ライフサイエンスコーパス: vorapaxar

1 for whom there is a clinical indication for vorapaxar.

2 ith or without the thrombin receptor blocker vorapaxar.

3 ignificantly lower in patients randomized to vorapaxar.

4 ry preventive therapy such as treatment with vorapaxar.

5 end point did not differ significantly with vorapaxar (11.3% versus 11.9%; hazard ratio, 0.94; 95% c

6 e, or peripheral arterial disease to receive vorapaxar (2.5 mg daily) or matching placebo and followe

7 ith a history of atherothrombosis to receive vorapaxar (2.5 mg daily) or matching placebo in a 1:1 ra

8 Vorapaxar, a novel thrombin receptor antagonist, reduces

9 ion crystal structure of human PAR1 bound to vorapaxar, a PAR1 antagonist.

10 The only marketed drug targeting a PAR is vorapaxar, a selective antagonist of PAR1 used to preven

11 ical outcome was increasingly favorable with vorapaxar across risk groups.

12 ing receiving standard antiplatelet therapy, vorapaxar administered for long-term secondary preventio

13 We aimed to assess efficacy and safety of vorapaxar among CABG patients.

14 thway was confirmed in human psoriasis using vorapaxar, an FDA-approved PAR1 antagonist, on explanted

15 ng occurred in 4.2% of patients who received vorapaxar and 2.5% of those who received placebo (hazard

16 arction and were assigned treatment (8898 to vorapaxar and 8881 to placebo).

17 xar, but not significantly different between vorapaxar and placebo (9.7% vs. 7.3%; HR: 1.36; 95% CI:

18 rtic valve stenosis; and antiplatelet agents vorapaxar and prasugrel for reducing cardiovascular even

19 More intensive antiplatelet therapy (vorapaxar and ticagrelor pooled) significantly reduced t

20 e or severe bleeding risk was increased with vorapaxar and was not significantly altered by planned t

21 ents-Thrombolysis in Myocardial Infarction) (vorapaxar) and PEGASUS-TIMI 54 (Prevention of Cardiovasc

22 rdiovascular disease/MI/ischemic stroke with vorapaxar, and intermediate-risk patients (1-2 risk indi

23 Vorapaxar antagonizes protease-activated receptor 1, the

24 e-activated G-protein-coupled receptors, the vorapaxar-binding pocket is superficial but has little s

25 Vorapaxar blocks the activity of that pathway.

26 n major bleeding was numerically higher with vorapaxar, but not significantly different between vorap

27 Bleeding occurred more frequently with vorapaxar compared with placebo (7.4% versus 4.5%; hazar

28 studies using a C-ring-truncated version of Vorapaxar culminated in the discovery of three leads, re

29 Vorapaxar did not reduce the risk of cardiovascular deat

30 n the rate of intracranial hemorrhage in the vorapaxar group (1.0%, vs. 0.5% in the placebo group; P<

31 ion occurred in 1259 patients (11.2%) in the vorapaxar group and 1417 patients (12.4%) in the placebo

32 oderate and severe bleeding were 7.2% in the vorapaxar group and 5.2% in the placebo group (hazard ra

33 roke occurred in 610 of 8898 patients in the vorapaxar group and 750 of 8881 in the placebo group (3-

34 had occurred in 1028 patients (9.3%) in the vorapaxar group and in 1176 patients (10.5%) in the plac

35 n, or stroke occurred in 822 patients in the vorapaxar group versus 910 in the placebo group (14.7% a

36 te or severe bleeding was more common in the vorapaxar group versus the placebo group (241/8880 [3.4%

37 ) in the placebo group (hazard ratio for the vorapaxar group, 0.87; 95% confidence interval [CI], 0.8

38 The structure of PAR1 in complex with vorapaxar has been reported previously.

39 the protease-activated receptor-1 antagonist vorapaxar, have shown ischaemic benefit.

40 ints (efficacy and safety) was improved with vorapaxar (hazard ratio, 0.79 [95% confidence interval,

41 d, double-blind, placebo-controlled trial of vorapaxar in 26 449 patients with stable atherosclerotic

42 d, double-blind, placebo-controlled trial of vorapaxar in 26,449 patients with previous atherothrombo

43 We examined the efficacy of vorapaxar in patients with and without DM who qualified

44 moderate/severe bleeding was increased with vorapaxar in patients with DM (4.4% versus 2.6%; hazard

45 d, double-blind, placebo-controlled trial of vorapaxar in patients with stable atherosclerosis.

