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1  mean sitting DBP and SBP, respectively, for irbesartan).
2 n coronary artery disease patients receiving irbesartan.
3 he presence of the AT(1) receptor antagonist irbesartan.
4 effect of that dose when coadministered with irbesartan.
5          Safety of sparsentan was similar to irbesartan.
6        TEAEs with sparsentan were similar to irbesartan.
7 F-PEF) on patients' lives and the effects of irbesartan.
8 specific mortality rates between placebo and irbesartan.
9 ibrosis that was prevented by treatment with irbesartan.
10 nvolved, Ang II was added in the presence of irbesartan (10 micromol/L), a specific AT(1) receptor an
11 re made over 24 h following randomization to irbesartan 12.5 mg, 37.5 mg, 75 mg, 150 mg or placebo.
12 f aliskiren 150 mg was comparable to that of irbesartan 150 mg (8.9+/-0.7 and 12.5+/-1.2 mm Hg, least
13 red mean sitting DBP significantly more than irbesartan 150 mg (P<0.05).
14          Aliskiren 150 mg is as effective as irbesartan 150 mg in lowering blood pressure.
15 or an indistinguishable monotherapy control (irbesartan 150 mg).
16 al doses of aliskiren (150, 300, or 600 mg), irbesartan 150 mg, or placebo.
17 bolic syndrome in a double-blinded manner to irbesartan 150 mg/d (n=14), lipoic acid 300 mg/d (n=15),
18      Patients were randomized 1:1 to receive irbesartan (150 mg/day titrated to 300 mg/day) or placeb
19  quickly accessing the antihypertensive drug irbesartan (2).
20 ber of AT(1) receptor antagonists, including irbesartan (3).
21 o to receive sparsentan 400 mg once daily or irbesartan 300 mg once daily, stratified by estimated gl
22 th indapamide 1.5 mg/d, ramipril 10 mg/d (or irbesartan 300 mg/d), and amlodipine 10 mg/d were random
23 thy due to type 2 diabetes to treatment with irbesartan (300 mg daily), amlodipine (10 mg daily), or
24 ressure-lowering drugs each at quarter-dose (irbesartan 37.5 mg, amlodipine 1.25 mg, hydrochlorothiaz
25 aily caloric intake); 6 received alcohol and irbesartan (5 mg.kg(-1).d(-1) PO); and 8 were controls.
26 ge -5.9+/-0.9 mm Hg and -5.3+/-0.9 mm Hg for irbesartan 75 mg and 150 mg, respectively) after 12 week
27                                              Irbesartan, a long acting selective angiotensin-1 recept
28 vement in MLHFQ scores was not observed with irbesartan after 6 months (mean adjusted difference, 0.4
29                               Treatment with irbesartan, aliskiren and amlodipine were associated wit
30 lly induced RAS, RAS + treatment with either irbesartan, aliskiren or amlodipine or sham-surgery.
31  (I-Preserve) trial and to determine whether irbesartan altered the distribution of mode of death in
32 e interaction of assigned study medications (irbesartan, amlodipine, and placebo) on progressive rena
33  diabetes and overt nephropathy treated with irbesartan, amlodipine, or placebo in addition to conven
34                  Patients were randomized to irbesartan, amlodipine, or placebo, with other antihyper
35                               Treatment with irbesartan, amlodipine, or placebo.
36 ound 7 clearly demonstrated superiority over irbesartan (an AT(1) receptor antagonist) in the normal
37 st, significantly reduced proteinuria versus irbesartan, an angiotensin II receptor blocker, at 36 we
38                  We evaluated the ability of irbesartan, an angiotensin receptor blocker, and lipoic
39                          The AT(1)R blockers irbesartan and candesartan abrogated antifibrotic signal
40 /d (n=14), lipoic acid 300 mg/d (n=15), both irbesartan and lipoic acid (n=15), or matching placebo (
41 contrast, the highest cancer signals for the irbesartan and losartan recalls detected in March 2019 (
42                                  Conversely, irbesartan and losartan were largely G protein-selective
43 rol exposures, while the changes in RORs for irbesartan and losartan were only 20-30% higher.
