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1  of gefitinib; PBTC-014: phase I/II study of tipifarnib).
2 Fs), which sensitized nontransfected MEFs to tipifarnib.
3 escued by the farnesyl transferase inhibitor Tipifarnib.
4 that was further enhanced by the addition of tipifarnib.
5 ose-limiting toxicities occurred with 21-day tipifarnib.
6 farnib versus 5 of 30 (17%) receiving 21-day tipifarnib.
7  courses of a farnesyltransferase inhibitor, tipifarnib.
8 s with AML who are more likely to respond to tipifarnib.
9 mor (median, 100%; range, 55% to 100%) after tipifarnib.
10 hours), and predose trough concentrations of tipifarnib.
11 hway alterations, which confer resistance to tipifarnib.
12                            Patients received tipifarnib 300 mg twice daily on days 1-21 of each 28-da
13                                              Tipifarnib (300 mg bid for 21 days every 4 weeks) shows
14 n age, 77 years) received 224 cycles of oral tipifarnib (300-600 mg twice daily for 14 or 21 days) pl
15                                              Tipifarnib, 300 mg orally twice daily, was administered
16 : 3A (tipifarnib 600, etoposide 100) and 8A (tipifarnib 400, etoposide 200).
17 in 50% of two 14-day tipifarnib cohorts: 3A (tipifarnib 600, etoposide 100) and 8A (tipifarnib 400, e
18 rs PI3K-mTOR and HRAS via the combination of tipifarnib, a farnesyltransferase (FTase) inhibitor, and
19 ioma to determine the efficacy and safety of tipifarnib, a farnesyltransferase inhibitor, dosed at th
20 fects of FTase inhibition in RMS we utilized tipifarnib, a potent and selective FTase inhibitor, in i
21 Exposure of MLL-AF6-rearranged AML blasts to tipifarnib, a RAS inhibitor, leads to cell autophagy and
22  Importantly, we investigate the efficacy of tipifarnib, a recently identified exosome biogenesis inh
23                                              Tipifarnib, an orally bioavailable inhibitor of farnesyl
24 macokinetic properties, the newly discovered tipifarnib analogues are ideal leads for the development
25                      We rationally developed tipifarnib analogues that display reduced affinity for h
26                               We synthesized tipifarnib analogues that no longer bind to protein farn
27 cell apoptosis induced by the combination of tipifarnib and bortezomib.
28 p at the 4-position of the quinoline ring of tipifarnib and by replacing the amino group by OMe.
29                      Combined treatment with tipifarnib and MEK inhibition sensitized cells to tipifa
30 arnesylation inhibition, rather than dose of tipifarnib, and escalation beyond 300 mg bid might not r
31                       This study establishes tipifarnib as a potential therapeutic option in T-cell l
32 farnesyltransferase inhibitors (FTI) such as tipifarnib as the most effective drugs in preventing rel
33                  Data from RNA-seq show that tipifarnib at IC(50) after 72 h downregulated a great va
34 the pharmacokinetics and pharmacodynamics of tipifarnib at MTD in patients on and off EIAEDs.
35            The farnesyltransferase inhibitor tipifarnib blocked mutant HRAS-PI3K signaling and synerg
36                                              Tipifarnib caused dose-dependent up-regulation of Bim in
37 ete remissions occurred in 50% of two 14-day tipifarnib cohorts: 3A (tipifarnib 600, etoposide 100) a
38 way through c-Raf to Bim that contributes to tipifarnib cytotoxicity in human lymphoid cells but also
39                                     Finally, tipifarnib decreased the levels of phosphorylated Akt an
40              This pediatric phase I trial of tipifarnib determined the maximum-tolerated dose (MTD),
41                                        Since tipifarnib displays high oral bioavailability and accept
42 nesyltransferase inhibition was noted at all tipifarnib dose levels, as measured in peripheral-blood
43            The farnesyltransferase inhibitor tipifarnib exhibits modest activity against acute myelog
44                  These results indicate that tipifarnib has activity in lymphoma, particularly in hea
45                       Combined alpelisib and tipifarnib has potential to benefit >45% of patients wit
46 ested the oral farnesyltransferase inhibitor tipifarnib in 158 older adults with previously untreated
47 arnib and MEK inhibition sensitized cells to tipifarnib in all settings, including in MEFs with PI3K
48               The pharmacokinetic profile of tipifarnib in children is similar to that in adults, and
49 ), pharmacokinetics, and pharmacodynamics of tipifarnib in children with refractory solid tumors and
50 e assessable patients taking EIAEDs received tipifarnib in escalating doses from 300 to 700 mg bid fo
51 ca(H1047R) transduction led to resistance to tipifarnib in Hras(G13R)-transfected MEFs in the presenc
52 we examined the mechanism of cytotoxicity of tipifarnib in human lymphoid cell lines.
