ライフサイエンスコーパス: icatibant

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 , plasma pool C1-INH, and the B2R antagonist icatibant.

6 l ester or bradykinin B2 receptor antagonist icatibant.

7 E attacks and decide when to self-administer icatibant.

8 89 of 97 patients used a single injection of icatibant.

9 rable with results from controlled trials of icatibant.

10 ment with the bradykinin receptor antagonist icatibant.

11 on of the bradykinin B2-receptor antagonist, icatibant (0.5 mg/kg).

12 s of captopril alone (25 mg), captopril plus icatibant (100 microg per kilogram of body weight), the

13 treated with approved therapies (pdC1-INH or icatibant), 15% were with tranexamic acid, and 35% were

14 thin 6 hours of presentation to subcutaneous icatibant 30 mg or placebo at 0 and 6 hours later.

15 evere attacks were treated with subcutaneous icatibant 30 mg; two moderate attacks resolved without t

16 pate in the OLE phase and receive open-label icatibant (30 mg subcutaneously) for the treatment of cu

17 e in the United States in December 2009) and icatibant (a selective bradykinin B2 receptor antagonist

18 efficacy and safety of single injections of icatibant, a bradykinin B(2) receptor antagonist, in the

19 Icatibant, a bradykinin B2 receptor antagonist, is an es

20 Recently, icatibant, a bradykinin receptor antagonist, has been us

21 Accordingly, this effect was prevented by icatibant, a clinically available B2 receptor antagonist

22 ract to treatment with 30 mg of subcutaneous icatibant, a selective bradykinin B2 receptor antagonist

23 , a specific bradykinin-receptor antagonist, icatibant acetate (HOE 140), was used to determine the c

24 and 31 received treatment, with 13 receiving icatibant and 18 receiving placebo.

25 symptoms to drug administration was 1 h with icatibant and 2 h with pd-C1INH and median time from dru

26 treatments were self-administered: 93% with icatibant and 59% with pd-C1-INH.

27 s and its signaling mediators was blocked by icatibant and dominant-negative Akt, indicating a kinin

28 rd therapy required rescue intervention with icatibant and prednisolone; 1 patient required tracheoto

29 (angiotensin-converting enzyme inhibitors + icatibant), and 5) shocked mice treated with a single bo

30 Icatibant appeared to provide effective symptom relief a

31 ours (interquartile range, 3.0 to 16.0) with icatibant as compared with 27.1 hours (interquartile ran

32 h cardiovascular disease, nor in those using icatibant at a frequency above label guidelines.

33 dynamic effect of B2 receptor blockade using icatibant (B2 receptor antagonist) was studied using a p

34 with and without the B2 receptor antagonist icatibant (B2-ant); or (c) an AT1-ant with and without a

35 Icatibant did not alter the renal hemodynamic response t

36 t of C57BL/6 mice with PETN, L-NA, C1-INH or icatibant did not change B2R protein expression.

37 One patient randomized to icatibant did not complete the visual analog scale and w

38 No safety data are available on icatibant, ecallantide, or recombinant human C1-INH (rhC

39 Fifty-four patients received icatibant for 374 attacks (176 cutaneous, 168 abdominal,

40 r STZ injection, could as well be reduced by icatibant given for the final 2 weeks of the experimenta

41 Significantly more patients in the icatibant group than in the standard-therapy group had c

42 Icatibant has been reported to decrease time-to-resoluti

43 e second BK2A tested was the newer compound, icatibant (Hoe 140; D-Arg,[Hyp3,Thi5,D-Tic7,Oic8]-bradyk

44 ting enzyme inhibitors and a single bolus of icatibant (HOE-140) immediately before anesthesia (angio

45 ficacy and safety of repeated treatment with icatibant in adult patients experiencing HAE attacks dur

46 We describe our experience with icatibant in eight patients with angioedema because of a

47 as to assess the safety of self-administered icatibant in patients with HAE type I or II.

48 study monitoring safety and effectiveness of icatibant in the real-world setting.

49 A single icatibant injection achieved complete symptom resolution

50 all, 89.8% of attacks resolved with a single icatibant injection.

51 The B2 receptor antagonist icatibant is approved for treatment of attacks of heredi

52 ly reported AE; rescue medications including icatibant (N = 3) and C1-inhibitor concentrate (N = 6) w

53 Icatibant-naive patients were treated by an HCP prior to

54 Notably, no SAEs related to icatibant occurred in patients with cardiovascular disea

55 + kinin B(2) receptor antagonist (B(2)-ant) (icatibant) (only BN).

56 The Icatibant Outcome Survey (IOS) is an observational study

57 During volume-targeted hemorrhagic shock, icatibant prevented blood pressure lowering in the angio

58 e of the B(2)R by systemic administration of icatibant prevented the beneficial effect of bone marrow

59 nce and ease of use supports the adoption of icatibant self-administration in clinical practice.

60 A similar icatibant-sensitive enhancement of citric acid-evoked co

61 The coadministration of icatibant significantly attenuated the hypotensive effec

62 re trained to self-administer a single 30-mg icatibant subcutaneous injection to treat their next att

63 Bradykinin-B2-receptor (B2R) blockade by icatibant substantially impaired recruitment of circulat

64 tion of edema was significantly shorter with icatibant than with combination therapy with a glucocort

65 ymptom score) was significantly shorter with icatibant than with standard therapy (2.0 hours vs. 11.7

66 Second treatment was required in 12.7% of icatibant-treated attacks and in 1.9% of pdC1-INH-treate

67 We analyzed safety data from 3025 icatibant-treated attacks in 557 patients (enrolled betw

68 ere conducted in patients with at least five icatibant-treated attacks throughout the FAST-2 OLE phas

69 nstrated the efficacy and safety of repeated icatibant treatment for HAE attacks.

70 ution of symptoms was similar in placebo and icatibant treatment groups (P = .19 for the primary symp

71 Symptom improvement following icatibant treatment occurred in 0.5 (0.25-2.10) h and co

72 ession induced by NO, bradykinin, C1-INH, or icatibant unlikely contribute to bradykinin-induced angi

73 ed in AEs occurring in on-label vs off-label icatibant users.

74 Median attack duration with icatibant was 8 and 11.5 h with pd-C1 INH.

75 Icatibant was generally well tolerated.

76 e after the administration of captopril plus icatibant was similar to that after the administration o