44 rtan-associated cancer signals compared with irbesartan and losartan, although they all contained the
45                   Primary event rates in the irbesartan and placebo groups were 100.4 and 105.4 per 1
46 d tolerability profile comparable to that of irbesartan and placebo, in patients with mild-to-moderat
47 le were the formation of valsartan acid from irbesartan and valsartan, the persistence of N-desmethyl
48                            Administration of irbesartan and/or lipoic acid to patients with the metab
49                               Treatment with irbesartan and/or lipoic acid was associated with statis
50 40.3+/-11.3 years of age) were randomized to irbesartan, and 28 (64% female; 40.7+/-11.0 years of age
51 gliflozin, finerenone, atrasentan, losartan, irbesartan, and aliskiren in patients with CKD.
52 nals of association between ARBs (valsartan, irbesartan, and losartan) and reported neoplasm AEs usin
53 he exaggerated renal vasodilator response to irbesartan, and the therapeutic effectiveness of interru
54 , that started with the quadpill (containing irbesartan at 37.5 mg, amlodipine at 1.25 mg, indapamide
55                                              Irbesartan, at once-daily doses of 75 mg and 150 mg, ind
56 ed for telemesartan and, to a lesser extent, irbesartan based on a partial agonist action on PPAR-gam
57       All of these effects were inhibited by irbesartan but not PD 123319 or divalinil.
58  weeks with the angiotensin receptor blocker irbesartan, but not with the thiazide-type diuretic chlo
59 dividuals were enrolled in the international Irbesartan Diabetic Nephropathy Trial (IDNT) and followe
60 iabetic nephropathy and were enrolled in the Irbesartan Diabetic Nephropathy Trial (IDNT) and had a b
61 tensive patients with type 2 diabetes in the Irbesartan Diabetic Nephropathy Trial (IDNT), a randomiz
62 L) trial with independent replication in the Irbesartan Diabetic Nephropathy Trial (IDNT).
63                  The primary outcomes of the Irbesartan Diabetic Nephropathy Trial were doubling of s
64                               Treatment with irbesartan did not affect overall mortality or the distr
65                                              Irbesartan did not improve the outcomes of patients with
66                                              Irbesartan did not substantially improve MLHFQ scores du
67 change in aortic Z score was also reduced by irbesartan (difference in means -0.10 per year, 95% CI -
68  placebo were reallocated to one of the four irbesartan doses, treatment was continued for 12 weeks a
69 ed coronary artery disease were treated with irbesartan for a 12-week period.
70 onary artery disease (CAD) were treated with irbesartan for a 24-week period.
71 e Atrial Fibrillation Clopidogrel Trial With Irbesartan for Prevention of Vascular Events, there was
72  sparsentan versus -4.4%, -15.8 to 8.7, with irbesartan; geometric least-squares mean ratio 0.60, 95%
73 er in the sparsentan group (-49.8%) than the irbesartan group (-15.1%), resulting in a between-group
74 0% lower in the sparsentan group than in the irbesartan group (-42.8%, 95% CI -49.8 to -35.0, with sp
75 h the risk related to WRF was greater in the irbesartan group (HR: 1.66; 95% CI: 1.21 to 2.28; p = 0.
76 group versus 26 (13%) of 202 patients in the irbesartan group (relative risk 0.7, 95% CI 0.4 to 1.2).
77 line aortic root diameter was 34.4 mm in the irbesartan group (SD 5.8) and placebo group (5.5).
78 mary outcome occurred in 742 patients in the irbesartan group and 763 in the placebo group.
79 .53 mm per year (95% CI 0.39 to 0.67) in the irbesartan group compared with 0.74 mm per year (0.60 to
80  group (P=0.003) and 37 percent lower in the irbesartan group than in the amlodipine group (P<0.001).
81 ne concentration was 33 percent lower in the irbesartan group than in the placebo group (P=0.003) and
82 tion increased 24 percent more slowly in the irbesartan group than in the placebo group (P=0.008) and
83 igned to the sparsentan group and 203 to the irbesartan group.
84 lower rate of eGFR decline than those in the irbesartan group.
