ライフサイエンスコーパス: cilostazol

1 heir sensitivities to inhibition by cGMP and cilostazol.

2 ction, and the phosphodiesterase 3 inhibitor cilostazol.

3 proved by endothelium-targeted drugs such as cilostazol.

4 ebo (0.02, -0.01 to 0.05; P=0.18), or versus cilostazol (-0.01, -0.04 to 0.02; P=0.36), despite incre

5 muM) and the phosphodiesterase-3 inhibitors cilostazol (10 muM) and milrinone (2.5 muM) restored ele

6 l/L) or the phosphodiesterase III inhibitors cilostazol (10 mumol/L) or milrinone (5 mumol/L) diminis

7 antation to receive, in addition to aspirin, cilostazol 100 mg BID or placebo for 6 months; clopidogr

8 nequally (2:1) to 12 weeks of treatment with cilostazol 100 mg PO BID or placebo.

9 scranial ultrasound), with noninferiority to cilostazol 100 mg twice daily.

10 mg, once per day) alone, or a combination of cilostazol (100 mg, twice per day) with aspirin or clopi

11 nt and were randomized to ISMN (40-60 mg/d), cilostazol (200 mg/d), ISMN-cilostazol (40-60 and 200 mg

12 MN (40-60 mg/d), cilostazol (200 mg/d), ISMN-cilostazol (40-60 and 200 mg/d, respectively), or no stu

13 lacebo-controlled trial to determine whether cilostazol, a drug that suppresses intimal proliferation

14 In this study, we assessed whether cilostazol, a phosphodiesterase III inhibitor, could pro

15 ], 0.80 [95% CI, 0.59 to 1.09]; P = .16) nor cilostazol (aHR, 0.77 [95% CI, 0.57 to 1.05]; P = .10) a

16 d elevated CD39 protein (2-fold [P<0.05] for cilostazol and 2.5-fold [P<0.01] for milrinone), while m

17 ualised rate 2.2%) on dual therapy including cilostazol and 64 (7%) of 947 patients (annualised rate

18 lecular models show that the PDE3 inhibitors cilostazol and milrinone share some of common residues b

19 HUVEC ATPase activity increased by 25% with cilostazol and milrinone treatment (P<0.05 and P<0.01, r

20 UVECs) were treated with the PDE3 inhibitors cilostazol and milrinone, then analyzed using qRT-PCR, i

21 Cilostazol and sildenafil did not have negative pharmaco

22 Cilostazol and sildenafil may benefit tuberculosis patie

23 rance in the lung, while the addition of the cilostazol and sildenafil reduced the time to clearance

24 pharmacokinetic interactions between PDE-Is (cilostazol and sildenafil) and rifampin.

25 ance, and relapse when types 3 and 5 PDE-Is (cilostazol and sildenafil, respectively) and rolipram we

26 or angiotensin receptor blockers [ARBs], and cilostazol) and lifestyle counseling (exercise or diet c

27 anscription, inhibitors of PDE3 (siguazodan, cilostazol) and PDE4 (rolipram, GSK256066, roflumilast N

28 Quinidine, cilostazol, and milrinone suppress the hypothermia-induc

29 and examines the effectiveness of quinidine, cilostazol, and milrinone to prevent hypothermia-induced

30 A, F972A and Q975A showed increased K(i) for cilostazol but no difference for milrinone from the reco

31 Cilostazol did not change ATP release in either age grou

32 enosis or a sham operation and fed normal or cilostazol diet for three months.

33 the PDE3 selective inhibitors milrinone and cilostazol each suppressed thrombin-induced cAMP-depende

34 oup clinical trial evaluated the efficacy of cilostazol for treatment of stable, moderately severe in

35 rowing, occurred in 22.0% of patients in the cilostazol group and in 34.5% of the placebo group (P=0.

36 Exercise training and cilostazol improve walking capacity.

37 Cilostazol improved walking distances, significantly inc

38 SE: 2.4%), ACEI/ARB in 28.4% (SE: 2.0%), and cilostazol in 4.7% (SE: 1.0%) of visits.

39 also assessing medical therapies, including cilostazol, in patients with intracranial stenosis.

40 gs increased headaches (P=1.1x10(-4)), while cilostazol increased moderate-severe diarrhea (P=0.013).

41 Cilostazol is a new phosphodiesterase inhibitor that sup

42 whether dual antiplatelet therapy involving cilostazol is safe and appropriate for long-term use.

43 The data suggest cilostazol is safe and well tolerated for the treatment

44 the mutants), and diminished sensitivity to cilostazol (K(i) of the mutants were 18- to 371-fold hig

45 d for each experiment based on solubility of cilostazol, milrinone, and 8-Br-cAMP.

46 rmability), diamide (cell-stiffening agent), cilostazol (phosphodiesterase 3 inhibitor), or vehicle c

47 afil-placebo: 0.08, 0.05-0.10; P=4.9x10(-8); cilostazol-placebo, 0.06, 0.03-0.09; P=5.1x10(-5)).

48 Given that cilostazol prevents stroke recurrence without increasing

49 Cilostazol reduced dependence in 320 patients (aHR, 0.31

50 Combination ISMN-cilostazol reduced the composite (aHR, 0.58 [95% CI, 0.3

51 Supervised exercise programs and cilostazol remain the first-line medical therapies for c

52 Treatment with the drug cilostazol resulted in a significantly larger minimal lu

53 nonconserved T844 may be responsible for the cilostazol selectivity of PDE3A.

54 Altogether cilostazol showed potential to ameliorate the gliovascul

55 ition of the mutant enzymes by milrinone and cilostazol, specific inhibitors of PDE3.

56 and the well-characterized PDE3A inhibitor, cilostazol, to modulate 3',5'-cyclic adenosine monophosp

57 Restenosis was significantly lower in cilostazol-treated diabetics (17.7% versus 37.7%, P=0.01

58 sions after hypoperfusion was reduced in the cilostazol-treated group.

59 ments in walking performance observed in the cilostazol-treated group.

60 The minimal luminal diameter at 6 months for cilostazol-treated patients was 1.77 mm for the analysis

61 Cilostazol treatment reduced the impairment in working m

62 d after hypoperfusion, were ameliorated with cilostazol treatment.

63 t the LACI-2 trial was feasible and ISMN and cilostazol were well tolerated and safe.

64 The combination of cilostazol with aspirin or clopidogrel had a reduced inc