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. 2008 Jul 1;99(2):294–304. doi: 10.1038/sj.bjc.6604459

Table 2. Chemotherapy drugs and doses used in this study.

Drug Concentrations used in this study Published human peak intratumour or plasma concentrations
Soluble TRAIL 1 μg ml−1 100 ng ml−1 Not reported
F-LZ-TRAIL 100 ng ml−1 10 ng ml−1 Not reported
Superkiller TRAIL 100 ng ml−1 Not reported
Anti-DR5 3 μg ml−1 0.3 μg ml−1 Not reported
Cisplatin 54 μg ml−1 5.4 μg ml−1 Peak tumour concentration after embolisation was 54 μg ml−1, after perfusion was 11.4 μg ml−1 (Tegeder et al, 2003). Peak plasma concentrations ranged from 1.5 μg ml−1 (Riva et al, 2000; Urien et al, 2005) to around 4 μg ml−1 (Siegel-Lakhai et al, 2005; Watanabe et al, 2003)
Carboplatin 44 μg ml−1 4.4 μg ml−1 Peak glioma concentration was 13 μg ml−1, peak plasma concentration was 44 μg ml−1 (Whittle et al, 1999)
CCNU 9 μg ml−1 900 ng ml−1 90 ng ml−1 Peak plasma concentration of active metabolites was reported to be 9 μg ml−1 (Lee et al, 1985) or 1–2 μg ml−1 (Kastrissios et al, 1996)
Temozolomide 13.7 μg ml−1 1.37 μg ml−1 Peak plasma concentration was 13.7 μg ml−1 (Brada et al, 1999)
Etoposide 10.5 μg ml−1 1.05 μg ml−1 Peak tumour concentration was 1.04–4.80 μg g−1. Peak plasma concentration was 7–10.5 μg ml−1 (Kiya et al, 1992)
Vincristine 40.4 ng ml−1 4 ng ml−1 Peak plasma concentration was 40.5 ng ml−1 but rapidly decreased to 5 ng ml−1 (Groninger et al, 2005)
Procarbazine 540 ng ml−1 54 ng ml−1 Peak plasma concentration was 540 ng ml−1 (He et al, 2004)