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. Author manuscript; available in PMC: 2009 Jan 1.
Published in final edited form as: Mol Cancer Ther. 2008 Jan;7(1):79–89. doi: 10.1158/1535-7163.MCT-07-0584

Figure 3. Impact of axitinib treatment on hepatic activation of CPA and export of its active metabolite, 4-OH-CPA.

Figure 3

A. Mice bearing 9L tumors were treated with vehicle or axitinib (25 mg/kg, i.p. sid) for 4 days. 24 hr after the last drug injection, liver microsomes were isolated (21) and CPA 4-hydroxylase activity was assayed by HPLC (23) following in vitro incubation with 0.2 or 2 mM of CPA. Data shown are mean ± SE based on n = 3 livers/group. The levels of 4-OH-CPA in liver (B) and plasma (C) were measured by HPLC 15 min after injection of a single test dose of CPA (140 mg/kg, i.p.). The 15 min time point corresponds to the Tmax (4-OH-CPA) (see Fig. 4B, below). None of the values shown is significantly different than the day 0 (untreated) controls (n = 3 mice/group, p > 0.05 for all treatments compared to controls). Numbers along the x-axis indicate the time period of drug treatment, as described in Fig. 2.