ライフサイエンスコーパス: CCR5 antagonist

1 c prostate cancer burden was reduced by oral CCR5 antagonist.

2 roc (VCV), an investigational small-molecule CCR5 antagonist.

3 atient is necessary prior to treating with a CCR5 antagonist.

4 e inflamed lesion, which can be blocked by a CCR5 antagonist.

5 ase with previous HIV-1 strains resistant to CCR5 antagonists.

6 classes, including integrase inhibitors and CCR5 antagonists.

7 d was completely resistant to small molecule CCR5 antagonists.

8 human immunodeficiency virus type 1 (HIV-1) CCR5 antagonists.

9 combination with a variety of small molecule CCR5 antagonists.

10 to retrieve new chemical entities as potent CCR5 antagonists.

11 present a particularly attractive target for CCR5 antagonists.

12 competition underlies inhibitory effects of CCR5 antagonists and explains why adaptive HIV-1 mutatio

13 by which HIV envelopes acquire resistance to CCR5 antagonists and may have more general implications

14 were cross resistant to other small-molecule CCR5 antagonists, and were isolated from the patient's p

15 Maraviroc, a CCR5 antagonist antiretroviral drug, might provide benef

16 ins isolated from a patient treated with the CCR5 antagonist aplaviroc (APL) that were drug resistant

17 Furthermore, the CCR5 antagonist aplaviroc was converted to a full agonis

18 ternative coreceptor for HIV-1 entry, CXCR4; CCR5 antagonists are not effective in patients harboring

19 In addition to virologic effects, CCR5 antagonists are under investigation for immune-modu

20 an oxime-piperidine compound, is a specific CCR5 antagonist as determined in multiple receptor bindi

21 e series of piperidine- and piperazine-based CCR5 antagonists as anti-HIV-1 agents reported by Scheri

22 a-associated herpesvirus, is a high affinity CCR5 antagonist, but lacks efficacy as a coreceptor inhi

23 Therefore, we propose that a CCR5 antagonist can serve for HCC cancer prevention and

24 e identification of a novel potent series of CCR5 antagonists containing the imidazolidinylpiperidiny

25 Maraviroc is a new CCR5 antagonist designed to block HIV entry.

26 he design and development of next generation CCR5 antagonists, docking models for major classes of CC

27 ance to vicriviroc (VCV), an investigational CCR5 antagonist, during 28 weeks of therapy.

28 ist-resistant viruses, then continued use of CCR5 antagonists even in the face of virologic failure c

29 (SCH 351125) as an orally bioavailable human CCR5 antagonist for the treatment of HIV-1 infection.

30 CCR5 is a co-receptor for HIV and CCR5 antagonists have been investigated as inhibitors of

31 A large number of small-molecule CCR5 antagonists have been reported that show potent act

32 d 1,3,4-trisubstituted pyrrolidines as human CCR5 antagonists have recently been disclosed.

33 ated by mapping onto it a diverse set of six CCR5 antagonists identified by five different pharmaceut

34 , which may impose constraints on the use of CCR5 antagonists in certain regions of the world.

35 research will further elucidate the role of CCR5 antagonists in combating HIV disease.

36 Further studies of CCR5 antagonists in the dampening of immune activation a

37 ese viruses remained sensitive to most other CCR5 antagonists, including vicriviroc and aplaviroc.

38 CCR5 antagonists inhibit HIV entry by binding to a corec

39 CCR5 antagonists inhibit HIV-1 entry by blocking the int

40 Although resistance to one CCR5 antagonist is often associated with broad cross-res

41 Maraviroc, a CCR5 antagonist, is active against R5 but not X4 or dual

42 CC Envs exhibited partial resistance to the CCR5 antagonist maraviroc (MVC) on cells expressing high

43 failure on treatment regimens containing the CCR5 antagonist maraviroc (MVC).

44 The CCR5 antagonist maraviroc is approved for use in treatme

45 We tested the in vitro effect of the CCR5 antagonist maraviroc on lymphocyte function and che

46 y to the fusion inhibitor enfuvirtide or the CCR5 antagonist maraviroc were observed.

