ライフサイエンスコーパス: lonafarnib

1 e received pravastatin, zoledronic acid, and lonafarnib.

2 ng toxicities (DLTs) and pharmacokinetics of lonafarnib.

3 oionization efficiency of both clozapine and lonafarnib.

4 :1 in group 1 and 2:1 in group 2) to receive lonafarnib 100 mg (group 1) or lonafarnib 200 mg (group

5 2) to receive lonafarnib 100 mg (group 1) or lonafarnib 200 mg (group 2) twice daily for 28 days with

6 nducted an in vitro screen for resistance to lonafarnib, a farnesyl protein transferase inhibitor tha

7 Lonafarnib activated caspase-8 and its downstream caspas

8 estimate the MTD based on actual dosages of lonafarnib administered and toxicities observed during t

9 Here we show that the FTI lonafarnib affects the microtubule cytoskeleton resultin

10 at the protein farnesyltransferase inhibitor lonafarnib ameliorates some aspects of cardiovascular an

11 anistically, we show that the combination of lonafarnib and paclitaxel inhibits the in vitro deacetyl

12 th paclitaxel, similar to the combination of lonafarnib and paclitaxel.

13 nvestigated the modulation of DR5 by the FTI lonafarnib and the involvement of DR5 up-regulation in F

14 Group 1 placebo patients received open-label lonafarnib as group 2 participants.

15 important, supporting bortezomib followed by lonafarnib as the optimal schedule.

16 identified 9 mutations clustering around the lonafarnib binding site.

17 pharmacological delay (0.75 days [SE 0.24]), lonafarnib effectiveness in blocking HDV production was

18 S received the farnesyltransferase inhibitor lonafarnib for a minimum of 2 y.

19 nd tolerability of the prenylation inhibitor lonafarnib in patients with chronic delta hepatitis.

20 Lonafarnib increased CHOP expression, whereas silencing

21 By analyzing the DR5 promoter, we found that lonafarnib induced a CCAAT/enhancer-binding protein homo

22 yl ketone or small interfering RNA abrogated lonafarnib-induced apoptosis, indicating that lonafarnib

23 P-dependent DR5 up-regulation contributes to lonafarnib-induced apoptosis.

24 ssion using small interfering RNA attenuated lonafarnib-induced apoptosis.

25 DR5-mediated extrinsic apoptotic pathway in lonafarnib-induced apoptosis.

26 ereas silencing of CHOP expression abrogated lonafarnib-induced DR5 expression.

27 onafarnib-induced apoptosis, indicating that lonafarnib induces caspase-8-dependent apoptosis.

28 These results thus indicate that lonafarnib induces CHOP-dependent DR5 up-regulation.

29 rnesyl transferase inhibitor (FTI) SCH66336 (lonafarnib) inhibits the proliferation of STI571-resista

30 ose levels, the recommended phase II dose of lonafarnib is 115 mg/m2/dose administered twice daily by

31 with HGPS provide preliminary evidence that lonafarnib may improve vascular stiffness, bone structur

32 Comparisons with lonafarnib monotherapy treatment reveal additional bone

33 mprovement rates exceeded those of the prior lonafarnib monotherapy treatment trial.

34 on to descriptive comparisons with the prior lonafarnib monotherapy trial.

35 used to test either single agent bortezomib, lonafarnib, or the combination on MM signaling and apopt

36 Lonafarnib (SCH66336) is a farnesyl transferase inhibito

37 c study of the farnesyltransferase inhibitor lonafarnib (SCH66336) was conducted in children with rec

38 ized that combining a Ras pathway inhibitor (lonafarnib, SCH66336) with a proteasome inhibitor (borte

39 Lonafarnib serum concentrations correlated with HDV RNA

40 Treatment of chronic HDV with lonafarnib significantly reduces virus levels.

41 In addition, the lonafarnib/taxane combination is synergistic only in cel

42 ght into the putative molecular basis of the lonafarnib/taxane synergistic antiproliferative combinat

43 and made them resistant to the FTI SCH66336/lonafarnib to model emerging drug resistance in a patien

44 Lonafarnib up-regulated DR5 expression, increased cell-s

45 Lonafarnib was administered orally twice daily at dose l

46 s treated with a combination of imatinib and lonafarnib, we identified farnesyl protein transferase m

47 tiproliferative effects of Taxol and the FTI lonafarnib when used either as single agents or in combi

48 eatment with the combination of low doses of lonafarnib with paclitaxel markedly enhanced tubulin ace

49 ctional HDAC6 is required for the synergy of lonafarnib with taxanes.