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1 n, and (4) norepinephrine-infused rats given bosentan.
2 and LFTs for patients taking ambrisentan and bosentan.
3 , an effect abrogated by the ETAR antagonist bosentan.
4 and testing behavior for ambrisentan but not bosentan.
5 ees) but no significant change in the use of bosentan.
6 CI, -34.4% to -18.5%) of ambrisentan but not bosentan.
7 of the administration of the ET-1 antagonist bosentan.
8 dynamics in symptomatic patients with PAH on bosentan.
9 0.05, paired t test) but was not additive to bosentan.
10 0 mg, 3% for sitaxsentan 100 mg, and 11% for bosentan.
11 ategy to optimize therapy in PAH patients on bosentan.
12               Starting from the structure of bosentan (1), we embarked on a medicinal chemistry progr
13 ied Langendorff perfusions, ERAs (BQ-123 and bosentan 10(-7,-6,-5) mol/L) decreased contractility in
14     (NH4)2SO4-ingesting animals infused with bosentan (10 mg/kg) to inhibit A- and B-type endothelin
15 0, and 60 minutes after a bolus injection of bosentan (10 mg/kg).
16       The nonselective ET-1 receptor blocker bosentan (100 mg.kg-1.d-1) had similar but less pronounc
17                                              Bosentan (100 mg/kg once daily) was administered by gava
18 r 4 weeks followed by either of two doses of bosentan (125 or 250 mg twice daily) for a minimum of 12
19 e, 68 patients (79%) were still treated with bosentan, 13 (15%) were discontinued, and 5 (6%) had die
20 ib were unaffected by losartan (10 mg/kg/h), bosentan (20 mg/kg/h), or a combination of phentolamine
21 ib were unaffected by losartan (10 mg/kg/h), bosentan (20 mg/kg/h), or a combination of phentolamine
22                                              Bosentan (20-50 microM) significantly inhibited endothel
23  were available for analysis in 39 patients (bosentan = 25, placebo = 14).
24 entan 50 mg was 24.2 m (p = 0.07) and for OL bosentan, 29.5 m (p = 0.05).
25 e randomized to three months of therapy with bosentan (30 mg/kg twice daily, n = 7) or no therapy at
26 (n=8), (3) concomitant ET receptor blockade (bosentan, 50 mg/kg BID) and rapid pacing (n=8), (4) conc
27 or 4 weeks, then 50 mg three times daily) or bosentan (62.5 mg twice daily for 4 weeks, then 125 mg t
28  with scleroderma) were randomly assigned to bosentan (62.5mg taken twice daily for 4 weeks then 125
29 ce (6MWD) of 200 to 450 m while treated with bosentan (70%) or sildenafil were randomized to inhaled
30  11 159 patients received a prescription for bosentan (7931 women [71.1%]; mean [SD] age, 47.7 [23.7]
31                                              Bosentan, a dual endothelin receptor blocker, has been u
32       We describe the efficacy and safety of bosentan, a dual endothelin-receptor antagonist that can
33                                              Bosentan, a dual-receptor antagonist, is approved by the
34          Acute intravenous administration of bosentan, a mixed endothelin-1 type A and type B recepto
35 tudy, we examined the effects of intravenous bosentan, a nonpeptide, competitive endothelin-1 recepto
36 ested this hypothesis in a 12-month trial of bosentan, a nonselective endothelin receptor antagonist,
37                        In patients receiving bosentan, a statistically significant improvement in han
38 AVS patient sera and treated with or without bosentan-a clinically approved ET1 receptor inhibitor.
39 bjects and increased to control values after bosentan administration.
40 itions and control rats fed normal chow or a bosentan admix both produced similar (P > 0.05) panretin
41                                              Bosentan also improved the Borg dyspnea index and WHO fu
42                                         Oral bosentan, an endothelin A/B receptor antagonist, decreas
43                                              Bosentan, an endothelin A/B receptor antagonist, reduced
44 esigned to assess the hemodynamic effects of bosentan, an endothelin receptor antagonist, in patients
45 ly, inhibition of the endothelin system with bosentan, an endothelin receptor antagonist, was strongl
46 reatment with the current practice of adding bosentan, an endothelin receptor antagonist.
47                                         Oral bosentan, an ET A/B receptor antagonist, decreased dista
48                          Orally administered bosentan, an ET(A/B) receptor antagonist, decreased urin
49                      These data suggest that bosentan, an oral endothelin ET(A)/ET(B) receptor antago
50                                              Bosentan, an oral endothelin ET(A)/ET(B) receptor antago
51 ssion of ET-1 mRNA, and the acute effects of bosentan, an orally active ETA and ETB receptor antagoni
52 or the use of endothelin receptor inhibitors bosentan and ambrisentan improved drug penetration into
53 stinil), and endothelin pathway antagonists (bosentan and ambrisentan).