46 es P-TIMI 50 (Trial to Assess the Effects of Vorapaxar in Preventing Heart Attack and Stroke in Patie

47 The Trial to Assess the Effects of Vorapaxar in Preventing Heart Attack and Stroke in Patie

48 d, double-blind, placebo-controlled trial of vorapaxar in stable patients with prior myocardial infar

49 d, double-blind, placebo-controlled trial of vorapaxar in stable patients, including 3787 with sympto

50 Vorapaxar increased GUSTO moderate/severe bleeding (HR:

51 thelial cells to nanomolar concentrations of vorapaxar induces endothelial cell barrier dysfunction a

52 ntrast, orthosteric PAR1 antagonists such as vorapaxar inhibit all signaling downstream of PAR1.

53 PAR4 genotype did not affect vorapaxar inhibition of platelet PAR1 function, but a st

54 Vorapaxar inhibits platelet activation by antagonising t

55 Inhibiting PAR1 signaling with vorapaxar interrupts this process, reduces the burden of

56 Vorapaxar is a new oral protease-activated-receptor 1 (P

57 Vorapaxar is a novel antagonist of protease-activated re

58 Vorapaxar is a novel antiplatelet agent that selectively

59 Vorapaxar is an approved drug for the reduction of throm

60 Because vorapaxar is contraindicated in patients with a history

61 Subsequent to the discovery of Vorapaxar, medicinal chemistry efforts were continued to

62 of protease-activated receptor-1 antagonist vorapaxar (Merck, Whitehouse Station, New Jersey) versus

63 rotease-activated receptor 1 antagonism with vorapaxar reduced ALI overall and by type.

64 Vorapaxar reduced ARC definite ST (1.1% vs. 1.4%, hazard

65 Vorapaxar reduced cardiovascular death, MI, or stroke in

66 Vorapaxar reduced first ALI events by 41% (hazard ratio,

67 Inhibition of PAR-1 with vorapaxar reduced the risk of cardiovascular death or is

68 Vorapaxar reduces ALI in patients with symptomatic PAD w

69 Vorapaxar reduces cardiovascular death, myocardial infar

70 s to test the hypothesis that treatment with vorapaxar reduces the rate of coronary stent thrombosis

71 bition of protease-activated receptor 1 with vorapaxar reduces the risk of cardiovascular death or is

72 The efficacy and safety of vorapaxar (SCH 530348; MK-5348) were assessed by baselin

73 (Trial to Assess the Effects of Vorapaxar [SCH 530348; MK-5348] in Preventing Heart Atta

74 NCT00391872; Trial to Assess the Effects of Vorapaxar [SCH 530348; MK-5348] in Preventing Heart Atta

75 nts with peripheral artery disease; however, vorapaxar significantly reduced acute limb ischemia and

76 Vorapaxar significantly reduced the composite of cardiov

77 In patients with DM (n=3623), vorapaxar significantly reduced the primary end point (1

78 sity or Western diet/CCl 4 were treated with vorapaxar to determine effects on hepatocyte senescence

79 We used vorapaxar to determine if and how THBD-PAR1 signaling pr

80 th acute coronary syndromes, the addition of vorapaxar to standard therapy did not significantly redu

81 nts with previous MI and DM, the addition of vorapaxar to standard therapy significantly reduced the

82 Compared with placebo CABG patients, vorapaxar-treated patients had a 45% lower rate of the p

83 assist with therapeutic decision making for vorapaxar use for secondary prevention after MI.

84 occurred in 1031 of 6473 patients receiving vorapaxar versus 1102 of 6471 patients receiving placebo

85 ts (0.6%, 3-year Kaplan-Meier estimate) with vorapaxar versus 28 of 8849 (0.4%, 3-year Kaplan-Meier e

86 coronary syndrome patients undergoing CABG, vorapaxar was associated with a significant reduction in

87 The efficacy of vorapaxar was consistent across types of ALI.

88 cacy and safety of antiplatelet therapy with vorapaxar was modified by concurrent thienopyridine use.

89 increased bleeding, an efficacy signal with vorapaxar was noted on major ischemic outcomes, and prel

90 double-blind, randomized trial, we compared vorapaxar with placebo in 12,944 patients who had acute