ライフサイエンスコーパス: tadalafil

1 oration (vitamin D receptor, beta-estradiol, tadalafil).

2 n (0.4 mg) after the last dose of placebo or tadalafil.

3 tor downregulator and U.S. FDA approved drug Tadalafil.

4 e and were attenuated in WTs co-administered tadalafil.

5 ere similar for sildenafil and vardenafil or tadalafil.

6 As, 5 ng/mL for sildenafil, and 10 ng/mL for tadalafil.

7 PDE5 inhibitors sildenafil and vardenafil or tadalafil.

8 tan and sildenafil and 1.52 for bosentan and tadalafil.

9 out mice were treated with either vehicle or tadalafil.

10 ere injected i.p. with vehicle (10% DMSO) or tadalafil (1 mg/kg) with or without KT5823 (KT, PKG bloc

11 - 0.80, 3.7 +/- 0.29, and 11.7 +/- 0.70 nM), tadalafil (1.8 +/- 0.40, 2.4 +/- 0.60, 1.9 +/- 0.37, and

12 ce and block sizes of four, to receive daily tadalafil 10 mg or placebo for 12 weeks.

13 Effects of tadalafil (100 mg by mouth), ibutilide (0.002 mg/kg intr

14 Infarct size was reduced with tadalafil (13.2+/-1.7%) compared to vehicle (40.6+/-2.5%

15 ble patients from PHIRST received once-daily tadalafil 20 mg (T20 mg) or 40 mg (T40 mg) (n = 357) in

16 seven consecutive daily doses of placebo or tadalafil (20 mg).

17 0.71; 95% CL: 0.61-0.82; P < 0.0001) and vs tadalafil (28%; geometric mean ratio 0.72; 95% CL: 0.64-

18 95% CI, 0.79-2.61) for the addition of daily tadalafil, 3.50 (95% CI, 0.22-6.78) for the addition of

19 with SSc-PAH received ambrisentan 10 mg and tadalafil 40 mg daily for 36 weeks.

20 pertension and Response to Tadalafil) study, tadalafil 40 mg improved exercise capacity and delayed c

21 safety of M/T FDC vs macitentan 10 mg and vs tadalafil 40 mg monotherapies in PAH patients, including

22 5 patients had been randomized (placebo: 63; tadalafil: 62,).

23 Survival was increased with tadalafil (95%) compared with control (65%, P<0.05).

24 the time course of nitrate interaction with tadalafil, a phosphodiesterase 5 (PDE5) inhibitor with a

25 We tested whether tadalafil, a phosphodiesterase 5 inhibitor used to treat

26 ypertension who was receiving treatment with tadalafil, a phosphodiesterase 5 inhibitor, developed bi

27 We assessed the efficacy and safety of tadalafil, a phosphodiesterase type 5 inhibitor, in pati

28 is study was designed to evaluate effects of tadalafil, a phosphodiesterase-5 inhibitor used for the

29 ary arterial pressure more dramatically than tadalafil, a standard-of-care therapy for human pulmonar

30 We aimed to assess the effects of tadalafil--a PDE5 inhibitor--on exercise capacity and qu

31 Tadalafil abrogated high glucose stimulation of global p

32 ubicin-induced cardiotoxicity, and therefore tadalafil afforded no additional protection.

33 ved combination therapy with ambrisentan and tadalafil, ambrisentan and placebo, or tadalafil and pla

34 We conclude that tadalafil amelioration of high glucose stimulation of sy

35 adrenal cortex and is partially inhibited by tadalafil and other PDE inhibitors; its germline inactiv

36 erence in 6 min walking distance between the tadalafil and placebo groups was 0.5 m (95% CI -11.6 to

37 ean difference in the change in QTcI between tadalafil and placebo was 2.8 ms; tadalafil was equivale

38 creased QTcI by 6.9 and 8.9 ms compared with tadalafil and placebo, respectively.

39 n and tadalafil, ambrisentan and placebo, or tadalafil and placebo.