85 ere not different between the sparsentan and irbesartan groups.
86 es in mortality rate between the placebo and irbesartan groups.
87              In contrast, patients receiving irbesartan had a significantly lower incidence of conges
88 from acute lung injury by the AT1 antagonist irbesartan; however, this effect was again blocked by A7
89      The ARB was losartan in 17 patients and irbesartan in 1 patient.
90         The study examines sparsentan versus irbesartan in adults (aged >=18 years) with biopsy-prove
91 ngful reduction in proteinuria compared with irbesartan in adults with IgA nephropathy.
92 afety of the angiotensin II receptor blocker irbesartan in adults with vascular Ehlers-Danlos syndrom
93    We used data from the AVOID study and the Irbesartan in Diabetic Nephropathy Trial (IDNT) to estim
94 erved Ejection Fraction (PARAGON-HF) and the Irbesartan in Heart Failure With Preserved Ejection Frac
95                              The I-PRESERVE (Irbesartan in Heart Failure With Preserved Ejection Frac
96 istics and outcomes in the I-Preserve trial (Irbesartan in Heart Failure With Preserved Ejection Frac
97 n 3,595 patients included in the I-PRESERVE (Irbesartan in Heart Failure With Preserved Ejection Frac
98 s and outcomes of patients with HFpEF in the Irbesartan in Heart Failure with Preserved Ejection Frac
99 lure with preserved ejection fraction in the Irbesartan in Heart Failure with Preserved Ejection Frac
100 death in patients with HFPEF enrolled in the Irbesartan in Heart Failure With Preserved Ejection Frac
101 tality and morbidity) (EF>=45%), I-Preserve (Irbesartan in heart failure with Preserved ejection frac
102 ved Systolic Function [TOPCAT]; NCT00094302; Irbesartan in Heart Failure With Preserved Systolic Func
103 raction patients enrolled in the I-Preserve (Irbesartan in Heart Failure With Preserved Systolic Func
104 nd Preserved Systolic Function], I-PRESERVE [Irbesartan in Heart Failure With Preserved Systolic Func
105 es by international geographic region in the Irbesartan in Heart Failure with Preserved systolic func
106  in these trials, along with the I-PRESERVE (Irbesartan in Heart Failure with Preserved Systolic Func
107                                          The Irbesartan in HFPEF trial (I-PRESERVE) enrolled 4128 pat
108  preserved ejection fraction enrolled in the irbesartan in patients with heart failure and preserved
109 ong-term hemodynamic and clinical effects of irbesartan in patients with heart failure.
110 nt with sparsentan versus maximally titrated irbesartan in patients with IgA nephropathy resulted in
111         Therefore, we studied the effects of irbesartan in patients with this syndrome.
112                               Treatment with irbesartan in these patients significantly reduced level
113 RA, renal perfusion rose more in response to irbesartan in type 2 diabetes mellitus (714 +/- 83 to 93
114 e daily, then randomly assigned to 150 mg of irbesartan (increased to 300 mg as tolerated) or matchin
115       An additional renoprotective effect of irbesartan, independent of achieved SBP, was observed do
116                                              Irbesartan induced significant dose-related decreases in
117                                              Irbesartan is an orally active antagonist of the angiote
118                                              Irbesartan is associated with a reduction in the rate of
119          The angiotensin-II-receptor blocker irbesartan is effective in protecting against the progre
120 ry was increased by 67%, 44%, and 75% in the irbesartan, lipoic acid, and irbesartan plus lipoic acid
121 sent in recalled products include valsartan, irbesartan, losartan, metformin, ranitidine, and nizatid
122                 Our results show that use of irbesartan may retard the inflammatory process seen in p
123                    Our results indicate that irbesartan may suppress the atherosclerotic process by i
124                      PRA rose in response to irbesartan more gradually in the patients with type 2 di
125 seven dogs treated with the receptor blocker irbesartan (MR+AT(1)RB) started 24 h after induction of
126 ants were recruited and randomly assigned to irbesartan (n=104) or placebo (n=88), and all were follo
127 e randomly assigned to sparsentan (n=202) or irbesartan (n=202) and received treatment.