54    The first 2 agents approved in the class, bosentan and ambrisentan, initially carried boxed warnin
55 and precise method for the quantification of bosentan and its nine impurities with a short runtime of
56 0 individuals enrolled in the 3 datasets) vs bosentan and LFT monitoring (ie, proportion of initiator
57 functional capacity, or symptoms between the bosentan and placebo groups over 16 weeks.
58  for ambrisentan and sildenafil and 1.52 for bosentan and tadalafil.
59  up to 7 days), (3) sham-operated rats given bosentan, and (4) norepinephrine-infused rats given bose
60  163 patients, 77 were randomized to receive bosentan, and 86 were randomized to receive placebo.
61 ected, with seven (28.0%) patients receiving bosentan, and four (28.6%) receiving placebo achieving a
62 H); for observation only, an open-label (OL) bosentan arm was included.
63                                              Bosentan attenuated norepinephrine-induced increases in
64 ermore, the mixed ETA/B receptor antagonist, bosentan, blocked this process.
65 istance decreased by 223 dyn s cm(-)(5) with bosentan, but increased by 191 dyn s cm(-5) with placebo
66                                              Bosentan can reduce the development of new digital ulcer
67                                              Bosentan caused a dose-dependent fall in total pulmonary
68 r that was suppressed (P > 0.05) in rats fed bosentan chow admix.
69 P < 0.04) in the absence but not presence of bosentan, consistent with endothelin-mediated increased
70                                 Furthermore, bosentan decreased blood base excess in Nx animals (0.1
71                                              Bosentan decreased H(+) secretion and increased HCO(3) s
72 ent with the endothelin receptor antagonist, bosentan, decreased the development of new digital ulcer
73 Although many outcome variables were stable, bosentan did not reduce the frequency of clinically impo
74                        Next, we administered bosentan during the induction of liver injury in two mec
75            By contrast, in dogs treated with bosentan, EF tended to increase from 34 +/- 2% before in
76                       Treatment of mice with bosentan (endothelin-1 receptor antagonist) normalized t
77 cals, and antithrombotic agents (macitentan, bosentan, epoprostenol, selexipag, sildenafil, tadalafil
78                                        After bosentan, FE(NO), C(W), and urine NOx increased to contr
79 placebo was added to stable monotherapy with bosentan for 12 wk.
80 for severe Raynaud's and skin ulcers, and of bosentan for digital ulcers.
81                 For instance, macitentan and bosentan from endothelin receptor antagonists show major
82 ts filling prescriptions for ambrisentan and bosentan from July 1, 2007, to December 31, 2018.
83 (from 28.7 to 30.7 mL.kg(-1).min(-1)) in the bosentan group compared with 0.6 mL.kg(-1).min(-1) (from
84 e between the placebo group and the combined bosentan groups was 44 m (95 percent confidence interval
85                           Patients receiving bosentan had a 48% reduction in the mean number of new u
86                               Patients given bosentan had a reduced Borg dyspnoea index and an improv
87            At week 16, patients treated with bosentan had an improved six-minute walking distance; th
88                                              Bosentan had no effect on distal tubule HCO3 or H+ secre
89                                              Bosentan had no significant effect on heart rate or mean
90  Score; the endothelin-1 receptor antagonist bosentan has now been shown to reduce the number of new
91                                              Bosentan improved 6-minute walk distance (59 m; 95% CI,
92 nistered dual endothelin-receptor antagonist bosentan improved exercise capacity and cardiopulmonary
93 with the dual endothelin-1 receptor blocker, bosentan, improved cell engraftment independently of hep
94      The nonselective ET receptor antagonist bosentan improves exercise capacity and increases time t
95                                              Bosentan improves exercise capacity, exercise time, and
96 o, treatment with the FDA-approved compound, Bosentan, improves axon regeneration and reverses the ag
97 refore to examine the efficacy and safety of bosentan in Fontan patients.
98 role of prostacyclin (and its analogues) and bosentan in managing scleroderma-related pulmonary hyper
99 haled treprostinil as add-on therapy to oral bosentan in patients with pulmonary arterial hypertensio
100 f the dual endothelin-1 receptor antagonist, bosentan, in patients with PH and fibrotic IIP.
101                                              Bosentan increases exercise capacity and improves haemod
102                    H+ secretion was lower in bosentan-infused compared with baseline (NH4)2SO4 animal
103  in patients in WHO functional class I/II at bosentan initiation than in patients in WHO class III/IV
104 tion than in patients in WHO class III/IV at bosentan initiation.
105 gies to reduce or control fibrosis directly (bosentan, interferon gamma, and relaxin) have been disap
106                                  Intravenous bosentan is a potent but nonselective pulmonary vasodila
107     Endothelin-receptor antagonism with oral bosentan is an effective approach to therapy for pulmona
108           The endothelin-receptor antagonist bosentan is beneficial in patients with pulmonary arteri
109 gulated protein expression of TRPC6, whereas bosentan markedly downregulated TRPC6 protein levels.
