ライフサイエンスコーパス: atrasentan

1 of docetaxel plus prednisone with or without atrasentan.

2 tive endothelin A receptor (ET(A)R) blocker, atrasentan.

3 Participants were given atrasentan 0.75 mg orally daily during an enrichment per

4 ers were randomly assigned to receive either atrasentan 0.75 mg orally daily or placebo.

5 tio (UACR) of 100 to 3000 mg/g to placebo or atrasentan (0.25, 0.75, or 1.75 mg daily) for 8 weeks.

6 Patients were randomly assigned to receive atrasentan (0.75 mg per day) or matched placebo for 132

7 nner to either the ET(A) receptor antagonist atrasentan (10 mg) or placebo for 6 months.

8 5 mg/m(2) every 21 days, intravenously) with atrasentan (10 mg/day, orally) or placebo for up to 12 c

9 e to baseline was significantly greater with atrasentan (-38.1%) than with placebo (-3.1%), with a ge

10 ated with vehicle, ET(A) receptor antagonist atrasentan (5 mg x kg(-1) x day(-1)), or ET(B) receptor

11 Treatment with atrasentan (7.5 mg/kg/day) for 4 weeks reduced urinary a

12 Here, we examined the effect of atrasentan, a selective endothelin A receptor (ET(A)R) a

13 Atrasentan, a selective endothelin A receptor antagonist

14 increase in selectivity when the methoxy of Atrasentan (ABT-627) is replaced with methyl, and the be

15 tment with combined SGLT2i/atrasentan versus atrasentan alone decreased body weight, a surrogate for

16 Atrasentan also reduced the rate of all (first and subse

17 Atrasentan, an endothelin antagonist, binds selectively

18 Atrasentan, an endothelin receptor antagonist, has shown

19 n between the endothelin receptor antagonist atrasentan and pain and prescription of analgesics.

20 138.2 and 170.2 per 1000 person-years in the atrasentan and placebo group respectively (hazard ratio

21 adium-223, endothelin-A receptor antagonists atrasentan and zibotentan, proto-oncogene tyrosine-prote

22 f drugs that block endothelin receptors (eg, atrasentan) and non-steroidal mineralocorticoid receptor

23 tasis through the antialbuminuric effects of atrasentan, and they provide a mechanistic explanation f

24 In summary, atrasentan, at the doses tested, is generally safe and e

25 augmented in GK rats, which was reversed by atrasentan but exacerbated with A-192621.

26 e-proportional pharmacokinetics suggest that atrasentan can be easily and consistently dosed.

27 plied Cox regression to assess the effect of atrasentan compared to placebo on the risk of the first

28 patients (14 prostate) were treated at daily atrasentan doses of 10, 20, 30, 45, 60, and 75 mg (n = 3

29 responders and were randomly assigned to the atrasentan group (n=1325) or placebo group (n=1323).

30 79 (6.0%) of 1325 patients in the atrasentan group and 105 (7.9%) of 1323 in the placebo g

31 ccurred in 47 (3.5%) of 1325 patients in the atrasentan group and 34 (2.6%) of 1323 patients in the p

32 498 patients were randomly assigned to the atrasentan group and 496 to the placebo group.

33 58 (4.4%) patients in the atrasentan group and 52 (3.9%) in the placebo group died

34 n PFS was 9.2 months (95% CI 8.5-9.9) in the atrasentan group and 9.1 months (8.4-10.2) in the placeb

35 eported by 19 of 169 patients (11.2%) in the atrasentan group and in 14 of 170 (8.2%) in the placebo

36 Three deaths in the atrasentan group and seven in the placebo group were jud

37 etylcholine at 6 months from baseline in the atrasentan group compared with the placebo group (39.67%

38 278 (57%) of 492 patients in the atrasentan group had grade 3 and greater toxicity compar

39 eptor antagonists, were more frequent in the atrasentan group than in the placebo group.

40 survival was 17.8 months (16.4-19.8) in the atrasentan group versus 17.6 months (16.4-20.1) in the p

41 42, and 35% in the 0.25-, 0.75-, and 1.75-mg atrasentan groups (P=0.291, P=0.023, and P=0.073, respec

42 50, and 38% in the 0.25-, 0.75-, and 1.75-mg atrasentan groups, respectively (P=0.029 for 0.75 mg ver

43 udy demonstrates that 6-month treatment with atrasentan improves coronary microvascular endothelial f

44 rmacokinetics, and maximum-tolerated dose of atrasentan in cancer patients.

45 cal observations of reduced albuminuria with atrasentan in diabetic nephropathy.

46 canagliflozin, dapagliflozin, finerenone and atrasentan in patients with chronic kidney disease.

47 ective endothelin type A receptor antagonist atrasentan in reducing proteinuria in patients with IgA

48 Patients treated with atrasentan initiated fewer analgesics including NSAIDs a

49 of canagliflozin, dapagliflozin, finerenone, atrasentan, losartan, irbesartan, and aliskiren in patie

50 port the long-term effects of treatment with atrasentan on major renal outcomes.

51 Participants were randomized to receive atrasentan or placebo (1834 each arm).

52 ress on treatment were permitted to continue atrasentan or placebo for up to 52 weeks.

53 Atrasentan prevented this increase, whereas A-192621 cau

54 and cocultured with pericytes confirmed that atrasentan reduced endothelial heparanase expression and

55 Atrasentan reduced the risk of renal events in patients

56 2 diabetes and CKD, the selective ET(A) ERA, atrasentan, reduced albuminuria and kidney function decl

57 e selective endothelin A receptor antagonist atrasentan reduces albuminuria without causing significa

58 6% of those receiving 0.25, 0.5, and 1.75 mg atrasentan, respectively (P=0.007 for 1.75 mg versus pla

59 Blocking the ET(A)R with atrasentan restored glomerular thrombomodulin protein le

60 In this prespecified interim analysis, atrasentan resulted in a significant and clinically mean

61 Adverse events were consistent with atrasentan's pharmacologic vasodilatory effect.

62 Compared with placebo, atrasentan significantly reduced UACR only in the 0.75-

63 the endothelin receptor-specific antagonist, atrasentan, thereby blocking engagement of the up-regula

64 Therefore we tested the potential of atrasentan to stabilize the endothelial glycocalyx in di

65 nsmission electron microscopy, revealed that atrasentan treatment increases glycocalyx coverage in di

66 MMP-2 activity in diabetes was prevented by atrasentan treatment.

67 -of-run-in for placebo and end-of-run-in for atrasentan) until end-of-treatment.

68 hat six-weeks treatment with combined SGLT2i/atrasentan versus atrasentan alone decreased body weight

69 The effect of atrasentan versus placebo on chronic GFR slope was 0.72

70 with a randomized withdrawal (SONAR testing atrasentan vs placebo).

71 Thus, atrasentan was associated with reduced pain-related even

72 Atrasentan was rapidly absorbed; the time to maximum obs

73 Atrasentan, when added to docetaxel, does not improve ov

74 of the endothelin receptor antagonist (ERA) atrasentan while effects on albuminuria and kidney prote

75 d use of ET(A) receptor antagonist (ABT-627; Atrasentan) with Taxotere will be superior in inducing a