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1 ced susceptibility and virologic response to tipranavir.
2 pic susceptibility and virologic response to tipranavir.
8 of the novel non-peptidic protease inhibitor tipranavir co-administered with ritonavir plus an optimi
10 linical trials of this compound (PNU-140690, Tipranavir) for treatment of HIV infection are currently
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/
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
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
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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