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Carbamazepine is not a substrate for p-glycoprotein

Owen, A. and Pirmohamed, M. and Tettey, J.N.A. and Morgan, P. and Chadwick, D. and Park, B.K. (2001) Carbamazepine is not a substrate for p-glycoprotein. British Journal of Clinical Pharmacology, 51 (4). pp. 345-349. ISSN 0306-5251

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Abstract

Aims to determine whether the anticonvulsant carbamazepine (CBZ), a known CYP3A4 substrate, is also a substrate for the multidrug efflux transporter P-glycoprotein (Pgp). The role of Pgp in the transport of CBZ was assessed in three systems: (a) in mdr1a/1b(−/−) and wild-type mice after administration of 2 mg kg−1 and 20 mg kg−1, which served as a model for brain penetration; (b) in Caco-2 cells, an in vitro model of the intestinal epithelium that is known to express high Pgp levels; and (c) by flow cytometry in lymphocytes using rhodamine 123, a fluorescent substrate for PgP. Brain penetration of both doses of CBZ at 1 h and 4 h was comparable in wild-type and mdr1a/1b(−/−) mice. Transport across the Caco-2 cell monolayer was Pgp-independent, and was not affected by the Pgp inhibitor PSC-833. CBZ had no effect on rhodamine 123 efflux from lymphocytes, in contrast to verapamil, which increased fluorescence intensity fivefold. CBZ is not a substrate for Pgp. Its efficacy is unlikely to be affected by Pgp over-expression in the brain. Furthermore, the interaction of CBZ with drugs that modulate both CYP3A4 and Pgp function such as verapamil is probably due to inhibition of CYP3A4 and not Pgp.