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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
10 ce and block sizes of four, to receive daily tadalafil 10 mg or placebo for 12 weeks.
11                                   Effects of tadalafil (100 mg by mouth), ibutilide (0.002 mg/kg intr
12                Infarct size was reduced with tadalafil (13.2+/-1.7%) compared to vehicle (40.6+/-2.5%
13 ble patients from PHIRST received once-daily tadalafil 20 mg (T20 mg) or 40 mg (T40 mg) (n = 357) in
14  seven consecutive daily doses of placebo or tadalafil (20 mg).
15  with SSc-PAH received ambrisentan 10 mg and tadalafil 40 mg daily for 36 weeks.
16 pertension and Response to Tadalafil) study, tadalafil 40 mg improved exercise capacity and delayed c
17                  Survival was increased with tadalafil (95%) compared with control (65%, P<0.05).
18  the time course of nitrate interaction with tadalafil, a phosphodiesterase 5 (PDE5) inhibitor with a
19                            We tested whether tadalafil, a phosphodiesterase 5 inhibitor used to treat
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
23            We aimed to assess the effects of tadalafil--a PDE5 inhibitor--on exercise capacity and qu
24                                              Tadalafil abrogated high glucose stimulation of global p
25 ubicin-induced cardiotoxicity, and therefore tadalafil afforded no additional protection.
26 ved combination therapy with ambrisentan and tadalafil, ambrisentan and placebo, or tadalafil and pla
27                             We conclude that tadalafil amelioration of high glucose stimulation of sy
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
31 creased QTcI by 6.9 and 8.9 ms compared with tadalafil and placebo, respectively.
32 n and tadalafil, ambrisentan and placebo, or tadalafil and placebo.
33          The hemodynamic interaction between tadalafil and sublingual nitroglycerin lasted 24 h, but
34  production was significantly increased with tadalafil and was abolished with KT.
35 , subjects crossed over to either placebo or tadalafil, and nitrate dosing was repeated.
36 cation of ambrisentan, bosentan, sildenafil, tadalafil, and their main metabolites.
37 for 3-isobutyl-1-methylxanthine, sildenafil, tadalafil, and UK-122764, but mutants containing a compl
38                                  Sildenafil, tadalafil, and vardenafil each competitively inhibit cGM
39 odiesterase-5 (PDE5) inhibitors (sildenafil, tadalafil, and vardenafil) are agents currently in clini
40                                              Tadalafil at 5 mg once per day was commenced after 1 wee
41                               Treatment with tadalafil at a dose of 2 or 10 mg/kg significantly impro
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
45 on by two structurally unrelated inhibitors, tadalafil (Cialis) and vardenafil (Levitra).
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
51                      However, treatment with tadalafil did not reduce infarct volume when compared to
52                                              Tadalafil does not improve exercise capacity or quality
53 duced AMPK phosphorylation and abrogated the tadalafil effect on high glucose stimulation of laminin
54 ng-term safety and durability of efficacy of tadalafil for pulmonary arterial hypertension.
55                 Other withdrawals within the tadalafil group happened after a transient ischaemic att
56 r, and relative potencies were vardenafil >> tadalafil &gt; sildenafil.
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
60                        The safety profile of tadalafil in PHIRST-2 was similar to that in PHIRST, wit
61                                              Tadalafil increased AMPK phosphorylation by stimulating
62 E inhibitor, and siRNA against CSE inhibited tadalafil-induced AMPK phosphorylation and abrogated the
63                         KT and PAG abolished tadalafil-induced protection (IS: 39.2+/-1% and 51.2+/-2
64 le guanylyl cyclase, respectively, abolished tadalafil induction of H2S and AMPK phosphorylation.
65                                              Tadalafil inhibited high glucose-induced activation of m
66                                              Tadalafil is a novel long-acting inhibitor of phosphodie
67                                              Tadalafil is an oral phosphodiesterase-5 inhibitor appro
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
70                                              Tadalafil is used to treat erectile dysfunction after pr
71                          PKG activation with tadalafil limits myocardial infarction and preserves LV
72  inhibitors, such as sildenafil, vardenafil, tadalafil, mirodenafil, and udenafil, and hormonal treat
73  ambrisentan monotherapy and 151 patients to tadalafil monotherapy).
74 ure events than the risk with ambrisentan or tadalafil monotherapy.
75  group), or 40 mg of tadalafil plus placebo (tadalafil-monotherapy group), all administered once dail
76 mbrisentan-monotherapy group, and 121 to the tadalafil-monotherapy group.
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
79                     Partners of men assigned tadalafil noted no significant effect on sexual satisfac
80 to evaluate the specificity of the effect of tadalafil on cGMP.
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
87                                    Moreover, tadalafil preserved fractional shortening (FS: 31+/-1.5%
88 l test of equivalence, placebo and high-dose tadalafil produced equivalent effects on the QT interval
89                                              Tadalafil rapidly augmented inducible NOS (iNOS) express
90                                              Tadalafil rapidly increased the expression and activity
91 ial combination therapy with ambrisentan and tadalafil reduces the risk of clinical failure events co
92  at 28 to 30 weeks and 1 year, predictors of tadalafil response; and adverse events.
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
96                                              Tadalafil selectively increased cGMP but not cyclic aden
97            Similar to other PDE5 inhibitors, tadalafil should not be administered in combination with
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
100 monary Arterial Hypertension and Response to Tadalafil Study; NCT00549302).
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
105                                           In tadalafil-treated podocytes, we examined the interaction
106                                    Moreover, tadalafil-treated rats showed greater ipsilateral SVZ ce
107                                 In addition, tadalafil treatment increased cerebral vascular density
108 overy of antimalarial compounds derived from tadalafil, using a drug-to-genome-to-drug approach.
109                 PDE5 inhibitors (sildenafil, tadalafil, vardenafil, etc.) are first-line treatments f
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
112                                              Tadalafil was not associated with significantly improved
113                                              Tadalafil was orally administered every 48 h at a dose o
114 was less, but affinity of H613A or F786A for tadalafil was weakened 37- and 17-fold, respectively.
115                     Long-term treatment with tadalafil was well tolerated in patients with pulmonary
116                     Plasma concentrations of tadalafil were measured to evaluate concentration-QT eff
117 s the target for sildenafil, vardenafil, and tadalafil, which are drugs for treatment of erectile dys
118             In WT mice, co-administration of tadalafil with doxorubicin reduced PKG Ialpha oxidation
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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