128                                The effect of irbesartan on each inflammatory marker is significant.
129         We aimed to determine the effects of irbesartan on the rate of aortic dilatation in children
130 aily) or irbesartan (target dose 300 mg oral irbesartan once daily) based on a permuted-block randomi
131 participants were all given 75 mg open label irbesartan once daily, then randomly assigned to 150 mg
132                  In addition, treatment with irbesartan or irbesartan plus lipoic acid decreased 8-is
133  randomly assigned them to receive 300 mg of irbesartan or placebo per day.
134 ) and development of WRF after initiation of irbesartan or placebo were examined.
135          Patients were randomized to receive irbesartan or placebo.
136 r either the angiotensin-II-receptor blocker irbesartan or the calcium-channel blocker amlodipine slo
137 sm AEs were 2-fold higher for valsartan than irbesartan (OR, 1.77 [95% CI, 1.47-2.13], P<0.0001) and
138                            With alcohol plus irbesartan, plasma Ang II, cardiac angiotensin-convertin
139    In addition, treatment with irbesartan or irbesartan plus lipoic acid decreased 8-isoprostane leve
140  and 75% in the irbesartan, lipoic acid, and irbesartan plus lipoic acid groups, respectively, compar
141                                              Irbesartan prevented the alcohol-induced decreases in LV
142                       Compared with placebo, irbesartan reduced the risk of severe symptomatic and as
143                           Eleven episodes of irbesartan-related hypotension were recorded, leading to
144     Treatment with the AT1 receptor blocker, irbesartan rescued the systolic dysfunction, normalized
145 gmented effect through coadministration with irbesartan, respectively.
146                               Treatment with irbesartan significantly decreased the pro-oxidative env
147                                              Irbesartan significantly reduced systolic blood pressure
148 e global, randomized clinical trials testing irbesartan, spironolactone, sacubitril/valsartan, and da
149 t dose 400 mg oral sparsentan once daily) or irbesartan (target dose 300 mg oral irbesartan once dail
150 onsymptomatic arterial events was lower with irbesartan than with placebo (risk ratio, 0.37 [95% CI,
151 sly reported in HFrEF but more frequent with irbesartan than with placebo.
152 erability comparable to those of placebo and irbesartan; the incidence of adverse events and number o
153 ximal suppression of inflammatory markers by irbesartan therapy in patients with CAD was seen at 12 w
154 ) patients and occurred more frequently with irbesartan treatment (8% vs. 4%).
155           Estimated GFR decreased early with irbesartan treatment and remained significantly lower th
156                      WRF after initiation of irbesartan treatment in HFpEF was associated with excess
157 symptomatic HF-PEF were randomly assigned to irbesartan (up to 300 mg daily) or placebo.
158  Also, venlafaxine, acesulfame, bezafibrate, irbesartan, valsartan, ibuprofen and naproxen displayed
159  from the sartan family: losartan potassium, irbesartan, valsartan, olmesartan medoxomil, and telmisa
160 curred in 8 of 29 patients (27.6%) receiving irbesartan versus 15 of 28 patients (53.6%) receiving pl
161                               Treatment with irbesartan was associated with a relative risk of end-st
162                               Treatment with irbesartan was associated with a risk of the primary com
163        In addition, the AT1 receptor blocker irbesartan was evaluated for its ability to suppress the
164                                              Irbesartan was well tolerated with no observed differenc
165                                              Irbesartan was well tolerated without evidence of dose-r
166                 The neurohormonal effects of irbesartan were highly variable and none of the changes
167 ses of an angiotensin II (AngII) antagonist, irbesartan, were assessed in eight healthy volunteers an
168 est rise in renal plasma flow in response to irbesartan, whereas renal plasma flow rose less and GFR
169  present in an AT(1) receptor antagonist (1, irbesartan) with key structural elements in a biphenylsu
170 ts were well balanced between sparsentan and irbesartan, with no new safety signals.
171 ose of the biphenyl AT(1) antagonists (e.g., irbesartan) would yield a compound with dual activity fo

 
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