 but n

12 timal CD4(+) T-cell recovery, subjects added maraviroc, a CCR5 antagonist, to their existing ART for

13 a recent study by Matsuzawa and colleagues, Maraviroc, a CCR5 inhibitor, was used as pre-exposure pr

14 mutant R5-tropic gp120 protein resistant to maraviroc, a small-molecule CCR5 inhibitor, and they dra

15 nefungin) and several anti-viral drugs (e.g. Maraviroc, Abacavir, Telbivudine, and Cidofovir) may inh

16 CCR5 to the HIV-1 cellular entry inhibitors maraviroc, AD101, CMPD 167, and vicriviroc dramatically

17 Maraviroc also reduced the growth-promoting effects of c

18 Treg frequency after treatment of PBMCs with maraviroc, although their in vitro suppressive function

19 e were 276 patients randomized (140 received maraviroc and 136 placebo).

20 pants were randomly assigned (140 to receive maraviroc and 136 to receive placebo).

21 platform will inform the appropriate use of maraviroc and future CCR5 blocking drugs in regions of t

22 Both maraviroc and ibalizumab are being studied for preventio

23 tarting ART that was intensified (iART) with maraviroc and raltegravir in an open-label fashion.

24 pression of maximal responses for aplaviroc, maraviroc and vicriviroc suggests that these modulators

25 the antiviral potency of the CCR5 antagonist maraviroc, and had favorable antiviral interactions with

26 rovirals, including dapivirine, rilpivirine, maraviroc, and new integrase inhibitors.

27 %) patients had IRIS events, 33 (24%) in the maraviroc arm and 31 (23%) in the placebo arm (p=0.88).

28 hans cells in the ex vivo system, suggesting Maraviroc as a useful candidate for pre-exposure prophyl

29 HIV-infected pregnant women receiving maraviroc as part of clinical care had intensive steady-

30 d26 vectors combined with the CCR5 inhibitor maraviroc as the vaginal microbicide led to significant

31 Maraviroc, as compared with placebo, resulted in signifi

32 CCR5 coreceptor; however, the mechanisms of maraviroc-associated immunomodulation in human immunodef

33 These findings partially explain maraviroc-associated immunomodulatory effects and open n

34 explain the impediments to the emergence of maraviroc-associated R5 drug resistance.

35 (standard dose raltegravir and dose-adjusted maraviroc based on baseline antiretroviral therapy), pat

36 The predicted Maraviroc binding site agrees with the recent structure

37 Maraviroc (CCR5 antagonist) or CCL5 immunodepletion dimi

38 only two compounds have reached the market: maraviroc (CCR5) for HIV infection and plerixafor (CXCR4

39 1, obtained from 20 patients who enrolled in maraviroc clinical trials and experienced treatment fail

40 AUCtau) and 0.70 (0.58-0.85) for the maximum maraviroc concentration.

41 d a greater impact than did the CCR5 blocker maraviroc, confirming the use of CXCR6 in primary lympho

42 We compared the effect of maraviroc-containing or -sparing combination ART (cART)

43 Maraviroc-containing PrEP for women may warrant further

44 Maraviroc-containing PrEP regimens were safe and well-to

45 in treatment-experienced patients beginning maraviroc-containing regimens.

46 The median ratio of maraviroc cord blood to maternal blood was 0.33 (range,

47 Therefore, maraviroc could benefit HIV-positive patients with resid

48 Moreover, maraviroc counterregulated ritonavir-induced lipoatrophy

49 fecting cell proliferation or viability, and maraviroc decreased pulmonary metastasis in a preclinica

50 PBMC) in the presence of the CCR5 antagonist maraviroc, despite the fact that maraviroc was capable o

51 mAb ROAb13 and the small molecule inhibitor maraviroc, did not interfere with binding to CCR5 for ei

52 Because maraviroc does not bind to murine CCR5, we used human-CC

53 ty was statistically demonstrated for either maraviroc dosage compared with placebo at 24 weeks of tr

54 Collectively, these data suggest that maraviroc effectively protects against GVHD by modulatin

55 R5-/- mice or human-CCR5ki mice treated with maraviroc exhibited decreased PA-SMC proliferation and r

56 Overall maraviroc exposure during pregnancy was decreased, with

57 ese results may have relevance for trials of maraviroc for HIV preexposure prophylaxis and graft-vers

