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 ive either a 48-hour intravenous infusion of
serelaxin (
30 mug per kilogram of body weight per day) o
6 lus 48-h intravenous infusions of placebo or
serelaxin (
30 mug/kg per day) within 16 h from presentat
7 fewer deaths at day 180 (placebo, 65 deaths;
serelaxin,
42; HR 0.63, 95% CI 0.42-0.93; p=0.019).
8 up to day 60 (placebo, 47.7 [SD 12.1] days;
serelaxin,
48.3 [11.6]; p=0.37).
9 vents [60-day Kaplan-Meier estimate, 13.0%];
serelaxin,
76 events [13.2%]; hazard ratio [HR] 1.02 [0.
10 AHF) to evaluate the therapeutic efficacy of
serelaxin,
a recombinant form of human relaxin-2.
11 Serelaxin,
a recombinant form of the naturally occurring
12 Serelaxin administration improved these markers, consist
13 Serelaxin also decreased lipid accumulation in kidney in
14 Renal plasma flow increased by 29% with
serelaxin and 14% with placebo (13% relative increase wi
15 Filtration fraction increased by 36% with
serelaxin and 62% with placebo (16% relative decrease wi
16 rimarily, we assessed the difference between
serelaxin and placebo on renal plasma flow (para-aminohi
17 ential of selective renal vasodilation using
serelaxin as a new treatment for renal dysfunction in ci
18 We hypothesized that
serelaxin could ameliorate renal vasoconstriction and re
19 Treatment of DOCA-salt rats with
serelaxin decreased renal inflammation, including the ex
20 monstrated in a transfected cell system that
serelaxin did not directly bind to AT(1)Rs but that cons
21 ized for acute heart failure, an infusion of
serelaxin did not result in a lower incidence of death f
22 n the randomized clinical study, infusion of
serelaxin for 120 min increased total renal arterial blo
23 with osmotic minipumps delivering vehicle or
serelaxin for another 4 weeks.
24 e had occurred in 227 patients (6.9%) in the
serelaxin group and in 252 (7.7%) in the placebo group (
25 ed in 285 of the 3274 patients (8.7%) in the
serelaxin group and in 290 of the 3271 patients (8.9%) i
26 Recombinant relaxin-2 (
serelaxin)
has shown beneficial effects in acute heart f
27 Serelaxin improved the VAS AUC primary dyspnoea endpoint
28 The renal hemodynamic effects of
serelaxin in patients with chronic heart failure are unk
29 tic targeting of renal vasoconstriction with
serelaxin in the rat models increased kidney perfusion,
30 In patients with chronic heart failure,
serelaxin increased renal plasma flow and reduced the in
31 tients were randomized 1:1 to treatment with
serelaxin intravenous (i.v.) infusion (for 60 min at 80
32 Serelaxin is a promising therapy for acute heart failure
33 Serelaxin is a recombinant form of human relaxin-2, a va
34 s studies have suggested that treatment with
serelaxin may result in relief of symptoms and in better
35 1161 patients were randomly assigned to
serelaxin (
n=581) or placebo (n=580).
36 NGS: 1161 patients were randomly assigned to
serelaxin (
n=581) or placebo (n=580).
37 In this study, the effects of
serelaxin on cardiac and renal function, fibrosis, infla
38 ard models were used to assess the effect of
serelaxin on each mode of death, on the basis of pre-spe
39 In the RELAX-AHF study, the effects of
serelaxin on mortality were primarily driven by reductio
40 m of this study was to assess the effects of
serelaxin on short-term changes in markers of organ dama
41 al of this study was to assess the effect of
serelaxin on specific modes of death in patients with AH
42 y blocked the antifibrotic effects of either
serelaxin or an AT(2)R agonist (compound 21).
43 with AHF to 48 h of therapy with intravenous
serelaxin or placebo.
44 62% with placebo (16% relative decrease with
serelaxin;
P=0.0019) during 8 to 24 hours.
45 14% with placebo (13% relative increase with
serelaxin;
P=0.0386), whereas GFR changes did not differ
46 Treatment with
serelaxin prevented cardiac and renal dysfunction in DOC
47 Serelaxin prevented cardiac and renal fibrosis, as deter
48 h) treatment of primary cardiomyocytes with
serelaxin (
recombinant human relaxin-2) increased the ca
49 Serelaxin (
recombinant human relaxin-2) is a peptide mol
50 Serelaxin,
recombinant human relaxin-2, is a vasoactive
51 Serelaxin reduced 180-day mortality, with similar effect
52 Studies have shown that
serelaxin requires the angiotensin II (AngII) type 2 rec
53 In summary,
serelaxin reversed DOCA-salt induced cardiac and renal d
54 Candesartan also ameliorated
serelaxin'
s antifibrotic actions in the left ventricle o
55 the Treatment of Acute Heart Failure) study,
serelaxin,
the recombinant form of human relaxin-2, redu
56 iac tissue and plasma samples extracted from
serelaxin-
treated mice at day 28.
57 e RELAX-AHF trial tested the hypothesis that
serelaxin-
treated patients would have greater dyspnoea r
58 There was no apparent impact of
serelaxin treatment on HF deaths or non-CV deaths.
59 Serelaxin treatment was associated with significant redu
60 Serelaxin treatment was well tolerated and safe, support
61 brogated antifibrotic signal transduction of
serelaxin via RXFP1 in vitro and in vivo.
62 Early administration of
serelaxin was associated with a reduction of 180-day mor
63 Treatment of acute heart failure with
serelaxin was associated with dyspnoea relief and improv
64 ATION: Treatment of acute heart failure with
serelaxin was associated with dyspnoea relief and improv
65 The treatment effect of
serelaxin was most pronounced on other CV deaths (hazard
66 In a pilot study,
serelaxin was safe and well tolerated with positive clin
67 Administration of
serelaxin was safe and well tolerated, with no detriment
68 amined the signal transduction mechanisms of
serelaxin when applied to primary rat renal and human ca
69 Recombinant human relaxin-2 (
serelaxin),
which has organ-protective actions mediated