40 The hemodynamic interaction between tadalafil and sublingual nitroglycerin lasted 24 h, but

41 were identified, including multiple azoles, Tadalafil and Torin-1.

42 se-5 inhibitors (PDE-5i, such as Sildenafil, Tadalafil and Vardenafil, mainly prescribed to treat ere

43 widely-used drugs for erectile dysfunction, tadalafil and vardenafil, trigger bone gain in mice thro

44 production was significantly increased with tadalafil and was abolished with KT.

45 and endothelin pathways (eg, ambrisentan and tadalafil), and has shown demonstrable improvement in mo

46 sentan, epoprostenol, selexipag, sildenafil, tadalafil, and beraprost) form a similar class with a si

47 , subjects crossed over to either placebo or tadalafil, and nitrate dosing was repeated.

48 elexipag) versus initial double (macitentan, tadalafil, and placebo) oral therapy in newly diagnosed,

49 study, evaluated initial triple (macitentan, tadalafil, and selexipag) versus initial double (maciten

50 cation of ambrisentan, bosentan, sildenafil, tadalafil, and their main metabolites.

51 for 3-isobutyl-1-methylxanthine, sildenafil, tadalafil, and UK-122764, but mutants containing a compl

52 Sildenafil, tadalafil, and vardenafil each competitively inhibit cGM

53 odiesterase-5 (PDE5) inhibitors (sildenafil, tadalafil, and vardenafil) are agents currently in clini

54 (finasteride), phosphodiesterase inhibitors (tadalafil), anticholinergics (trospium), and beta3 agoni

55 CB1158 and tadalafil are promising drugs in reducing radiation-indu

56 Tadalafil at 5 mg once per day was commenced after 1 wee

57 Treatment with tadalafil at a dose of 2 or 10 mg/kg significantly impro

58 hypertension were randomized 1:1 to receive tadalafil at a target dose of 40 mg or placebo.

59 , D803P, L804M, N806D, I813L, S815K) reduces tadalafil binding affinity to levels characteristic of P

60 rogated the preservation of LV function with tadalafil by decline in FS to 17+/-1% and 23+/-3%, respe

61 inding site for the PDE5-selective inhibitor tadalafil (Cialis(R)) with the corresponding class-speci

62 on by two structurally unrelated inhibitors, tadalafil (Cialis) and vardenafil (Levitra).

63 resent study, we investigated the effects of tadalafil (Cialis), a long acting PDE5 inhibitor, on bra

64 ITION [a Study of First-Line Ambrisentan and Tadalafil Combination Therapy in Subjects with Pulmonary

65 rapy with 10 mg of ambrisentan plus 40 mg of tadalafil (combination-therapy group), 10 mg of ambrisen

66 c BP fell below 85 mm Hg in more subjects on tadalafil compared with placebo (p < 0.05), with no diff

67 diotherapy for prostate cancer, daily use of tadalafil compared with placebo did not result in improv

68 wenty-one participants were assigned 5 mg of tadalafil daily and 121 were assigned placebo for 24 wee

69 s were randomized to M/T FDC, macitentan, or tadalafil depending on their PAH treatment (treatment-na

70 However, treatment with tadalafil did not reduce infarct volume when compared to

71 Tadalafil does not improve exercise capacity or quality

72 r (CB1158) or phosphodiesterase-5 inhibitor (tadalafil) during radiation therapy (RT) successfully ab

73 duced AMPK phosphorylation and abrogated the tadalafil effect on high glucose stimulation of laminin

74 m) with fixed moderate-dose hydroxyurea plus tadalafil (experimental arm) in 64 males (aged 18-40 yea

75 Macitentan and tadalafil FDC significantly improved PVR vs monotherapie

76 and taurine for reducing muscle cramps, and tadalafil for improving sexual dysfunction in men.

77 ng-term safety and durability of efficacy of tadalafil for pulmonary arterial hypertension.

78 signal of higher all-cause mortality in the tadalafil group (hazard ratio, 5.10 [95% CI, 1.10-23.69]

79 nts occurred in 29 participants (48%) in the tadalafil group and 35 (56%) in the placebo group.

