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1 43 AEs in 17 patients (3.1%) were related to icatibant.
2 ) in two patients were considered related to icatibant.
3 reached and sustained with a single bolus of icatibant.
4  shocked mice treated with a single bolus of icatibant.
5 in response to compound 48/80, AG-30/5C, and Icatibant.
6 , plasma pool C1-INH, and the B2R antagonist icatibant.
7 l ester or bradykinin B2 receptor antagonist icatibant.
8 E attacks and decide when to self-administer icatibant.
9 89 of 97 patients used a single injection of icatibant.
10 rable with results from controlled trials of icatibant.
11 ment with the bradykinin receptor antagonist icatibant.
12 on of the bradykinin B2-receptor antagonist, icatibant (0.5 mg/kg).
13 s of captopril alone (25 mg), captopril plus icatibant (100 microg per kilogram of body weight), the
14 treated with approved therapies (pdC1-INH or icatibant), 15% were with tranexamic acid, and 35% were
15 thin 6 hours of presentation to subcutaneous icatibant 30 mg or placebo at 0 and 6 hours later.
16 evere attacks were treated with subcutaneous icatibant 30 mg; two moderate attacks resolved without t
17 pate in the OLE phase and receive open-label icatibant (30 mg subcutaneously) for the treatment of cu
18 care: 62.6 +/- 2.7%, pdC1INH: 64.9 +/- 7.5%, icatibant: 66.7 +/- 4.8%; p = 0.4), with no significant
19 e in the United States in December 2009) and icatibant (a selective bradykinin B2 receptor antagonist
20  efficacy and safety of single injections of icatibant, a bradykinin B(2) receptor antagonist, in the
21                                              Icatibant, a bradykinin B(2) receptor antagonist, promot
22                                              Icatibant, a bradykinin B2 receptor antagonist, is an es
23                                    Recently, icatibant, a bradykinin receptor antagonist, has been us
24    Accordingly, this effect was prevented by icatibant, a clinically available B2 receptor antagonist
25                         We aimed to evaluate icatibant, a competitive antagonist of the bradykinin B2
26                                              Icatibant, a selective bradykinin B(2) receptor antagoni
27 ract to treatment with 30 mg of subcutaneous icatibant, a selective bradykinin B2 receptor antagonist
28 , a specific bradykinin-receptor antagonist, icatibant acetate (HOE 140), was used to determine the c
29 dy, both a bradykinin B2 receptor inhibitor (icatibant acetate) and plasma-derived C1 inhibitor (pdC1
30 and 31 received treatment, with 13 receiving icatibant and 18 receiving placebo.
31 symptoms to drug administration was 1 h with icatibant and 2 h with pd-C1INH and median time from dru
32  treatments were self-administered: 93% with icatibant and 59% with pd-C1-INH.
33 s and its signaling mediators was blocked by icatibant and dominant-negative Akt, indicating a kinin
34 rd therapy required rescue intervention with icatibant and prednisolone; 1 patient required tracheoto
35  (angiotensin-converting enzyme inhibitors + icatibant), and 5) shocked mice treated with a single bo
36                                              Icatibant appeared to provide effective symptom relief a
37 ours (interquartile range, 3.0 to 16.0) with icatibant as compared with 27.1 hours (interquartile ran
38 h cardiovascular disease, nor in those using icatibant at a frequency above label guidelines.
39 dynamic effect of B2 receptor blockade using icatibant (B2 receptor antagonist) was studied using a p
40  with and without the B2 receptor antagonist icatibant (B2-ant); or (c) an AT1-ant with and without a
41                               Treatment with icatibant (bradykinin-B2-antagonist) or anakinra (interl
42                                              Icatibant caused MC degranulation via a pertussis toxin-
43                                              Icatibant did not alter the renal hemodynamic response t
44 t of C57BL/6 mice with PETN, L-NA, C1-INH or icatibant did not change B2R protein expression.
