ライフサイエンスコーパス: maraviroc

1 CR5 co-receptor than the standard antagonist Maraviroc.

2 1; p=0.49) for tacrolimus, methotrexate, and maraviroc.

3 receptor antagonists, including the HIV drug maraviroc.

4 re administration of the antiretroviral drug maraviroc.

5 cline partially reversed after discontinuing maraviroc.

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

7 was blocked by the CCR5-specific antagonist, maraviroc.

8 4 events with tacrolimus, methotrexate, and maraviroc.

9 neurons were suppressed by a CCR5 antagonist Maraviroc.

10 near an allosteric binding site for the drug maraviroc.

11 ich is inhibited by the CCL5/CCR5 antagonist maraviroc.

12 rminants with the FDA-approved HIV inhibitor Maraviroc.

13 ructure of CCR5 receptor cocrystallized with Maraviroc.

14 or tacrolimus, methotrexate, and maraviroc (maraviroc 300 mg orally twice daily from day -3 to day 3

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

16 C-ART plus placebo or maraviroc (300 mg twice daily with dose modification) fo

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

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

19 tezomib; 92 to tacrolimus, methotrexate, and maraviroc; 92 to tacrolimus, mycophenolate mofetil, and

20 Maraviroc, a CCR5 antagonist antiretroviral drug, might

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

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

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

24 found different degrees of responsiveness to maraviroc, a known immunomodulatory CCR5 antagonist, and

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

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

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

28 Maraviroc administrated in postnatal PAE rats, reduces t

29 Maraviroc also reduced the growth-promoting effects of c

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

31 peutic targeting of CCL4-CCR5 signaling with maraviroc, an FDA-approved antiviral drug, significantly

32 bone-targeted nanoparticles (NP) to deliver Maraviroc, an inhibitor of C-C chemokine receptor type 5

33 receptor, CCR5, we examined the efficacy of maraviroc, an inhibitor of CCR5 and a Food and Drug Admi

34 ics simulations to design heterobifunctional maraviroc analogues consisting of a drug fragment connec

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

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

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

38 Both maraviroc and ibalizumab are being studied for preventio

39 These results suggest that low-dose maraviroc and other CCR5 antagonists may be helpful for

40 dard ART"), with some (34.7%) also receiving maraviroc and raltegravir for the first 24 weeks (hereaf

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

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

43 therapeutics used in HIV, [small molecules (maraviroc and vicriviroc) and a humanized mAb (leronlima

44 d 78 [85%] for tacrolimus, methotrexate, and maraviroc) and cardiac (43 [47%], 44 [49%], and 43 [47%]

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

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

47 %) patients had IRIS events, 33 (24%) in the maraviroc arm and 31 (23%) in the placebo arm (p=0.88).

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

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

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

51 Maraviroc, as compared with placebo, resulted in signifi

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

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

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

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

56 The predicted Maraviroc binding site agrees with the recent structure

57 atural amino acids that were adjacent to the maraviroc binding site.

58 We aimed to evaluate regimens using either maraviroc, bortezomib, or post-transplantation cyclophos

59 Maraviroc (CCR5 antagonist) or CCL5 immunodepletion dimi

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

61 1, obtained from 20 patients who enrolled in maraviroc clinical trials and experienced treatment fail

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

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

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

65 Maraviroc-containing PrEP for women may warrant further

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

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

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

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

70 Moreover, maraviroc counterregulated ritonavir-induced lipoatrophy

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

72 NP-mediated Maraviroc delivery partially restored the BMME, signific

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

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

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

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

77 DTG-based (n = 92), or DTG intensified with maraviroc (DTG/MVC, n = 35).

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

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

80 Overall maraviroc exposure during pregnancy was decreased, with

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

82 Tetherable low-affinity maraviroc fragments displayed an increase in potency for

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

84 rbidity was 11.1 per 100 person-years in the maraviroc group and 11.2 per 100 person-years in the pla

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

86 %) patients had IRIS events, 33 (24%) in the maraviroc group and 31 (23%) in the placebo group (p=0.7

87 37 participants (26%) in the maraviroc group had grade 3 or 4 adverse events compared

88 nts (207 in the placebo group and 202 in the maraviroc group) who received more than 1 dose were incl

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

90 Maraviroc had no significant effect on development of IR

91 Maraviroc had no significant effect on frequency, time o

92 A CCR5 inhibitor Maraviroc has been approved for blocking HIV entry; howe

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

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

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

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

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

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

99 Maraviroc inhibited CCR5 internalization and lymphocyte

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

101 During maraviroc intensification, plasma lipopolysaccharide dec

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

103 Incorporation of maraviroc into the experimental model blunted airway hyp

104 Maraviroc is a new CCR5 antagonist designed to block HIV

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

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

107 Although only the CCR5 antagonist maraviroc is US Food and Drug Administration-approved (f

108 Exposure to maraviroc limits the evolution and associated systemic i

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

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

111 after HCT); or tacrolimus, methotrexate, and maraviroc (maraviroc 300 mg orally twice daily from day

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

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

114 ected as a mutation conferring resistance to maraviroc (MVC) in vitro.

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

116 Maraviroc (MVC) is a candidate for human immunodeficienc

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

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

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

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

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

122 he immunologic effects of the CCR5 inhibitor maraviroc (MVC), despite approval for clinical use, have

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

124 nt HIV-1s, but did not show activity against maraviroc (MVC)-resistant HIV-1.

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

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

127 ring patient adherence to the antiretroviral maraviroc (MVC).

128 were also obtained in cultures treated with maraviroc (MVC).

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

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

131 fected macaques and the potential effects of maraviroc on T-cell activation.

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

133 .20 log(10) copies/mL for those who received maraviroc once (P =.83) or twice (P +.38) daily, respect

134 60 cells/microL among patients who received maraviroc once daily, and 62 cells/microL among patients

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

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

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

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

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

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

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

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

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

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

145 owever, oral administration of a low dose of maraviroc protected glia limitans partially, maintained

146 on, inhibition of the CCL5/CCR5 pathway with maraviroc provided unique benefits in reducing airway hy

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

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

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

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

151 g a European Medicines Agency-approved drug, maraviroc, reduced immune cell infiltration, alleviated

152 The FDA-approved CCR5 antagonist, maraviroc, reduced TGFbeta1(+)CCR5(+) neutrophil numbers

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

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

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

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

157 ed to identify molecular changes that confer maraviroc resistance.

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

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

160 Maraviroc saliva AUCs were approximately 70% lower than

161 C-C chemokine receptor type 5 (CCR5) blocker maraviroc (Selzentry).

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

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

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

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

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

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

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

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

170 pported by the ability of the CCR5 inhibitor maraviroc to blunt reactivation.

171 -supportive signals and can be targeted with maraviroc to disrupt the metastatic niche as a safe and

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

173 Addition of maraviroc to standard c-ART does not improve clinical ou

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

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

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

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

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

179 Accordingly, maraviroc treatment also protected both the nigrostriata

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

181 Maraviroc treatment was associated with a lower incidenc

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

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

184 62 cells/microL among patients who received maraviroc twice daily.

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

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

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

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

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

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

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

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

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

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

195 inhibitor enfuvirtide or the CCR5 antagonist maraviroc were observed.

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

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

198 Drug Administration-approved CCR5 inhibitor (maraviroc) with assessment of airway resistance, inflamm