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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.
9                            Patients received tipifarnib 300 mg twice daily on days 1-21 of each 28-da
10                                              Tipifarnib (300 mg bid for 21 days every 4 weeks) shows
11 n age, 77 years) received 224 cycles of oral tipifarnib (300-600 mg twice daily for 14 or 21 days) pl
12                                              Tipifarnib, 300 mg orally twice daily, was administered
13 : 3A (tipifarnib 600, etoposide 100) and 8A (tipifarnib 400, etoposide 200).
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
17                                              Tipifarnib, an orally bioavailable inhibitor of farnesyl
18 macokinetic properties, the newly discovered tipifarnib analogues are ideal leads for the development
19                      We rationally developed tipifarnib analogues that display reduced affinity for h
20                               We synthesized tipifarnib analogues that no longer bind to protein farn
21 cell apoptosis induced by the combination of tipifarnib and bortezomib.
22 p at the 4-position of the quinoline ring of tipifarnib and by replacing the amino group by OMe.
23 arnesylation inhibition, rather than dose of tipifarnib, and escalation beyond 300 mg bid might not r
24 the pharmacokinetics and pharmacodynamics of tipifarnib at MTD in patients on and off EIAEDs.
25                                              Tipifarnib caused dose-dependent up-regulation of Bim in
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
28                                     Finally, tipifarnib decreased the levels of phosphorylated Akt an
29              This pediatric phase I trial of tipifarnib determined the maximum-tolerated dose (MTD),
30                                        Since tipifarnib displays high oral bioavailability and accept
31 nesyltransferase inhibition was noted at all tipifarnib dose levels, as measured in peripheral-blood
32            The farnesyltransferase inhibitor tipifarnib exhibits modest activity against acute myelog
33                  These results indicate that tipifarnib has activity in lymphoma, particularly in hea
34 ested the oral farnesyltransferase inhibitor tipifarnib in 158 older adults with previously untreated
35               The pharmacokinetic profile of tipifarnib in children is similar to that in adults, and
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
38 we examined the mechanism of cytotoxicity of tipifarnib in human lymphoid cell lines.
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
42  not in lines (SKW6.4 and Hs445) that resist tipifarnib-induced apoptosis.
43                                              Tipifarnib inhibited signaling downstream of the farnesy
44                                              Tipifarnib is active and well tolerated in older adults
45                                              Tipifarnib is an inhibitor of human protein farnesyltran
46                             We conclude that tipifarnib is tolerable, can induce disease stabilizatio
47                                         Oral tipifarnib is well tolerated in children receiving the d
48                                     R115777 (tipifarnib) is the first farnesyltransferase inhibitor (
49 rted that the cancer drug clinical candidate tipifarnib kills the causative agent of Chagas disease,
50                                              Tipifarnib may be safely combined with dose-dense AC usi
51  protein farnesyltransferase (PFT) inhibitor tipifarnib, now in phase III anticancer clinical trials,
52                                     In vivo, tipifarnib plus etoposide decreased ribosomal S6 protein
53 We subsequently conducted a phase 1 trial of tipifarnib plus etoposide in adults over 70 years of age
54                                              Tipifarnib plus etoposide is a promising orally bioavail
55 ing modes of the substrate lanosterol and of Tipifarnib, providing a basis for the design of derivati
56                                              Tipifarnib (R115777), an inhibitor of human protein farn
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
59                               Treatment with tipifarnib suppressed FTase (but not geranylgeranyltrans
60        Together, these data demonstrate that tipifarnib synergizes with bortezomib by inducing protei
61                                              Tipifarnib (T) exhibits modest activity in elderly adult
62                                      Because tipifarnib undergoes extensive hepatic metabolism, MTD 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.
66                                              Tipifarnib was administered twice daily for 21 days, rep
67 dy of the oral farnesyltransferase inhibitor tipifarnib was conducted in 93 adult patients with relap
68                                              Tipifarnib was taken orally for 21 days of a 28-day cycl
69 f this classifier for predicting response to tipifarnib was validated in an independent set of 58 sam
70               The plasma pharmacokinetics of tipifarnib were highly variable but not age dependent.
71 ven in the presence of EIAEDs, the levels of tipifarnib were still sufficient to potently inhibit FTa
72 results, we examined the effect of combining tipifarnib with other agents.
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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