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1 ced susceptibility and virologic response to tipranavir.
2 pic susceptibility and virologic response to tipranavir.
3 E24 (IC(50): lopinavir, 18.4 +/- 4.6 microM; tipranavir, 1.2 +/- 0.4 microM).
4                                              Tipranavir, a nonpeptidic HIV-1 protease inhibitor, has
5      Thermodynamically, the good response of tipranavir arises from a unique behavior: it compensates
6 -log10 copies/ml-lower virologic response to tipranavir at week 24 of treatment.
7                          Characterization of tipranavir binding to wild-type protease, active site mu
8 of the novel non-peptidic protease inhibitor tipranavir co-administered with ritonavir plus an optimi
9                                Structurally, tipranavir establishes a very strong hydrogen bond netwo
10 linical trials of this compound (PNU-140690, Tipranavir) for treatment of HIV infection are currently
11                                    Moreover, tipranavir forms hydrogen bonds directly to Ile50, while
12 ool for predicting the virologic response to tipranavir in protease inhibitor-experienced patients.
13 /L33I/M46I/I54V/L63I/V82A/I84V/L90M, and the tipranavir in vitro-selected mutant I13V/V32L/L33F/K45I/
14                                              Tipranavir inhibits wild-type protease with high potency
15                                              Tipranavir is a novel, nonpeptidic protease inhibitor of
16                   The non-peptidic inhibitor tipranavir is distinctive in its consistently strong eff
17          These analyses demonstrate that the tipranavir mutation score is a potentially valuable tool
18                                            A tipranavir mutation score was developed from these analy
19  contribute to multiple-regression models of tipranavir-related phenotype and of virologic response.
20 tes displaying an increasing number of these tipranavir resistance-associated mutations had a reduced
21                          The high potency of tipranavir results from a very large favorable entropy c
22                      486 (65.1%) patients on tipranavir-ritonavir and 192 (26.1%) on CPI-ritonavir re
23    3324 patients were screened; 746 received tipranavir-ritonavir and 737 CPI-ritonavir.
24 ment failure was significantly longer in the tipranavir-ritonavir group than in the CPI-ritonavir gro
25 ved and maintained treatment response in the tipranavir-ritonavir group than in the CPI-ritonavir gro
26  and triglycerides were more frequent in the tipranavir-ritonavir group than in the CPI-ritonavir gro
27                 Compared with CPI-ritonavir, tipranavir-ritonavir with an optimised background regime
28              A lower number of points in the tipranavir score and a greater number of active drugs in
29 e III trials revealed that each point in the tipranavir score was associated with a 0.16-log10 copies
30 ion, Ki values of amprenavir, darunavir, and tipranavir were determined to be 135, 10, and 82 pM, res
31  sequences were susceptible to darunavir and tipranavir, whereas 47% showed resistance to lopinavir,
32 ata from phase II and III clinical trials of tipranavir with protease inhibitor-experienced patients

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