58 e principal obstacle to the CCR5-antagonist, maraviroc, from being more widely used in anti-HIV-1 the

59 in placebo group; p=0.072); 25 (18%) in the maraviroc group and 21 (15%) in the placebo group had se

60 %) patients had IRIS events, 33 (24%) in the maraviroc group and 31 (23%) in the placebo group (p=0.7

61 37 participants (26%) in the maraviroc group had grade 3 or 4 adverse events compared

62 the placebo group in MOTIVATE 1; 45% in both maraviroc groups vs. 18% in MOTIVATE 2; P<0.001 for both

63 Maraviroc had no significant effect on development of IR

64 Maraviroc had no significant effect on frequency, time o

65 The CCR5 inhibitor maraviroc has been hypothesized to decrease T-cell activ

66 tests" to determine virus susceptibility to maraviroc have been developed primarily for HIV-1 subtyp

67 cted to determine the safety and efficacy of maraviroc in combination with optimized background thera

68 , and is a predictor of virologic success on maraviroc in therapy-experienced patients.

69 In the late model, maraviroc inhibited atherosclerotic progression by reduc

70 wth of human and human-CCR5ki mouse PA-SMCs; maraviroc inhibited both effects.

71 Maraviroc inhibited CCR5 internalization and lymphocyte

72 tein 1beta) levels increased 2.4-fold during maraviroc intensification (P < .001).

73 During maraviroc intensification, plasma lipopolysaccharide dec

74 ne activation and apoptosis decreased during maraviroc intensification; this decline partially revers

75 Maraviroc is a new CCR5 antagonist designed to block HIV

76 The CCR5 antagonist maraviroc is approved for use in treatment-naive and tre

77 Maraviroc is the first antiretroviral (ART) drug to targ

78 Exposure to maraviroc limits the evolution and associated systemic i

79 The entry inhibitor drug maraviroc makes the cell coreceptor CCR5 unavailable for

80 e of the only marketed CCR5 entry inhibitor, maraviroc, makes it necessary to develop new CCR5 allost

81 iated immunopathology and are susceptible to maraviroc-mediated CCR5 blockade.

82 CCR5 inhibitors such as vicriviroc (VVC) and maraviroc (MVC) are allosteric modulators that impair HI

83 Maraviroc (MVC) is a candidate drug for HIV preexposure

84 Maraviroc (MVC) is a candidate for human immunodeficienc

85 Maraviroc (MVC) is a CCR5 antagonist that inhibits HIV-1

86 Maraviroc (MVC) is a potent CCR5 coreceptor antagonist t

87 ed partial resistance to the CCR5 antagonist maraviroc (MVC) on cells expressing high levels of CCR5,

88 ngle-dose pharmacokinetics of low-osmolar 1% maraviroc (MVC), 1% tenofovir (TFV), or 1% MVC/1% TFV co

89 bicide candidates in clinical development is Maraviroc (MVC), a small-molecule drug that binds the CC

90 We compared maraviroc (MVC)- to tenofovir disoproxil fumarate (TDF)-

91 TAK-779, an investigational antagonist, and maraviroc (MVC).

92 ment regimens containing the CCR5 antagonist maraviroc (MVC).

93 (n = 12), saquinavir/ritonavir (n = 2), and maraviroc (n = 3).

94 d the in vitro effect of the CCR5 antagonist maraviroc on lymphocyte function and chemotaxis.

95 Our aim was to evaluate the effect of maraviroc on Tregs.

96 .20 log(10) copies/mL for those who received maraviroc once (P =.83) or twice (P +.38) daily, respect

97 60 cells/microL among patients who received maraviroc once daily, and 62 cells/microL among patients

98 three antiretroviral regimens consisting of maraviroc once daily, maraviroc twice daily, or placebo,

99 More patients receiving maraviroc once or twice daily had HIV-1 RNA levels of le

100 baseline in CD4 counts was also greater with maraviroc once or twice daily than with placebo (increas

101 to receive optimized background therapy plus maraviroc (once or twice daily) or placebo.

102 The CCR5 antagonists maraviroc or vicriviroc, developed to block CCR5 HIV cor

103 three ligands with a similar pharmacophore (Maraviroc, PF-232798, and Aplaviroc) bind to a specific

104 hich treatment-experienced patients received maraviroc plus optimized background therapy.

