ライフサイエンスコーパス: vardenafil

1 ated PDE5A1 catalytic domain in complex with vardenafil.

2 effect on affinity for cAMP, sildenafil, or vardenafil.

3 .60, 1.9 +/- 0.37, and 2.7 +/- 0.25 nM); and vardenafil (0.091 +/- 0.031, 0.38 +/- 0.07, 0.27 +/- 0.0

4 At peak exercise, vardenafil 10 mg did not alter blood pressure, heart rat

5 Relative to placebo, vardenafil 10 mg did not alter exercise treadmill time (

6 Vardenafil 10 mg did not impair the ability of patients

7 ertional angina due to ischemic CAD received vardenafil 10 mg or placebo, followed by ETT (5 to 10 me

8 ed mild major depression received placebo or vardenafil, 10 mg/day, for 4 weeks, with the option to t

9 The effect of vardenafil, a potent and highly selective phosphodiester

10 Vardenafil, a potent PDE5 inhibitor (K(i) = 0.2 nM), was

11 method was applied in a formal synthesis of vardenafil, a well-known representative of this class of

12 Sildenafil and vardenafil affinity were not significantly affected in P

13 binding affinity of [(3)H]tadalafil or [(3)H]vardenafil, an effect presumably mediated by cGMP bindin

14 Studies of sildenafil and vardenafil analogs demonstrated that higher potency of v

15 cGMP signaling pathways, FASS-LTP identified vardenafil and Bay-73-6691 (phosphodiesterase-5 and -9 i

16 pecially for vardenafil, and that binding of vardenafil and sildenafil differs substantially.

17 erase-5 (PDE5) is the target for sildenafil, vardenafil, and tadalafil, which are drugs for treatment

18 major determinant of potency, especially for vardenafil, and that binding of vardenafil and sildenafi

19 PDE5) inhibitors (sildenafil, tadalafil, and vardenafil) are agents currently in clinical use for non

20 GAF-B had 7- to 18-fold higher affinity for vardenafil-based compounds compared with those lacking a

21 Both [(3)H]vardenafil binding and hydrolytic activity of transducin

22 f membrane-associated PDE6 holoenzyme, [(3)H]vardenafil binding increases in proportion to the extent

23 e filtration assay we used to quantify [(3)H]vardenafil binding to PDE6 required histone II-AS to sta

24 Under these conditions, [(3)H]vardenafil binds stoichiometrically to both the alpha- a

25 amma1-60 binding to the GAF domain increased vardenafil but not cGMP affinity, indicating that substr

26 It is noteworthy that the binding of vardenafil causes loss of the divalent metal ions that h

27 erectile function domain score was 22.9 with vardenafil compared to 14.9 with placebo.

28 the conformation of the H-loop in the PDE5A1-vardenafil complex is different from those of any known

29 In addition, the molecular configuration of vardenafil differs from that of sildenafil when bound to

30 Sildenafil, tadalafil, and vardenafil each competitively inhibit cGMP hydrolysis by

31 PDE5 inhibitors (sildenafil, tadalafil, vardenafil, etc.) are first-line treatments for erectile

32 [(3)H]vardenafil fails to bind to either the PDE6 holoenzyme o

33 The HAM-D score was lower in the vardenafil group (7.9) than in the placebo group (10.1).

34 each inhibitor, and relative potencies were vardenafil >> tadalafil > sildenafil.

35 Vardenafil has higher affinity to phosphodiesterase-5 (P

36 nt study assessed the safety and efficacy of vardenafil in men with erectile dysfunction and untreate

37 hosphodiesterase-5 inhibitors sildenafil and vardenafil induces a parallel release of Abeta due to a

38 analogs demonstrated that higher potency of vardenafil is caused by differences in its double ring.

39 These mutations fail to alter vardenafil (Levitra(R)) affinity for the active site.

40 mice with the phosphodiesterase-5 inhibitor vardenafil (Levitra) mobilized FoxO3a to the nucleus of

41 al administration of sildenafil (Viagra) and vardenafil (Levitra), inhibitors of cGMP-specific PDE5,

42 unrelated inhibitors, tadalafil (Cialis) and vardenafil (Levitra).

43 addition, prolonged incubation of PDE6 with vardenafil or sildenafil (but not 3-isobutyl-1-methylxan

44 sk estimates were similar for sildenafil and vardenafil or tadalafil.

45 tions for the PDE5 inhibitors sildenafil and vardenafil or tadalafil.

46 and nonselective inhibitors, and that higher vardenafil potency over sildenafil and tadalafil results

47 6 amino acids in GAF-B are required for high vardenafil potency.

48 Vardenafil produced statistically significant and clinic

49 in, which forms bidentate bonds with 5'-GMP, vardenafil, sildenafil, and 3-isobutyl-1-methylxanthine

50 For PDE5(Q817A), vardenafil, sildenafil, and IBMX inhibitory potencies we

51 Change in affinity for cGMP, vardenafil, sildenafil, or IBMX in Y612F, H613A, L765A,

52 Catalytic-site affinities for cGMP, vardenafil, sildenafil, tadalafil, or 3-isobutyl-1-methy

53 Affinity of V782A for cGMP, vardenafil, sildenafil, tadalafil, or IBMX was reduced 5

54 erapy agent, adriamycin, in combination with vardenafil survived significantly longer than rats treat

55 urthermore, a phosphodiesterase 5 inhibitor, vardenafil, synergizes with EGCG to induce cancer cell d

56 se-5 (PDE-5) inhibitors, such as sildenafil, vardenafil, tadalafil, mirodenafil, and udenafil, and ho

57 ssion were observed in patients treated with vardenafil versus placebo.

58 Treatment with vardenafil was the most important predictor for return t

59 Vardenafil was well tolerated and highly efficacious in