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. 2016 Oct;44(10):1709–1719. doi: 10.1124/dmd.116.072363

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Copyright © 2016 by The Author(s)

This is an open access article distributed under the CC BY-NC Attribution 4.0 International license.

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Fig. 4. — Metabolism of erythro- and threohydrobupropion by recombinant P450 enzymes and human liver microsomes. (A) Erythro- and threo-4′-OH-hydrobupropion formation from erythro- and threohydrobupropion in a panel of P450 supersomes. (B) Inhibition of erythro- and threo-4′-OH-hydrobupropion formation from erythro- and threohydrobupropion in HLM as percentage of control following incubation in the presence of selective P450 inhibitors or a CYP2B6 inhibitory antibody (MAB-2B6). Control 1 is the control for the reversible inhibitors montelukast (2C8 MONT), sulfaphenazole (2C9 SULF), (+)-N-3-benzylnirvanol (2C19 N-BENZ), and quinidine (2D6 QUIN). Control 2 is the control for time-dependent inhibitors troleandomycin (3A4 TAO) and furafylline (1A2 FURA). *p < 0.05 in comparison to control, one-way analysis of variance. (C and D) Formation kinetics of threo-4′-OH-hydrobupropion (C) and erythro-4′OH-hydrobupropion (D) in CYP2C19 supersomes.