45                    One patient randomized to icatibant did not complete the visual analog scale and w
46 d (1:1) to treatment with either three 30-mg icatibant doses/d for 3 consecutive days plus standard c
47 ments (plasma-derived C1 esterase inhibitor, icatibant, ecallantide [United States only], and recombi
48              No safety data are available on icatibant, ecallantide, or recombinant human C1-INH (rhC
49                 Fifty-four patients received icatibant for 374 attacks (176 cutaneous, 168 abdominal,
50 r STZ injection, could as well be reduced by icatibant given for the final 2 weeks of the experimenta
51 occurred in 27 of 37 patients (73.0%) in the icatibant group and 20 of 36 patients (55.6%) in the con
52 ficacy ensued in 37 patients (100.0%) in the icatibant group and 30 patients (83.3%) in the control g
53           Significantly more patients in the icatibant group than in the standard-therapy group had c
54                       No patient died in the icatibant group, compared with 6 patients (16.7%) in the
55                                              Icatibant has been reported to decrease time-to-resoluti
56 ter attack duration; effectiveness/safety of icatibant has been shown across a broad range of patient
57 e second BK2A tested was the newer compound, icatibant (Hoe 140; D-Arg,[Hyp3,Thi5,D-Tic7,Oic8]-bradyk
58 ting enzyme inhibitors and a single bolus of icatibant (HOE-140) immediately before anesthesia (angio
59  have demonstrated that the effectiveness of icatibant in a real-world setting is comparable to effic
60 ficacy and safety of repeated treatment with icatibant in adult patients experiencing HAE attacks dur
61              We describe our experience with icatibant in eight patients with angioedema because of a
62 as to assess the safety of self-administered icatibant in patients with HAE type I or II.
63  2009 to monitor the effectiveness/safety of icatibant in routine clinical practice.
64 study monitoring safety and effectiveness of icatibant in the real-world setting.
65                                     A single icatibant injection achieved complete symptom resolution
66 all, 89.8% of attacks resolved with a single icatibant injection.
67                   The B2 receptor antagonist icatibant is approved for treatment of attacks of heredi
68 e prediction that the FDA-approved molecule, icatibant, might be able to interrupt this feedback loop
69 ly reported AE; rescue medications including icatibant (N = 3) and C1-inhibitor concentrate (N = 6) w
70                                              Icatibant-naive patients were treated by an HCP prior to
71                  Notably, no SAEs related to icatibant occurred in patients with cardiovascular disea
72 + kinin B(2) receptor antagonist (B(2)-ant) (icatibant) (only BN).
73    Survivors of COVID-19 treated with either icatibant or pdC1INH as a supplement to standard-care un
74                                          The Icatibant Outcome Survey (IOS) is an observational study
75                                          The Icatibant Outcome Survey is an ongoing observational reg
76    During volume-targeted hemorrhagic shock, icatibant prevented blood pressure lowering in the angio
77 e of the B(2)R by systemic administration of icatibant prevented the beneficial effect of bone marrow
78 nce and ease of use supports the adoption of icatibant self-administration in clinical practice.
79                                    A similar icatibant-sensitive enhancement of citric acid-evoked co
80 nstrates the novel finding that AG-30/5C and Icatibant serve as G protein-biased agonists for MRGPRX2
81  reducing myocardial injury and edema, while icatibant showed less favorable effects, and highlights
82                      The coadministration of icatibant significantly attenuated the hypotensive effec
83 re trained to self-administer a single 30-mg icatibant subcutaneous injection to treat their next att
84     Bradykinin-B2-receptor (B2R) blockade by icatibant substantially impaired recruitment of circulat
85 tion of edema was significantly shorter with icatibant than with combination therapy with a glucocort
86 ymptom score) was significantly shorter with icatibant than with standard therapy (2.0 hours vs. 11.7
87                                       Adding icatibant to standard care was safe and improved both CO
88    Second treatment was required in 12.7% of icatibant-treated attacks and in 1.9% of pdC1-INH-treate
89            We analyzed safety data from 3025 icatibant-treated attacks in 557 patients (enrolled betw
90 ere conducted in patients with at least five icatibant-treated attacks throughout the FAST-2 OLE phas
91 nstrated the efficacy and safety of repeated icatibant treatment for HAE attacks.
92 ution of symptoms was similar in placebo and icatibant treatment groups (P = .19 for the primary symp
93                Symptom improvement following icatibant treatment occurred in 0.5 (0.25-2.10) h and co
94 ession induced by NO, bradykinin, C1-INH, or icatibant unlikely contribute to bradykinin-induced angi
95 ed in AEs occurring in on-label vs off-label icatibant users.
96                  Median attack duration with icatibant was 8 and 11.5 h with pd-C1 INH.
97                                              Icatibant was generally well tolerated.
98 e after the administration of captopril plus icatibant was similar to that after the administration o