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. Author manuscript; available in PMC: 2011 Oct 1.
Published in final edited form as: Pharmacogenet Genomics. 2010 Oct;20(10):611–618. doi: 10.1097/FPC.0b013e32833e0cb5

Table 2.

Comparison of the activities of POR variants in various assays

Drug Metabolism Steroidogenesis
CYP 3A4 1A2 2C19 17 19
Reaction 6β-OH T 1-OH M 4-OH M 3-OH Q N- deMe E EOMCC EOMCC 17α-OH 17, 20 lyase aromatase
WT 100 100 100 100 100 100 100 100 100 100
Q153R 129 94 92 150 76 144 284 31 27 ND
A287P 17 17 14 3 nil nil nil 40 21 104
R457H nil nil nil 1 nil nil nil 3 nil 1
A503V 77 61 74 89 97 85 113 68 58 ND

All data are Vmax/Km, shown as a percentage of the wild-type control, set at 100%; ND, not done. The reactions assayed are: 6β-hydroxylation of testosterone (6β-OH T), 1-hydroxylation (1-OH M) and 4-hydroxylation (4-OH M) of midazolam, 3-hydroxylation of quinidine (3-OH Q), and N-demethylation of erythromycin (N-deMe E) by CYP3A4 (Table 1–4 of this work); activation of fluorogenic EOMCC by CYP1A2 and CYP2C19 (from [30]); 17α-hydroxylation of progesterone (17α OH) and 17,20 lyase cleavage of 17OH-pregnenolone by CYP17 (from [19]); aromatization of androstenedione to estrone by CYP19 (from [41]).