“…The CYP2B6 substrate selectivity comprises many diverse chemicals, including not only clinically used drugs but also many environmental chemicals such as pesticides (Turpeinen et al, 2006; Hodgson and Rose, 2007; Turpeinen and Zanger, 2012). Therapeutically important drugs metabolized primarily by CYP2B6 include the prodrug cyclophosphamide, which is converted to the direct precursor of the cytotoxic metabolites, phosphoramide mustard and acrolein, by 4-hydroxylation (Huang et al, 2000; Roy et al, 2005), the non-nucleoside reverse transcriptase inhibitor (NNRTI), efavirenz, which is 8-hydroxylated to become pharmacologically inactive (Ward et al, 2003; Desta et al, 2007), the atypical antidepressant and smoking cessation agent bupropion, which is converted to pharmacologically active hydroxybupropion (Faucette et al, 2000; Hesse et al, 2000; Turpeinen et al, 2005b), the anesthetics propofol (Court et al, 2001; Oda et al, 2001) and ketamine (Desta et al, 2012), the analgesic pethidine (meperidine; Ramírez et al, 2004); the μ-opioid receptor agonist, methadone (Totah et al, 2008), the antimalarial artemisinin (Svensson and Ashton, 1999; Asimus and Ashton, 2009), among numerous additional metabolic pathways of other drugs, to which CYP2B6 contributes in part, such as the antiretroviral, nevirapine (Erickson et al, 1999), and many others (Turpeinen and Zanger, 2012). Metabolic pathways suitable as probe for CYP2B6 activity include S-mephenytoin N -demethylation (Ko et al, 1998), bupropion hydroxylation (Faucette et al, 2000; Fuhr et al, 2007) and efavirenz, based on in vitro investigations (Ward et al, 2003; Desta et al, 2007).…”