ライフサイエンスコーパス: valdecoxib

1 d 3,4,5-trisubstituted isoxazoles, including valdecoxib.

2 s compared to the combination of aspirin and valdecoxib.

3 ffect sizes derived from trials of celecoxib/valdecoxib.

4 ed as constrained analogues of celecoxib and valdecoxib.

5 mides, different from those of celecoxib and valdecoxib.

6 Rats were treated with vehicle or valdecoxib 15 min before or 1.5, 3 and 6 h after cerebra

7 (-1)+ATV 10 mg x kg(-1) x d(-1); PIO+ATV and valdecoxib, a selective cyclooxygenase-2 (COX-2) inhibit

8 Valdecoxib administered at 1.5 h after ischemia signific

9 The use of parecoxib and valdecoxib after CABG was associated with an increased i

10 ple, HCV NS5B and COX-2 inhibitors including valdecoxib and celecoxib derivatives) and precursors of

11 Valdecoxib and its intravenous prodrug parecoxib are use

12 lted in more consistent associations between valdecoxib and MI across sequential monitoring periods.

13 toxicity of rofecoxib, celecoxib, parecoxib, valdecoxib and naproxen.

14 bo alone, both the group given parecoxib and valdecoxib and the group given placebo and valdecoxib ha

15 Both valdecoxib and zileuton abrogated the PIO+ATV increase i

16 inhibitors (coxibs), particularly rofecoxib, valdecoxib, and parecoxib, increases risk for cardiovasc

17 and most hydrogen bonds are chlorthalidone, valdecoxib, and ZINC14824819, which interact with the Rd

18 the study period (celecoxib, rofecoxib, and valdecoxib), as well as oral formulations of diclofenac,

19 ages of 200 mg/day and 100 mg twice daily or valdecoxib at a dosage of 10 mg/day (0.26 and 0.16, resp

20 d to the withdrawal of rofecoxib (Vioxx) and valdecoxib (Bextra), but the mechanisms underlying these

21 rofecoxib (Vioxx), celecoxib (Celebrex), and valdecoxib (Bextra), have been developed for treating ar

22 market entry for 3 medications and outcomes (valdecoxib for myocardial infarction (MI), aripiprazole

23 Two compounds (celecoxib and valdecoxib) from the diarylheterocycle class of cyclooxy

24 d valdecoxib and the group given placebo and valdecoxib had a higher proportion of patients with at l

25 xib, etoricoxib, lumiracoxib, rofecoxib, and valdecoxib have been developed and the greatest recent g

26 of coxibs (etoricoxib, celecoxib, rofecoxib, valdecoxib) in patients with hip and/or knee OA.

27 e results suggest that COX-2 inhibition with valdecoxib is effective when initiated both before and a

28 2.3 nM) was similar to the affinity of [(3)H]valdecoxib (K(D) = 3.2 nM).

29 io (EOR) in the months immediately following valdecoxib market entry implausibly suggested a 12-fold

30 ket', affected the binding affinity of [(3)H]valdecoxib more than that of [(3)H]celecoxib.

31 day 10; intravenous placebo followed by oral valdecoxib; or placebo for 10 days.

32 populations (40 rofecoxib, 37 celecoxib, 29 valdecoxib + parecoxib, 15 etoricoxib, and 6 lumiracoxib

33 Valdecoxib reduced basal brain prostaglandin E(2) concen

34 1/2) = 98 min) for [(3)H]celecoxib and [(3)H]valdecoxib, respectively.

35 quent among the patients given parecoxib and valdecoxib than among those given placebo (2.0 percent v

36 ecoxib for at least 3 days, followed by oral valdecoxib through day 10; intravenous placebo followed

37 rties and binding constants of celecoxib and valdecoxib to COX-2.

38 Valdecoxib treatment was associated with a decrease in i

39 oxib/etoricoxib trials than in the celecoxib/valdecoxib trials.

40 selective cyclooxygenase (COX)-2 inhibitor, valdecoxib, were investigated in a rat model of temporar

41 Recently, two COX-2 drugs, rofecoxib and valdecoxib, were withdrawn from the United States market