47 INK128 enhanced the antiviral potency of the CCR5 antagonist maraviroc, and had favorable antiviral i

48 onuclear cells (PBMC) in the presence of the CCR5 antagonist maraviroc, despite the fact that maravir

49 ood mononuclear cells in the presence of the CCR5 antagonist maraviroc, suggesting that non-CCR5 entr

50 ced sensitivities to VCV and to the licensed CCR5 antagonist maraviroc.

51 The CCR5 antagonists maraviroc or vicriviroc, developed to b

52 There is one CCR5 antagonist, maraviroc, that is FDA-approved for tre

53 Moreover, treatment with a CCR5 antagonist, maraviroc, was protective against C5a-A

54 The principal obstacle to the CCR5-antagonist, maraviroc, from being more widely used

55 f basal breast cancer cells and suggest that CCR5 antagonists may be used as an adjuvant therapy to r

56 Additionally, CCR5 antagonists may not reduce the HIV-1 RNA load when

57 ed the effects of a potent, highly selective CCR5 antagonist, Merck's compound 167 (CMPD 167), in an

58 Using a selective CCR5 antagonist, methionine-RANTES, CCL2 expression was

59 more potent than a mixture of mu agonist and CCR5 antagonist monovalent ligands.

60 predicted the binding site of the dual CCR2/CCR5 antagonist N-dimethyl-N-[4-[[[2-(4-methylphenyl)-6,

61 Maraviroc (CCR5 antagonist) or CCL5 immunodepletion diminished 95%

62 C series) that contain mu opioid agonist and CCR5 antagonist pharmacophores linked through homologous

63 adaptive amino acid changes had no impact on CCR5 antagonist resistance but made virus more sensitive

64 olates from three participants who developed CCR5 antagonist resistance during treatment with vicrivi

65 on mechanism that underlies the emergence of CCR5 antagonist resistance.

66 In contrast to previous reports in which CCR5 antagonist-resistant viruses interact predominantly

67 opism shift proves to be a common feature of CCR5-antagonist-resistant viruses, then continued use of

68 We describe the use of two CCR5 antagonists, Schering-C (SCH-C), which is specific

69 HIV CCR5 antagonists select for env gene mutations that enab

70 not efficiently blocked by a small-molecule CCR5 antagonist, suggesting that sMagi cells express as-

71 ibitors, and entry inhibitors, including the CCR5 antagonist TAK-779 and the CXCR4 antagonist AMD3100

72 RAPA enhanced the antiviral activity of the CCR5 antagonist TAK-779.

73 ced replication, cross-resistance to another CCR5 antagonist, TAK779, and increased sensitivity to am

74 Cenicriviroc, a small-molecule CCR5 antagonist that also has activity as a CCR2 antagon

75 Maraviroc (MVC) is a CCR5 antagonist that inhibits HIV-1 entry by binding to

76 riviroc is a C-C motif chemokine receptor 5 (CCR5) antagonist that is in clinical development for the

77 We propose that the restoration of pre-CCR5 antagonist therapy HIV entry kinetics drives the se

78 tool for determining patient eligibility for CCR5 antagonist therapy.

79 T-cell recovery, subjects added maraviroc, a CCR5 antagonist, to their existing ART for 24 weeks.

80 ologic failure from a phase IIb study of the CCR5 antagonist vicriviroc (VCV) and identified one indi

81 gonists, docking models for major classes of CCR5 antagonists were created by using site-directed mut

82 inus are broadly cross-resistant to multiple CCR5 antagonists, whereas viruses that require both the

83 -350634 (1), a prototypical piperazine-based CCR5 antagonist, which is a potent inhibitor of HIV-1 en

84 Vicriviroc (VCV) is a CCR5 antagonist with nanomolar activity against human im

85 to the synthesis of Maraviroc, the selective CCR5 antagonist with potent activity against HIV-1 infec

86 the discovery of SCH 351125 (1), a selective CCR5 antagonist with potent activity against RANTES bind

87 We recently described a novel class of CCR5 antagonists with strong anti-HIV potency.

88 (VCV) is a chemokine (C-C motif) receptor 5 (CCR5) antagonist with potent anti-HIV activity that curr

89 rmations by many CC Envs was seen with other CCR5 antagonists, with replication-competent viruses, an