80 Other withdrawals within the tadalafil group happened after a transient ischaemic att

81 r, and relative potencies were vardenafil >> tadalafil > sildenafil.

82 to placebo and 17 patients (27%) assigned to tadalafil (hazard ratio, 1.02 [95% CI, 0.52-2.01]; P=0.9

83 and phosphodiesterase 5 inhibitors (such as tadalafil) improve lower urinary tract symptoms (mean im

84 trate that treatment of ischemic stroke with tadalafil improved functional recovery, which was associ

85 of which is 10-fold more potent compared to tadalafil in cell-based activity.

86 Study subjects from the clinical trial of tadalafil in PAH, a 16-week, parallel-group, randomized

87 n-to-treat population of the Ambrisentan and Tadalafil in Patients with Pulmonary Arterial Hypertensi

88 The safety profile of tadalafil in PHIRST-2 was similar to that in PHIRST, wit

89 Tadalafil increased AMPK phosphorylation by stimulating

90 E inhibitor, and siRNA against CSE inhibited tadalafil-induced AMPK phosphorylation and abrogated the

91 KT and PAG abolished tadalafil-induced protection (IS: 39.2+/-1% and 51.2+/-2

92 le guanylyl cyclase, respectively, abolished tadalafil induction of H2S and AMPK phosphorylation.

93 Tadalafil inhibited high glucose-induced activation of m

94 Tadalafil is a clinically relevant drug that blocks phos

95 Tadalafil is a novel long-acting inhibitor of phosphodie

96 Tadalafil is an oral phosphodiesterase-5 inhibitor appro

97 stereochemistry of all four stereoisomers of tadalafil is determined using vibrational circular dichr

98 , we contemplated that cardioprotection with tadalafil is mediated by hydrogen sulfide (H(2)S) signal

99 Tadalafil is used to treat erectile dysfunction after pr

100 PKG activation with tadalafil limits myocardial infarction and preserves LV

101 Adding daily tadalafil, low-intensity shockwave therapy, vacuum erect

102 combination of the ERA macitentan and PDE5i tadalafil (M/T FDC) in a once-daily, single tablet would

103 inhibitors, such as sildenafil, vardenafil, tadalafil, mirodenafil, and udenafil, and hormonal treat

104 re the Efficacy and Safety of Macitentan and Tadalafil Monotherapies With the Corresponding Fixed-dos

105 ambrisentan monotherapy and 151 patients to tadalafil monotherapy).

106 ure events than the risk with ambrisentan or tadalafil monotherapy.

107 group), or 40 mg of tadalafil plus placebo (tadalafil-monotherapy group), all administered once dail

108 mbrisentan-monotherapy group, and 121 to the tadalafil-monotherapy group.

109 t M/T FDC (n = 108), macitentan (n = 35), or tadalafil (n = 44).

110 0 patients were randomly assigned to receive tadalafil (n=60) or placebo (n=60), of whom 56 (93%) ver

111 al in healthy men were compared (placebo and tadalafil [n = 90], with a subset [n = 61] receiving all

112 Partners of men assigned tadalafil noted no significant effect on sexual satisfac

113 to evaluate the specificity of the effect of tadalafil on cGMP.

114 ial combination therapy with ambrisentan and tadalafil on long-term outcomes in patients with pulmona

115 eriments the influence of the PDE5 inhibitor tadalafil on the development of doxorubicin-induced card

116 addition increased binding affinity of [(3)H]tadalafil or [(3)H]vardenafil, an effect presumably medi

117 affinities for cGMP, vardenafil, sildenafil, tadalafil, or 3-isobutyl-1-methylxanthine (IBMX) were re

118 y of V782A for cGMP, vardenafil, sildenafil, tadalafil, or IBMX was reduced 5.5-, 23-, 10-, 3-, and 1

119 onophosphate biological pathway (sildenafil, tadalafil, or riociguat), prostacyclin pathway agonists

