ライフサイエンスコーパス: dacomitinib

1 irreversible EGFR tyrosine kinase inhibitor dacomitinib.

2 20 insertion mutants restored sensitivity to dacomitinib.

3 inantly grade 1 to 2, and more frequent with dacomitinib.

4 ed 878 patients and randomly assigned 439 to dacomitinib (256 KRAS wild type) and 439 (263 KRAS wild

5 and were then randomly allocated 2:1 to oral dacomitinib 45 mg once-daily or matched placebo centrall

6 assigned participants (1:1) to receive oral dacomitinib 45 mg/day (in 28-day cycles) or oral gefitin

7 randomly assigned patients in a 1:1 ratio to dacomitinib (45 mg/day) or erlotinib (150 mg/day) with m

8 progression-free survival was 2.6 months for dacomitinib (95% CI 1.9-2.9) and erlotinib (95% CI 1.9-3

9 In this report, we show that dacomitinib, a pan-ErbB receptor inhibitor, diminished g

10 Dacomitinib, a pan-HER inhibitor, is approved for first-

11 Dacomitinib, an irreversible pan-HER inhibitor, had show

12 FS was 2.21 months for patients treated with dacomitinib and 1.84 months for patients treated with er

13 t) was 2.86 months for patients treated with dacomitinib and 1.91 months for patients treated with er

14 FS was 3.71 months for patients treated with dacomitinib and 1.91 months for patients treated with er

15 , 2013, we randomly assigned 480 patients to dacomitinib and 240 patients to placebo.

16 were reported in 52 (12%) patients receiving dacomitinib and 40 (9%) patients receiving erlotinib.

17 al was 9.53 months for patients treated with dacomitinib and 7.44 months for patients treated with er

18 185 (39%) of 477 patients who received dacomitinib and 86 (36%) of 239 patients who received pl

19 tations seldom achieve clinical responses to dacomitinib and afatinib, two covalent quinazoline-based

20 ents were reported in 21 (9%) patients given dacomitinib and in ten (4%) patients given gefitinib.

21 99804) has been assigned the nomenclature of dacomitinib and is currently under clinical evaluation.

22 We did a trial of dacomitinib as initial systemic therapy in clinically an

23 Moreover, dacomitinib attenuated migration and invasion of the EOC

24 y enhanced the sensitivity of SCCHN cells to dacomitinib by the loss of both translesion synthesis an

25 optimal dosing schedule for osimertinib and dacomitinib combination therapy.

26 l lung cancer showed favourable efficacy for dacomitinib compared with erlotinib.

27 A combination of osimertinib and dacomitinib could therefore induce more durable response

28 Dacomitinib demonstrated significantly improved PFS vers

29 Dacomitinib did not improve overall survival compared wi

30 Dacomitinib did not increase overall survival and cannot

31 nhibitors (Afatinib, Gefitinib, Osimertinib, Dacomitinib, Erlotinib), confirming the biological relev

32 Two treatment-related deaths occurred in the dacomitinib group (one related to untreated diarrhoea an

33 4 months (IQR 15.6-29.6) for patients in the dacomitinib group and 24.4 months (11.5-38.9) for those

34 ew was 14.7 months (95% CI 11.1-16.6) in the dacomitinib group and 9.2 months (9.1-11.0) in the gefit

35 was 2.6 months (95% CI 1.9-2.8) in both the dacomitinib group and the erlotinib group (stratified ha

36 However, patients in the dacomitinib group had longer progression-free survival t

37 nts were diarrhoea (47 [11%] patients in the dacomitinib group vs ten [2%] patients in the erlotinib

38 Dacomitinib had encouraging clinical activity as initial

39 Compared with placebo, patients allocated dacomitinib had significantly longer time to deteriorati

40 We designed BR.26 to assess whether dacomitinib improved overall survival in heavily pretrea

41 (version 1.0) to investigate the activity of dacomitinib in all patients with a baseline scan and at

42 nvestigation on the therapeutic potential of dacomitinib in treatment of the chemoresistant EOC.

43 ted therapies, are sensitive to afatinib and dacomitinib in vitro.

44 Dacomitinib is a covalent pan-HER inhibitor that has sho

45 Dacomitinib is a second-generation, irreversible EGFR ty

46 Dacomitinib is an irreversible pan-EGFR family tyrosine

47 Dacomitinib is an irreversible pan-HER tyrosine-kinase i

48 e patients were randomly assigned to receive dacomitinib (n=227) or gefitinib (n=225).

49 ted qualitative differences in the effect of dacomitinib on overall survival for patients with KRAS-m

50 Compared with placebo, the effect of dacomitinib on overall survival seemed similar in patien

51 We gave dacomitinib orally once daily (45 mg or 30 mg) until pro

52 nts who derived extended clinical benefit to dacomitinib (P = 0.04).

53 This randomized, open-label trial compared dacomitinib (PF-00299804), an irreversible inhibitor of

54 Introduction of Gly770 into two dacomitinib-resistant EGFR exon 20 insertion mutants res

55 identify potential predictive biomarkers for dacomitinib sensitivity, we performed whole exome sequen

56 INTERPRETATION: Dacomitinib significantly improved progression-free surv

57 erization domain mutations show responses to dacomitinib treatment followed by within-pathway resista

58 clinically achieved a partial response after dacomitinib treatment.

59 o (median 6.83 months [95% CI 6.08-7.49] for dacomitinib vs 6.31 months [5.32-7.52] for placebo; haza

60 events were diarrhoea (59 [12%] patients on dacomitinib vs no controls), acneiform rash (48 [10%] vs

61 is acneiform (31 [14%] of 227 patients given dacomitinib vs none of 224 patients given gefitinib), di

62 Irreversible EGFR inhibition with dacomitinib was not superior to erlotinib in an unselect

63 We aimed to compare dacomitinib with erlotinib in a phase 3 study.