ライフサイエンスコーパス: argatroban

1 ifibatide); or DTIs (r-hirudin, bivalirudin, argatroban).

2 outcome were lower in the patients receiving argatroban.

3 fluorogenic substrate, and (iv) titration of argatroban (0-1.5 microg/mL) into plugs and measurement

4 Argatroban 2 microg x kg x min, adjusted to achieve acti

5 nt (fondaparinux = 133, danaparoid = 59, and argatroban = 47) for suspected or confirmed HIT.

6 Intravenous infusion of argatroban, a direct thrombin inhibitor, alleviated neur

7 study evaluating the efficacy and safety of argatroban, a direct thrombin inhibitor, as anticoagulan

8 44) received 2 microgram. kg(-1). min(-1) IV argatroban, adjusted to maintain the activated partial t

9 Argatroban administration significantly reduced hepatic

10 urred in 37.5% of heparin, 32.0% of low-dose argatroban and 25.5% of high-dose argatroban patients (p

11 onal costs, fondaparinux prevailed over both argatroban and bivalirudin in terms of cost ($151 vs $12

12 inux has similar effectiveness and safety as argatroban and danaparoid in patients with suspected HIT

13 Argatroban and lepirudin are well studied and approved d

14 direct thrombin inhibitors (DTI; lepirudin, argatroban) and danaparoid.

15 Argatroban anticoagulation, compared with historical con

16 ice were given the direct thrombin inhibitor argatroban approximately 15 mg/kg/day or its vehicle via

17 Argatroban, as compared with heparin, appears to enhance

18 e conducted a cost-effectiveness analysis of argatroban, bivalirudin, and fondaparinux for the treatm

19 rin agents such as fondaparinux, danaparoid, argatroban, bivalirudin, or one of the new direct-acting

20 switching to a nonheparin anticoagulant (ie, argatroban, danaparoid) upon clinical suspicion.

21 Argatroban did not significantly impact hepatic steatosi

22 Analysis of the argatroban dose-response data with a competitive inhibit

23 nearly a half, whereas doubling the dose of argatroban from its IC50 would decrease coagulation acti

24 In the argatroban group, baseline platelet counts were signific

25 c analyses demonstrated that permeation with argatroban had no significant effects on clot structure.

26 In vitro and in vivo studies have shown that argatroban has advantages over heparin for the inhibitio

27 The antithrombotic activity of argatroban has been quantified in fibrin clot permeation

28 Hirudin and argatroban have found their niche for the treatment of p

29 to heparin, low-dose argatroban or high-dose argatroban in addition to TPA.

30 were hemorrhagic (one per group, none during argatroban infusion); 30 (86%) were present at or within

31 m was developed to titrate an anticoagulant (argatroban) into blood samples and to measure the clotti

32 clot permeation system have also shown that argatroban is a potent inhibitor of clot-bound thrombin,

33 We conclude that argatroban is an effective inhibitor of thrombin bound t

34 nd is not approved in the United States; and argatroban is contraindicated in patients with impaired

35 84 (43.1%) had been treated first-line with argatroban, lepirudin, danaparoid, and fondaparinux, res

36 th the alternative nonheparin anticoagulants argatroban, lepirudin, or danaparoid.

37 29 patients (21.5%) received treatment with argatroban, lepirudin, or fondaparinux: 10 of 10 heparin

38 a small-molecule, direct thrombin inhibitor, argatroban, on reperfusion induced by tissue plasminogen

39 and adverse events averted compared with IV argatroban or bivalirudin infusions.

40 hin 6 h were randomized to heparin, low-dose argatroban or high-dose argatroban in addition to TPA.

41 arin with a direct thrombin inhibitor (e.g., argatroban or lepirudin) or the heparinoid danaparoid (w

42 First-line therapies for HIT are argatroban or lepirudin.

43 ieved in 42.1% of heparin, 56.8% of low-dose argatroban (p = 0.20 vs. heparin) and 58.7% of high-dose

44 p = 0.20 vs. heparin) and 58.7% of high-dose argatroban patients (p = 0.13 vs. heparin).

45 f low-dose argatroban and 25.5% of high-dose argatroban patients (p = 0.23).

46 d in 2.6% and 4.3% of low-dose and high-dose argatroban patients, respectively.

47 Argatroban reduced both alpha-smooth muscle actin expres

48 Argatroban reduced serum triglyceride and cholesterol le

49 ed cognitive deficit, whereas rats receiving argatroban retained intact learning and memory.

50 tissue-type plasminogen activator (tPA), on argatroban's ability to inhibit thrombin.

51 creased the available thrombin activity, yet argatroban still inhibited this clot-associated thrombin

52 Argatroban therapy vs. control significantly reduces the

53 Argatroban therapy, relative to control subjects, also s

54 Argatroban-treated patients achieved therapeutic activat

55 tio, 4.10; 95% CI, 1.12-15.01; p =.033), and argatroban-treated patients had significantly reduced od

56 new thrombosis, was reduced significantly in argatroban-treated patients versus control subjects with

57 In HITTS, the composite incidence in argatroban-treated patients was 43.8% versus 56.5% in co

58 s with heparin-induced thrombocytopenia (767 argatroban-treated patients, 193 historical controls).

59 analysis of the composite end point favored argatroban treatment in HIT (P=0.010) and HITTS (P=0.014

60 was significantly more frequent in high-dose argatroban versus heparin patients: 57.1% versus 20.0% (

61 The Hill coefficient for argatroban was the lowest, at 1.7 +/- 0.2 (95% confidenc

62 all molecule active site inhibitors, such as argatroban, were the observation that fibrinopeptide A h