ライフサイエンスコーパス: bosutinib

1 nd-generation TKIs nilotinib, dasatinib, and bosutinib.

2 tinib, dasatinib, ponatinib, rebastinib, and bosutinib.

3 samples were less sensitive to dasatinib and bosutinib.

4 lled with imatinib, dasatinib, nilotinib, or bosutinib.

5 Eighty-five percent of patients on bosutinib, 100% on nilotinib, and 33% on imatinib had no

6 of kidney enlargement was reduced by 66% for bosutinib 200 mg/d versus placebo (1.63% versus 4.74%, r

7 ey volume >/=750 ml were randomized 1:1:1 to bosutinib 200 mg/d, bosutinib 400 mg/d, or placebo for <

8 were randomized 1:1:1 to bosutinib 200 mg/d, bosutinib 400 mg/d, or placebo for </=24 months.

9 onse (MMR) rate at 12 months was higher with bosutinib (41%; 95% CI, 35% to 47%) compared with imatin

10 luated the efficacy and safety of once-daily bosutinib 500 mg in leukemia patients after resistance/i

11 part 2 evaluated the efficacy and safety of bosutinib 500 mg once-daily dosing.

12 We assessed the safety and tolerability of bosutinib 500 mg per day in a phase 1/2 study in chronic

13 CyR) rate at 12 months was not different for bosutinib (70%; 95% CI, 64% to 76%) versus imatinib (68%

14 Compound 1 (SKI-606, bosutinib), a 7-alkoxy-4-[(2,4-dichloro-5-methoxyphenyl)

15 alpha-Parvin and PINCH-1 sensitizes cells to bosutinib, a clinically approved SRC/ABL kinase inhibito

16 Bosutinib, a dual Src/Abl kinase inhibitor, has shown po

17 Bosutinib, a dual Src/Abl tyrosine kinase inhibitor (TKI

18 nvasive thyroid cancer cells; so, we explore bosutinib, a specific inhibitor for SRC, to explore SRC

19 Finally, bosutinib, a tyrosine kinase inhibitor, markedly reduced

20 SRC inhibitors (DGY-06-116, dasatinib, and bosutinib) also exhibit synergistic effects with MRTX849

21 te study assessed the efficacy and safety of bosutinib, an oral dual Src/Bcr-Abl tyrosine kinase inhi

22 Updated information regarding bosutinib and asciminib, the latter currently in clinica

23 ed to determine inhibition constants of both bosutinib and dasatinib.

24 A rational combination of bosutinib and gefitinib showed additive and synergistic

25 The safety profiles of bosutinib and imatinib were distinct; GI and liver-relat

26 e inhibitors (TKIs), including nilotinib and bosutinib and showed that they reduce the level of nucle

27 , with the addition of dasatinib, nilotinib, bosutinib, and ponatinib, deeper and more rapid reductio

28 ministration (FDA)-approved drugs dasatinib, bosutinib, and saracatinib that target ABL, SRC-family,

29 ib as well as SFK inhibitors dasatinib, PP1, bosutinib, and Src inhibitor 1 dramatically inhibited AN

30 cytogenetic and major molecular response to bosutinib appeared comparable with other published phase

31 d FDA-approved SRC inhibitors, dasatinib and bosutinib, are multitargeted kinase inhibitors.

32 of three CML-related deaths occurred on the bosutinib arm compared with eight on the imatinib arm.

33 ity map (K-Map), we identified and validated bosutinib as an effective compound that could inhibit pr

34 In conclusion, compared with placebo, bosutinib at 200 mg/d reduced kidney growth in patients

35 doses for 24 patients who initially received bosutinib at 400 mg/d were later reduced to 200 mg/d.

36 rs that inhibit SRC, including dasatinib and bosutinib, bind their target in the active "open" confor

37 last phase occurred in four patients (2%) on bosutinib compared with 10 patients (4%) on imatinib.

38 Time to CCyR and MMR was faster with bosutinib compared with imatinib (two-sided P < .001 for

39 ast phase, and fewer CML-related deaths with bosutinib compared with imatinib.

