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. 2012 Jul;342(1):33–40. doi: 10.1124/jpet.112.192195

Fig. 3.

Fig. 3.

Directional flux of vemurafenib in MDCKII cell monolayers. A and B, the transport of vemurafenib in wild-type (A) and Bcrp1-transfected (B) cells. KO, Ko143. C, the apparent permeability of vemurafenib in wild-type and Bcrp1 cells in both the A-to-B and B-to-A directions. In the Bcrp1-transfected cells, the B-to-A permeability of vemurafenib was significantly greater than the A-to-B permeability (***, p < 0.05). The addition of 0.2 μM Ko143, a potent Bcrp inhibitor, decreased this directionality in flux caused by Bcrp (#, p < 0.05). D and E, the transport of vemurafenib in wild-type (D) and MDR1-transfected (E) cells. LY, LY335979. F, the apparent permeability of vemurafenib in wild-type and MDR1 cells in both the A-to-B and B-to-A directions. In the MDR1-transfected cells, the B-to-A permeability of vemurafenib was significantly greater than the A-to-B permeability (***, p < 0.05). The addition of 1 μM LY335979, a potent P-gp inhibitor, abolished this directionality in flux caused by P-gp (#, p < 0.05), such that there was no significant difference in the permeability of vemurafenib in both directions. Data represent mean ± S.E. (n = 3–9 for all data sets).