53  of patients from a phase 2 study of the FTI tipifarnib in older adults with previously untreated acu
54                On the contrary, treatment of tipifarnib in TAC mice reduced circulating exosomes to b
55  value of the farnesyltransferase inhibitor, tipifarnib, in 25 TCL cell lines through the identificat
56 rkat, Molt3, H9, DoHH2, and RL) that undergo tipifarnib-induced apoptosis but not in lines (SKW6.4 an
57 ociated death domain or procaspase-8 undergo tipifarnib-induced apoptosis, whereas cells lacking casp
58  not in lines (SKW6.4 and Hs445) that resist tipifarnib-induced apoptosis.
59                                              Tipifarnib inhibited signaling downstream of the farnesy
60                                              Tipifarnib is active and well tolerated in older adults
61                                              Tipifarnib is an inhibitor of human protein farnesyltran
62 -matched strategy of combining alpelisib and tipifarnib is efficacious in PIK3CA- and HRAS-dysregulat
63                             We conclude that tipifarnib is tolerable, can induce disease stabilizatio
64                                         Oral tipifarnib is well tolerated in children receiving the d
65                                     R115777 (tipifarnib) is the first farnesyltransferase inhibitor (
66 rted that the cancer drug clinical candidate tipifarnib kills the causative agent of Chagas disease,
67                                              Tipifarnib may be safely combined with dose-dense AC usi
68 By blocking feedback reactivation of mTORC1, tipifarnib may prevent adaptive resistance to additional
69                                              Tipifarnib-mediated inhibition of exosome biogenesis and
70  protein farnesyltransferase (PFT) inhibitor tipifarnib, now in phase III anticancer clinical trials,
71 raf(G466E) transduction led to resistance to tipifarnib only in the presence of Kras(WT).
72                                     In vivo, tipifarnib plus etoposide decreased ribosomal S6 protein
73 We subsequently conducted a phase 1 trial of tipifarnib plus etoposide in adults over 70 years of age
74                                              Tipifarnib plus etoposide is a promising orally bioavail
75 ing modes of the substrate lanosterol and of Tipifarnib, providing a basis for the design of derivati
76                                              Tipifarnib (R115777), an inhibitor of human protein farn
77 the dose-dependent administration of the FTI tipifarnib (R115777, Zarnestra) to this HGPS mouse model
78                                              Tipifarnib reduced cell viability in these T-cell leukem
79                                              Tipifarnib reduced HRAS processing, and plasma membrane
80                   In HRAS-mutant cell lines, tipifarnib reduced two-dimensional and three-dimensional
81 onal cell growth, and in vivo treatment with tipifarnib resulted in tumor growth inhibition exclusive
82 B were associated as potential biomarkers of tipifarnib sensitivity and resistance, respectively.
83  RelB could serve as potential biomarkers of tipifarnib sensitivity and resistance.
84 ucleotide exchange factor RasGRP1 diminished tipifarnib sensitivity, suggesting that H-Ras or N-Ras i
85 enomic and/or immunohistochemical markers of tipifarnib sensitivity.
86                               Treatment with tipifarnib suppressed FTase (but not geranylgeranyltrans
87                                              Tipifarnib synergized with alpelisib at the level of mTO
88        Together, these data demonstrate that tipifarnib synergizes with bortezomib by inducing protei
89                                              Tipifarnib (T) exhibits modest activity in elderly adult
90 randomly assigned to groups with and without tipifarnib treatment (10 mg/kg 3 times/wk) and monitored
91                                              Tipifarnib treatment also drastically altered the miRNA
92                                              Tipifarnib treatment in TAC mice upregulated the express
93                                      Because tipifarnib undergoes extensive hepatic metabolism, MTD i
94  malignant glioma patients were treated with tipifarnib using an interpatient dose-escalation scheme.
95  achieved in 16 of 54 (30%) receiving 14-day tipifarnib versus 5 of 30 (17%) receiving 21-day tipifar
96 ith AC every 2 weeks plus G-CSF, the RPTD of tipifarnib was 200 mg bid administered on days 2 to 7.
97                                              Tipifarnib was administered twice daily for 21 days, rep
98 dy of the oral farnesyltransferase inhibitor tipifarnib was conducted in 93 adult patients with relap
99                      At the molecular level, Tipifarnib was not able to block HRAS activation, but im
100                                              Tipifarnib was taken orally for 21 days of a 28-day cycl
101 f this classifier for predicting response to tipifarnib was validated in an independent set of 58 sam
102               The plasma pharmacokinetics of tipifarnib were highly variable but not age dependent.
103 ven in the presence of EIAEDs, the levels of tipifarnib were still sufficient to potently inhibit FTa
104 results, we examined the effect of combining tipifarnib with other agents.
105 ssion ratio was found to predict response to tipifarnib with the greatest accuracy using a "leave one
106 of the farnesyltransferase (FTase) inhibitor tipifarnib (Zarnestra) in a phase 2 trial as well as its
107    The two FTase inhibitors (FTIs), R115777 (tipifarnib/Zarnestra) and BMS-214662, have undergone eva
108  inhibitors of prenylation (PTI) lonafarnib, tipifarnib, zoledronic acid, or atorvastatin at concentr

 
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