120 (ambrisentan-monotherapy group), or 40 mg of tadalafil plus placebo (tadalafil-monotherapy group), al

121 Moreover, tadalafil preserved fractional shortening (FS: 31+/-1.5%

122 l test of equivalence, placebo and high-dose tadalafil produced equivalent effects on the QT interval

123 Tadalafil rapidly augmented inducible NOS (iNOS) express

124 Tadalafil rapidly increased the expression and activity

125 ial combination therapy with ambrisentan and tadalafil reduces the risk of clinical failure events co

126 at 28 to 30 weeks and 1 year, predictors of tadalafil response; and adverse events.

127 ial combination therapy with ambrisentan and tadalafil resulted in a significantly lower risk of clin

128 igher vardenafil potency over sildenafil and tadalafil results from stronger contacts with Tyr-612, G

129 0 (79%; 95% CI, 70%-88%) assigned to receive tadalafil retained erectile function between weeks 28 an

130 Tadalafil selectively increased cGMP but not cyclic aden

131 Treatment with PDE5 inhibitors and daily tadalafil, shockwaves, or a vacuum device was associated

132 Similar to other PDE5 inhibitors, tadalafil should not be administered in combination with

133 ont combination therapy with ambrisentan and tadalafil significantly improved hemodynamics, RV struct

134 r iNOS and 1400W, an iNOS blocker, inhibited tadalafil stimulation of CSE expression and AMPK phospho

135 monary Arterial Hypertension and Response to Tadalafil Study; NCT00549302).

136 monary Arterial Hypertension and Response to Tadalafil) study, tadalafil 40 mg improved exercise capa

137 daily administration of the PDE-5 inhibitor, tadalafil (TAD) will attenuate inflammation, improve fas

138 esponding to maximum plasma concentration of tadalafil, the mean difference in the change in QTcI bet

139 mans, in whom vardenafil is more potent than tadalafil, the relative potencies were reversed with res

140 modeling revealed a higher binding energy of tadalafil to mouse PDE5A compared with vardenafil, due t

141 These findings do not support daily use of tadalafil to prevent erectile dysfunction in these patie

142 In tadalafil-treated podocytes, we examined the interaction

143 Moreover, tadalafil-treated rats showed greater ipsilateral SVZ ce

144 g a sheep model of advanced HF, we show that tadalafil treatment improves contractile function, rever

145 In addition, tadalafil treatment increased cerebral vascular density

146 ubules in HF and their restoration following tadalafil treatment involves the BAR domain protein Amph

147 Accompanying these effects, tadalafil treatment normalized BNP mRNA and prevented de

148 dication supply disruption, does not support tadalafil use in patients with heart failure with preser

149 overy of antimalarial compounds derived from tadalafil, using a drug-to-genome-to-drug approach.

150 men receiving PDE5Is, including sildenafil, tadalafil, vardenafil, and avanafil.

151 PDE5 inhibitors (sildenafil, tadalafil, vardenafil, etc.) are first-line treatments f

152 nding systolic BP at 8 and 24 h after taking tadalafil versus placebo (p < 0.02), with no significant

153 cI between tadalafil and placebo was 2.8 ms; tadalafil was equivalent to placebo (a priori, upper lim

154 Tadalafil was not associated with significantly improved

155 Tadalafil was orally administered every 48 h at a dose o

156 was less, but affinity of H613A or F786A for tadalafil was weakened 37- and 17-fold, respectively.

157 Long-term treatment with tadalafil was well tolerated in patients with pulmonary

158 Plasma concentrations of tadalafil were measured to evaluate concentration-QT eff

159 s the target for sildenafil, vardenafil, and tadalafil, which are drugs for treatment of erectile dys

160 In WT mice, co-administration of tadalafil with doxorubicin reduced PKG Ialpha oxidation

161 ion of the three-dimensional distribution of tadalafil within a Cialis tablet to a depth of >140 mum.

162 on, we hypothesized that PKG activation with tadalafil would limit myocardial ischemia/reperfusion (I