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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

31 Bosutinib demonstrated acceptable safety with manageable

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

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

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

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

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

37 Bosutinib exhibited an acceptable safety profile; the mo

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

39 Bosutinib had an acceptable safety profile; treatment-em

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

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

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

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

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

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

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

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

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

49 Bosutinib may offer a new treatment option for patients

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

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

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

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

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

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

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

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

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

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

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

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