105 Serum from patients receiving maraviroc prevented CCR5 internalization by CCL5 and blo

106 Pretreating the MK cultures with maraviroc prior to exposure to CCL5 reversed the augment

107 Patients who developed acute GVHD despite maraviroc prophylaxis showed increased T-cell activation

108 ding optimal use of recently approved drugs (maraviroc, raltegravir, and etravirine) in treatment-exp

109 PBMC samples from 181 maraviroc recipients at study entry in MOTIVATE or A4001

110 In ritonavir-treated mice, maraviroc reduced plaque areas and macrophage infiltrati

111 In a mouse model of genetic dyslipidemia, maraviroc reduced the atherosclerotic progression by int

112 treatment with the CCL5 receptor antagonist Maraviroc reduces TAM infiltration.

113 We assessed whether CCR5 blockade with maraviroc reduces the risk of IRIS.

114 We ascertained whether CCR5 blockade using maraviroc reduces the risk of IRIS.

115 sequence mutations are the key to conferring maraviroc resistance, the specific changes involved are

116 ed to identify molecular changes that confer maraviroc resistance.

117 revious data suggest that CCR5 blockade with maraviroc results in a low incidence of visceral GVHD.

118 by a general ritonavir-induced inflammation, maraviroc reversed the proinflammatory profile.

119 Maraviroc saliva AUCs were approximately 70% lower than

120 ransmitted viruses were more likely to use a maraviroc-sensitive conformation of CCR5, perhaps identi

121 We found that maraviroc significantly reduced the Treg frequency in bo

122 cells in the presence of the CCR5 antagonist maraviroc, suggesting that non-CCR5 entry pathways can s

123 in HIV-1 RNA from baseline was greater with maraviroc than with placebo: -1.66 and -1.82 log(10) cop

124 There is one CCR5 antagonist, maraviroc, that is FDA-approved for treatment of HIV-1 i

125 tion is directly applied to the synthesis of Maraviroc, the selective CCR5 antagonist with potent act

126 After stopping maraviroc, they were followed for an additional 24 weeks

127 llo-HSCT with standard GVHD prophylaxis plus maraviroc to a contemporary control cohort receiving sta

128 ly, 3 days or more of oral administration of Maraviroc to healthy volunteers conferred protection aga

129 Adding maraviroc to suppressive ART for 24 weeks was not associ

130 al reduction in the frequency of Tregs among maraviroc-treated peripheral blood mononuclear cells (PB

131 Compared with placebo-treated subjects, maraviroc-treated subjects unexpectedly experienced a gr

132 ssive function of Tregs was also analyzed in maraviroc-treated Tregs.

133 icantly correlated with inflammation whereas maraviroc treatment abolished this correlation.

134 At day 30, maraviroc treatment increased CCR5 expression on T cells

135 Maraviroc treatment was associated with a lower incidenc

136 Most women (12; 67%) received 150 mg of maraviroc twice daily with a protease inhibitor, 2 (11%)

137 regimens consisting of maraviroc once daily, maraviroc twice daily, or placebo, each of which include

138 62 cells/microL among patients who received maraviroc twice daily.

139 drop lectin and Griffithsin, and to T-20 and maraviroc, two anti-HIV drugs currently in clinical use.

140 -blind, placebo-controlled, phase 3 studies--Maraviroc versus Optimized Therapy in Viremic Antiretrov

141 ant differences in this ratio were found for maraviroc, vicriviroc, aplaviroc, Sch-C, TAK652, and TAK

142 Five clinical candidates: maraviroc, vicriviroc, aplaviroc, TAK-779, and TAK-220 w

143 er mL on antiretroviral therapy (ART) to add maraviroc vs placebo to their regimen for 24 weeks follo

144 igned-rank test was used to evaluate whether maraviroc was associated with an increase of at least 20

145 antagonist maraviroc, despite the fact that maraviroc was capable of blocking the CCR5-tropic strain

146 More pharmacologically available maraviroc was found in SP than BP.

147 Moreover, treatment with a CCR5 antagonist, maraviroc, was protective against C5a-ALI.

148 ratios for third-trimester versus postpartum maraviroc were 0.72 (90% confidence interval, .60-.88) f

149 inhibitor enfuvirtide or the CCR5 antagonist maraviroc were observed.

150 s no synergy was found between mAb 45523 and maraviroc, which do compete for binding to CCR5.

151 uced-intensity allogeneic HSCT that combined maraviroc with standard GVHD prophylaxis.