110 ment with the endothelin receptor antagonist bosentan may be effective in preventing new digital ulce
111 In addition to its efficacy as sole therapy, bosentan may have a role as part of a combination of dru
112 s with PAH with reduced exercise capacity on bosentan monotherapy is safe and efficacious.
113 catheter confirmed PH were randomized 2:1 to bosentan (n = 40) or placebo (n = 20).
114 = 9), and 3-month diabetic rats treated with bosentan (n = 5).
115 s, and WHO FC assessments third-party blind) bosentan (n = 60).
116 trol rats (n = 7), control rats treated with bosentan (n = 7), 3-month diabetic rats (n = 9), and 3-m
117 s, such as nitroglycerine, prostacyclin, and bosentan, offer opportunities for improving cell therapy
118 The present trial investigated the effect of bosentan on exercise capacity in a larger number of pati
119                        The greater effect of bosentan on IPAH-PASMCs than on normal PASMCs suggests t
120 nstrate that the antiproliferative effect of bosentan on PASMCs involves the downregulation of TRPC6
121 amined the effects of long-term therapy with bosentan on the progression of LV dysfunction and remode
122 tration of an ET receptor antagonist, either bosentan or macitentan, markedly attenuated PD-induced M
123 randomized 1:1 to 14 weeks of treatment with bosentan or placebo.
124 ith a decrease in oxygen saturation received bosentan or placebo.
125 among PAH patients who remain symptomatic on bosentan or sildenafil, inhaled treprostinil improves ex
126 (PAH) patients receiving therapy with either bosentan or sildenafil.
127 ion of the pan-ET-receptor (ET-R) antagonist Bosentan or the selective ET(B)-R antagonist BQ788 into
128 t alter the high-affinity binding of BQ-123, bosentan, or SB 209670.
129 ceiving placebo and 22.5% of those receiving bosentan (P not significant).
130        Studies evaluating anti-endothelin-1 (bosentan), phosphodiesterases inhibitors (sildenafil), a
131     However, the endothelin receptor blocker bosentan prevented the reduction in thin-filament calciu
132 ogs with moderate HF, long-term therapy with bosentan prevents the progression of LV dysfunction and
133      However, incubation of hepatocytes with bosentan protected cells from cytokine toxicity in vitro
134 Twelve patients with symptomatic PAH despite bosentan received either 30 microg of inhaled treprostin
135 isolated stellate cells from injured livers, bosentan reduced expression of activation markers, inclu
136                                              Bosentan reduced levels of type I collagen and cellular
137                               At 60 minutes, bosentan reduced LV end-diastolic pressure (17 +/- 2 ver
138                       Short-term intravenous bosentan reduced systemic vascular resistance and improv
139 othelin-A (ETA) and ETB receptor antagonist, bosentan, reduced portal pressure in portal hypertensive
140  Oral pretreatment with the clinical blocker bosentan resulted in a dose-dependent partial blockade (
141                                              Bosentan reversed these abnormalities, suggesting that s
142 pared with untreated dogs, dogs treated with bosentan showed significantly less LV cardiomyocyte hype
143 (n=111); subgroups included monotherapy with bosentan, sildenafil, or epoprostenol and combination th
144 ssays for the quantification of ambrisentan, bosentan, sildenafil, tadalafil, and their main metaboli
145  had no additional effect in HiPro ingesting bosentan, supporting that ET mediated the increased dist
146 0.6-1.4, p<0.0001) greater in patients given bosentan than in those given placebo.
147 94 +/- 99 microEq/d, P < 0.04 versus without bosentan); the decrease was mediated by decreased HCO(3)
148                            In patients given bosentan, the distance walked in 6 min improved by 70 m
149 de BQ-123, the pyrimidinylbenzenesulfonamide bosentan, the indancarboxlic acid SB 209670, and the nap
150 ary arterial hypertension (PAH) treated with bosentan therapy, with or without concomitant prostanoid
151 ent in exercise capacity was observed in the bosentan-treated group compared with the placebo group,
152 into the vitreous of control and 5- to 7-day bosentan-treated nondiabetic rats.
153                                         Nine bosentan-treated patients improved 1 functional class, w
154 ated to >3-fold the upper limit of normal in bosentan-treated patients; this elevation is comparable
155 e after nerve injury is partially rescued by Bosentan treatment.
156 nderwent follow-up testing after 3 months of bosentan treatment.
157 s improved (46%) or was unchanged (44%) with bosentan treatment.
158  to receive placebo or to receive 62.5 mg of bosentan twice daily for 4 weeks followed by either of t
159     Post hoc analyses showed that background bosentan use and higher 6MWD at PHIRST baseline were ass
160                           Median exposure to bosentan was 14 months.
161 used by the addition of the hepatotoxic drug Bosentan was determined.
162  PASMCs, and the antiproliferative effect of bosentan was significantly enhanced in IPAH-PASMCs in co
163               The safety and tolerability of bosentan were also assessed.
164                               Macitentan and bosentan were associated with 64% and 56% of pulmonary A
165  heart or connective tissue disease) started bosentan with or without concomitant intravenous epopros

 
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