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1 omized within 16 h to intravenous placebo or serelaxin.
2  (Likert scale; placebo, 150 patients [26%]; serelaxin, 156 [27%]; p=0.70).
3        Adverse event rates were similar with serelaxin (20.5%) and placebo (25.0%).
4 89 mL/min per 1.73 m(2) received intravenous serelaxin 30 mug/kg per day or placebo for 24 hours.
5 lus 48-h intravenous infusions of placebo or serelaxin (30 mug/kg per day) within 16 h from presentat
6 fewer deaths at day 180 (placebo, 65 deaths; serelaxin, 42; HR 0.63, 95% CI 0.42-0.93; p=0.019).
7  up to day 60 (placebo, 47.7 [SD 12.1] days; serelaxin, 48.3 [11.6]; p=0.37).
8 vents [60-day Kaplan-Meier estimate, 13.0%]; serelaxin, 76 events [13.2%]; hazard ratio [HR] 1.02 [0.
9 AHF) to evaluate the therapeutic efficacy of serelaxin, a recombinant form of human relaxin-2.
10                                              Serelaxin, a recombinant form of the naturally occurring
11                                              Serelaxin administration improved these markers, consist
12                                              Serelaxin also decreased lipid accumulation in kidney in
13      Renal plasma flow increased by 29% with serelaxin and 14% with placebo (13% relative increase wi
14    Filtration fraction increased by 36% with serelaxin and 62% with placebo (16% relative decrease wi
15 rimarily, we assessed the difference between serelaxin and placebo on renal plasma flow (para-aminohi
16 ential of selective renal vasodilation using serelaxin as a new treatment for renal dysfunction in ci
17                         We hypothesized that serelaxin could ameliorate renal vasoconstriction and re
18             Treatment of DOCA-salt rats with serelaxin decreased renal inflammation, including the ex
19 n the randomized clinical study, infusion of serelaxin for 120 min increased total renal arterial blo
20 with osmotic minipumps delivering vehicle or serelaxin for another 4 weeks.
21                                              Serelaxin improved the VAS AUC primary dyspnoea endpoint
22             The renal hemodynamic effects of serelaxin in patients with chronic heart failure are unk
23 tic targeting of renal vasoconstriction with serelaxin in the rat models increased kidney perfusion,
24      In patients with chronic heart failure, serelaxin increased renal plasma flow and reduced the in
25 tients were randomized 1:1 to treatment with serelaxin intravenous (i.v.) infusion (for 60 min at 80
26                                              Serelaxin is a promising therapy for acute heart failure
27      1161 patients were randomly assigned to serelaxin (n=581) or placebo (n=580).
28 NGS: 1161 patients were randomly assigned to serelaxin (n=581) or placebo (n=580).
29                In this study, the effects of serelaxin on cardiac and renal function, fibrosis, infla
30 ard models were used to assess the effect of serelaxin on each mode of death, on the basis of pre-spe
31       In the RELAX-AHF study, the effects of serelaxin on mortality were primarily driven by reductio
32 m of this study was to assess the effects of serelaxin on short-term changes in markers of organ dama
33 al of this study was to assess the effect of serelaxin on specific modes of death in patients with AH
34 with AHF to 48 h of therapy with intravenous serelaxin or placebo.
35 62% with placebo (16% relative decrease with serelaxin; P=0.0019) during 8 to 24 hours.
36 14% with placebo (13% relative increase with serelaxin; P=0.0386), whereas GFR changes did not differ
37                               Treatment with serelaxin prevented cardiac and renal dysfunction in DOC
38                                              Serelaxin prevented cardiac and renal fibrosis, as deter
39                                              Serelaxin (recombinant human relaxin-2) is a peptide mol
40                                              Serelaxin, recombinant human relaxin-2, is a vasoactive
41                                              Serelaxin reduced 180-day mortality, with similar effect
42                                  In summary, serelaxin reversed DOCA-salt induced cardiac and renal d
43 the Treatment of Acute Heart Failure) study, serelaxin, the recombinant form of human relaxin-2, redu
44 e RELAX-AHF trial tested the hypothesis that serelaxin-treated patients would have greater dyspnoea r
45              There was no apparent impact of serelaxin treatment on HF deaths or non-CV deaths.
46                                              Serelaxin treatment was associated with significant redu
47                                              Serelaxin treatment was well tolerated and safe, support
48                      Early administration of serelaxin was associated with a reduction of 180-day mor
49        Treatment of acute heart failure with serelaxin was associated with dyspnoea relief and improv
50 ATION: Treatment of acute heart failure with serelaxin was associated with dyspnoea relief and improv
51                      The treatment effect of serelaxin was most pronounced on other CV deaths (hazard
52                            In a pilot study, serelaxin was safe and well tolerated with positive clin
53                            Administration of serelaxin was safe and well tolerated, with no detriment

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