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1 n (0.4 mg) after the last dose of placebo or tadalafil.
2 ere similar for sildenafil and vardenafil or tadalafil.
3 As, 5 ng/mL for sildenafil, and 10 ng/mL for tadalafil.
4 PDE5 inhibitors sildenafil and vardenafil or tadalafil.
5 tan and sildenafil and 1.52 for bosentan and tadalafil.
6 out mice were treated with either vehicle or tadalafil.
7 e and were attenuated in WTs co-administered tadalafil.
8 ere injected i.p. with vehicle (10% DMSO) or tadalafil (1 mg/kg) with or without KT5823 (KT, PKG bloc
9 - 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
13 ble patients from PHIRST received once-daily tadalafil 20 mg (T20 mg) or 40 mg (T40 mg) (n = 357) in
16 pertension and Response to Tadalafil) study, tadalafil 40 mg improved exercise capacity and delayed c
18 the time course of nitrate interaction with tadalafil, a phosphodiesterase 5 (PDE5) inhibitor with a
20 ypertension who was receiving treatment with tadalafil, a phosphodiesterase 5 inhibitor, developed bi
21 is study was designed to evaluate effects of tadalafil, a phosphodiesterase-5 inhibitor used for the
22 ary arterial pressure more dramatically than tadalafil, a standard-of-care therapy for human pulmonar
26 ved combination therapy with ambrisentan and tadalafil, ambrisentan and placebo, or tadalafil and pla
28 adrenal cortex and is partially inhibited by tadalafil and other PDE inhibitors; its germline inactiv
29 erence in 6 min walking distance between the tadalafil and placebo groups was 0.5 m (95% CI -11.6 to
30 ean difference in the change in QTcI between tadalafil and placebo was 2.8 ms; tadalafil was equivale
37 for 3-isobutyl-1-methylxanthine, sildenafil, tadalafil, and UK-122764, but mutants containing a compl
39 odiesterase-5 (PDE5) inhibitors (sildenafil, tadalafil, and vardenafil) are agents currently in clini
42 , D803P, L804M, N806D, I813L, S815K) reduces tadalafil binding affinity to levels characteristic of P
43 rogated the preservation of LV function with tadalafil by decline in FS to 17+/-1% and 23+/-3%, respe
44 inding site for the PDE5-selective inhibitor tadalafil (Cialis(R)) with the corresponding class-speci
46 resent study, we investigated the effects of tadalafil (Cialis), a long acting PDE5 inhibitor, on bra
47 rapy with 10 mg of ambrisentan plus 40 mg of tadalafil (combination-therapy group), 10 mg of ambrisen
48 c BP fell below 85 mm Hg in more subjects on tadalafil compared with placebo (p < 0.05), with no diff
49 diotherapy for prostate cancer, daily use of tadalafil compared with placebo did not result in improv
50 wenty-one participants were assigned 5 mg of tadalafil daily and 121 were assigned placebo for 24 wee
53 duced AMPK phosphorylation and abrogated the tadalafil effect on high glucose stimulation of laminin
57 trate that treatment of ischemic stroke with tadalafil improved functional recovery, which was associ
58 Study subjects from the clinical trial of tadalafil in PAH, a 16-week, parallel-group, randomized
59 n-to-treat population of the Ambrisentan and Tadalafil in Patients with Pulmonary Arterial Hypertensi
62 E inhibitor, and siRNA against CSE inhibited tadalafil-induced AMPK phosphorylation and abrogated the
64 le guanylyl cyclase, respectively, abolished tadalafil induction of H2S and AMPK phosphorylation.
68 stereochemistry of all four stereoisomers of tadalafil is determined using vibrational circular dichr
69 , we contemplated that cardioprotection with tadalafil is mediated by hydrogen sulfide (H(2)S) signal
72 inhibitors, such as sildenafil, vardenafil, tadalafil, mirodenafil, and udenafil, and hormonal treat
75 group), or 40 mg of tadalafil plus placebo (tadalafil-monotherapy group), all administered once dail
77 0 patients were randomly assigned to receive tadalafil (n=60) or placebo (n=60), of whom 56 (93%) ver
78 al in healthy men were compared (placebo and tadalafil [n = 90], with a subset [n = 61] receiving all
81 ial combination therapy with ambrisentan and tadalafil on long-term outcomes in patients with pulmona
82 eriments the influence of the PDE5 inhibitor tadalafil on the development of doxorubicin-induced card
83 addition increased binding affinity of [(3)H]tadalafil or [(3)H]vardenafil, an effect presumably medi
84 affinities for cGMP, vardenafil, sildenafil, tadalafil, or 3-isobutyl-1-methylxanthine (IBMX) were re
85 y of V782A for cGMP, vardenafil, sildenafil, tadalafil, or IBMX was reduced 5.5-, 23-, 10-, 3-, and 1
86 (ambrisentan-monotherapy group), or 40 mg of tadalafil plus placebo (tadalafil-monotherapy group), al
88 l test of equivalence, placebo and high-dose tadalafil produced equivalent effects on the QT interval
91 ial combination therapy with ambrisentan and tadalafil reduces the risk of clinical failure events co
93 ial combination therapy with ambrisentan and tadalafil resulted in a significantly lower risk of clin
94 igher vardenafil potency over sildenafil and tadalafil results from stronger contacts with Tyr-612, G
95 0 (79%; 95% CI, 70%-88%) assigned to receive tadalafil retained erectile function between weeks 28 an
98 ont combination therapy with ambrisentan and tadalafil significantly improved hemodynamics, RV struct
99 r iNOS and 1400W, an iNOS blocker, inhibited tadalafil stimulation of CSE expression and AMPK phospho
101 monary Arterial Hypertension and Response to Tadalafil) study, tadalafil 40 mg improved exercise capa
102 daily administration of the PDE-5 inhibitor, tadalafil (TAD) will attenuate inflammation, improve fas
103 esponding to maximum plasma concentration of tadalafil, the mean difference in the change in QTcI bet
104 These findings do not support daily use of tadalafil to prevent erectile dysfunction in these patie
108 overy of antimalarial compounds derived from tadalafil, using a drug-to-genome-to-drug approach.
110 nding systolic BP at 8 and 24 h after taking tadalafil versus placebo (p < 0.02), with no significant
111 cI between tadalafil and placebo was 2.8 ms; tadalafil was equivalent to placebo (a priori, upper lim
114 was less, but affinity of H613A or F786A for tadalafil was weakened 37- and 17-fold, respectively.
117 s the target for sildenafil, vardenafil, and tadalafil, which are drugs for treatment of erectile dys
119 ion of the three-dimensional distribution of tadalafil within a Cialis tablet to a depth of >140 mum.
120 on, we hypothesized that PKG activation with tadalafil would limit myocardial ischemia/reperfusion (I
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