1 n the cellular pharmacology of 64Cu and [14C]CBDCA was investigated in more detail using one cell pai

2 BDCA content upon exposure to 50 microM [14C]CBDCA.

3 18 days of PIXY321 beginning on day 1 of all CBDCA cycles, including cycle 1.

4 id from 2008/ATP7B cells for both copper and CBDCA.

5 TP7B directly mediates resistance to DDP and CBDCA by stably transfecting human carcinoma cells with

6 entration, this deficit remained for DDP and CBDCA, but accumulation of L-OHP was no longer CTR1-depe

7 sistance to cisplatin (DDP) and carboplatin (CBDCA) are often cross-resistant to copper and vice vers

8 ccumulation of cisplatin (DDP), carboplatin (CBDCA), and oxaliplatin (L-OHP).

9  the influx of cisplatin (DDP), carboplatin (CBDCA), oxaliplatin (L-OHP), and transplatin.

10 n) administered after high-dose carboplatin (CBDCA) treatment.

11 ed by three cycles of high-dose carboplatin (CBDCA)/Txl and one cycle of high-dose melphalan (MEL), e

12 hat CTR1 mediates the initial influx of DDP, CBDCA, and L-OHP and is a major determinant of responsiv

13 exposed to increasing concentrations of DDP, CBDCA, or L-OHP for 1 h.

14                         When exposed to DDP, CBDCA, or L-OHP at 2 microM, accumulation in the CTR1-/-

15 ant to a 1-h exposure to DDP (1.6-2.6-fold), CBDCA (1.5-1.6-fold), and copper (1.2-1.4-fold).

16  completely eliminated the initial influx of CBDCA and reduced the initial uptake of L-OHP by 68% but

17 tasis modulates the cellular pharmacology of CBDCA.

18      Patients with advanced cancers received CBDCA at 800 mg/m2 intravenously on day 0 of repeated 28

19 supplemented conditions, as was steady-state CBDCA content upon exposure to 50 microM [14C]CBDCA.

20 fold resistant to DDP, 2.0-fold resistant to CBDCA, but only 1.7-fold resistant to L-OHP.

21 expression of ATP7B regulates sensitivity to CBDCA as well as to DDP and copper and that a transporte

22 t A of the study, patients were treated with CBDCA alone during cycle 1 and then received PIXY321 on