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1 of gefitinib; PBTC-014: phase I/II study of tipifarnib).
2 that was further enhanced by the addition of tipifarnib.
3 ose-limiting toxicities occurred with 21-day tipifarnib.
4 farnib versus 5 of 30 (17%) receiving 21-day tipifarnib.
5 courses of a farnesyltransferase inhibitor, tipifarnib.
6 s with AML who are more likely to respond to tipifarnib.
7 mor (median, 100%; range, 55% to 100%) after tipifarnib.
8 hours), and predose trough concentrations of tipifarnib.
11 n age, 77 years) received 224 cycles of oral tipifarnib (300-600 mg twice daily for 14 or 21 days) pl
14 in 50% of two 14-day tipifarnib cohorts: 3A (tipifarnib 600, etoposide 100) and 8A (tipifarnib 400, e
15 ioma to determine the efficacy and safety of tipifarnib, a farnesyltransferase inhibitor, dosed at th
16 Exposure of MLL-AF6-rearranged AML blasts to tipifarnib, a RAS inhibitor, leads to cell autophagy and
18 macokinetic properties, the newly discovered tipifarnib analogues are ideal leads for the development
23 arnesylation inhibition, rather than dose of tipifarnib, and escalation beyond 300 mg bid might not r
26 ete remissions occurred in 50% of two 14-day tipifarnib cohorts: 3A (tipifarnib 600, etoposide 100) a
27 way through c-Raf to Bim that contributes to tipifarnib cytotoxicity in human lymphoid cells but also
31 nesyltransferase inhibition was noted at all tipifarnib dose levels, as measured in peripheral-blood
34 ested the oral farnesyltransferase inhibitor tipifarnib in 158 older adults with previously untreated
36 ), pharmacokinetics, and pharmacodynamics of tipifarnib in children with refractory solid tumors and
37 e assessable patients taking EIAEDs received tipifarnib in escalating doses from 300 to 700 mg bid fo
39 of patients from a phase 2 study of the FTI tipifarnib in older adults with previously untreated acu
40 rkat, Molt3, H9, DoHH2, and RL) that undergo tipifarnib-induced apoptosis but not in lines (SKW6.4 an
41 ociated death domain or procaspase-8 undergo tipifarnib-induced apoptosis, whereas cells lacking casp
49 rted that the cancer drug clinical candidate tipifarnib kills the causative agent of Chagas disease,
51 protein farnesyltransferase (PFT) inhibitor tipifarnib, now in phase III anticancer clinical trials,
53 We subsequently conducted a phase 1 trial of tipifarnib plus etoposide in adults over 70 years of age
55 ing modes of the substrate lanosterol and of Tipifarnib, providing a basis for the design of derivati
57 the dose-dependent administration of the FTI tipifarnib (R115777, Zarnestra) to this HGPS mouse model
58 ucleotide exchange factor RasGRP1 diminished tipifarnib sensitivity, suggesting that H-Ras or N-Ras i
63 malignant glioma patients were treated with tipifarnib using an interpatient dose-escalation scheme.
64 achieved in 16 of 54 (30%) receiving 14-day tipifarnib versus 5 of 30 (17%) receiving 21-day tipifar
65 ith AC every 2 weeks plus G-CSF, the RPTD of tipifarnib was 200 mg bid administered on days 2 to 7.
67 dy of the oral farnesyltransferase inhibitor tipifarnib was conducted in 93 adult patients with relap
69 f this classifier for predicting response to tipifarnib was validated in an independent set of 58 sam
71 ven in the presence of EIAEDs, the levels of tipifarnib were still sufficient to potently inhibit FTa
73 ssion ratio was found to predict response to tipifarnib with the greatest accuracy using a "leave one
74 of the farnesyltransferase (FTase) inhibitor tipifarnib (Zarnestra) in a phase 2 trial as well as its
75 The two FTase inhibitors (FTIs), R115777 (tipifarnib/Zarnestra) and BMS-214662, have undergone eva
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