40 matinib, and second-generation TKIs, such as bosutinib, dasatinib, and nilotinib, have improved CML-r

41 includes inhibitors of Src tyrosine kinase (bosutinib, dasatinib, cytarabine and saracatinib), which

42 We assessed interactions of bosutinib, dasatinib, imatinib, nilotinib, and ponatinib

43 Like in thyroid cells, bosutinib decreases oxidative PTEN in patient lymphoblas

44 Bosutinib demonstrated acceptable safety with manageable

45 Bcr-Abl inhibitors nilotinib, dasatinib, and bosutinib developed to override imatinib resistance are

46 ecreased soluble and insoluble TDP-43, while bosutinib did not affect the insoluble level.

47 ls of endogenous TDP-43, while nilotinib and bosutinib did not alter TDP-43, underscoring an indispen

48 Sensitivity to bosutinib did not correlate with ABL dependency; instead

49 Median bosutinib duration was 11.1 (range, 0.03-83.4) months.

50 The phase III Bosutinib Efficacy and Safety in Newly Diagnosed Chronic

51 Bosutinib exhibited an acceptable safety profile; the mo

52 IC50 value, 0.7 mum) followed by ponatinib > bosutinib > dasatinib > imatinib.

53 Bosutinib had an acceptable safety profile; treatment-em

54 atment period, patients receiving placebo or bosutinib had similar annualized eGFR decline.

55 Bosutinib has a different tolerability profile than othe

56 In this phase 1/2 study we evaluated bosutinib in patients with chronic phase imatinib-resist

57 potential treatment with SRC inhibitors like bosutinib in PTEN-wild-type SDHD-variant/mutation positi

58 bitors, we tested an Src inhibitor, SKI-606 (bosutinib), in the MMTV-PyVmT transgenic mouse model of

59 inhibition of Src family kinases by SKI-606 (bosutinib) induces C/EBPdelta expression in an SIAH2-dep

60 ong affected patients, 46% were managed with bosutinib interruption and 32% with dose reduction.

61 Bosutinib is an oral Src/Abl tyrosine kinase inhibitor.

62 Bosutinib is an oral, dual SRC/ABL tyrosine kinase inhib

63 Bosutinib is approved for adults with chronic myeloid le

64 These data suggest bosutinib is effective and tolerable in patients with ch

65 ently in clinical trials, will be presented; bosutinib is of particular interest as the drug's transi

66 not correlate with ABL dependency; instead, bosutinib likely induces these effects by acting as a SR

67 Bosutinib may offer a new treatment option for patients

68 A fourth drug, bosutinib, may also win FDA approval in 2011.

69 apy (n = 4) or receiving dasatinib (n = 27), bosutinib (n = 32), imatinib (n = 19), or nilotinib (n =

70 own agents such as Albendazole, Gemcitabine, Bosutinib, Neratinib, and Ponatinib.

71 e first-line treatment (imatinib, dasatinib, bosutinib, nilotinib, and asciminib) and 5 approved for

72 gression despite initial therapy (dasatinib, bosutinib, nilotinib, ponatinib, asciminib).

73 owed that LCK inhibitors, such as dasatinib, bosutinib, nintedanib, and WH-4-023, are able to induce

74 sistent with the profile in prior studies of bosutinib; no new toxicities were identified.

75 No significant difference was found with bosutinib (OR, 2.77; 95% CI, 0.39-19.77).

76 b, ponatinib), gastrointestinal disturbance (bosutinib), or increased amylase and lipase with pancrea

77 ong patients managed with dose interruption, bosutinib rechallenge was successful in 74%.

78 Accordingly, inhibition of Abl/Src with bosutinib reduced FcgammaRIIA-mediated glomerular neutro

79 GC cells treated with midostaurin or bosutinib significantly suppressed migration in vitro an

80 were targeted by a Src/Abl kinase inhibitor, bosutinib (SKI-606), or a specific-inhibitor of Axl (R42

81 owing IgG deposition that may be targeted by bosutinib to avert glomerular injury.

82 Whole-genome RNA sequencing following bosutinib treatment in ILK knockout cells identified bro

83 respectively; P=0.01) and by 82% for pooled bosutinib versus placebo (0.84% versus 4.74%, respective

84 liver-related events were more frequent with bosutinib, whereas neutropenia, musculoskeletal disorder

85 ronic Myeloid Leukemia (BELA) trial compared bosutinib with imatinib in newly diagnosed, chronic-phas