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 Clinical trials have demonstrated that lonafarnib, a farnesyltransferase inhibitor, extends the

8 We select lonafarnib, a licensed farnesyltransferase inhibitor, an

9 Lonafarnib activated caspase-8 and its downstream caspas

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

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

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

13 onance reveals RSV fusion protein binding of lonafarnib and co-crystallography identifies the lonafar

14 Combination treatment with Lonafarnib and Everolimus produced additional benefits s

15 We tested the effects of HGPS therapeutics Lonafarnib and Everolimus separately and together, curre

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

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

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

19 drug repurposing candidates and establishes lonafarnib as a bona fide fusion protein inhibitor.

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

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

22 farnib and co-crystallography identifies the lonafarnib binding site within RSV F.

23 identified 9 mutations clustering around the lonafarnib binding site.

24 Oral administration of lonafarnib dose-dependently reduces RSV virus load in a

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

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

27 s may provide cardiovascular benefits beyond Lonafarnib, if the Everolimus dose can be tolerated.

28 Lonafarnib improved shear stress response of HGPS iPSC-d

29 that the farnesyltransferase inhibitor (FTI) lonafarnib in addition to ALK TKIs act synergistically i

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

31 od and Drug Administration approved Zokinvy (lonafarnib) in November 2020 for treating these patients

32 Lonafarnib increased CHOP expression, whereas silencing

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

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

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

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

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

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

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

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

41 ith variant RSV fusion proteins confirm that lonafarnib inhibits RSV cell entry and that these mutati

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

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

44 Proof-of-concept studies demonstrated lonafarnib (LNF), a first-in-class oral prenylation inhi

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

46 Lonafarnib monotherapy did not improve bone or cartilage

47 Comparisons with lonafarnib monotherapy treatment reveal additional bone

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

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

50 in improved outcomes over that achieved with lonafarnib monotherapy.

51 utcomes of daily post-weaning treatment with lonafarnib on the composition and biomechanical phenotyp

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

53 ome under evaluation, including bulevirtide, lonafarnib, pegylated interferon lambda, and REP-2139 cr

54 itor rapamycin alone nor dual treatment with lonafarnib plus rapamycin improved outcomes over that ac

55 while treated with farnesylation inhibitors lonafarnib+/-pravastatin and zoledronate, within 3 seque

56 ial of different treatment combinations with lonafarnib, pravastatin, and zoledronic acid.

57 V cell entry and that these mutations confer lonafarnib resistance.

58 Lonafarnib resulted in 100% survival of the treated prog

59 irtide monotherapy and 19% after 48 weeks of lonafarnib, ritonavir, and pegylated interferon alfa tre

60 Lonafarnib (SCH66336) is a farnesyl transferase inhibito

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

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

63 Passaging of RSV with lonafarnib selects for phenotypic resistance and fixatio

64 Lonafarnib serum concentrations correlated with HDV RNA

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

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

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

68 in levels in HGPS plasma that decreased with lonafarnib therapy.

69 with either inhibitors of prenylation (PTI) lonafarnib, tipifarnib, zoledronic acid, or atorvastatin

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

71 Lonafarnib treatment resulted in an average per-visit pr

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

73 Lonafarnib was administered orally twice daily at dose l

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

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

76 ch blocks entry of HDV into hepatocytes, and lonafarnib, which interferes with HDV assembly, showed t

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

78 The lonafarnib with ritonavir for HDV-2 (LOWR-2) study's aim

79 The lonafarnib with ritonavir for HDV-2 (LOWR-2) study's aim

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