ライフサイエンスコーパス: atrasentan

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1 of docetaxel plus prednisone with or without atrasentan.

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

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

4 5 mg/m(2) every 21 days, intravenously) with atrasentan (10 mg/day, orally) or placebo for up to 12 c

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

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

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

8 Atrasentan, a selective endothelin A receptor antagonist

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

10 Atrasentan, an endothelin antagonist, binds selectively

11 Atrasentan, an endothelin receptor antagonist, has shown

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

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

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

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

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

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

18 498 patients were randomly assigned to the atrasentan group and 496 to the placebo group.

19 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

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

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

22 278 (57%) of 492 patients in the atrasentan group had grade 3 and greater toxicity compar

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

24 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

25 50, and 38% in the 0.25-, 0.75-, and 1.75-mg atrasentan groups, respectively (P=0.029 for 0.75 mg ver

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

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

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

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

30 Atrasentan prevented this increase, whereas A-192621 cau

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

32 6% of those receiving 0.25, 0.5, and 1.75 mg atrasentan, respectively (P=0.007 for 1.75 mg versus pla

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

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

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

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

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

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

39 Atrasentan was rapidly absorbed; the time to maximum obs

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

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

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