1 the low oxidation potential of the substrate phenacetin.

2                               In the case of phenacetin acetyl hydroxylation (acetol formation), larg

3 ed a set of p-alkoxyacylanilide analogues of phenacetin and found that variations in the O-alkyl and

4 d mixtures of drugs including aspirin (ASA), phenacetin, and caffeine.

5 sic/antipyretic drugs such as acetaminophen, phenacetin, antipyrine, and dipyrone, and is potently in

6 cetaminophen (APAF, the active metabolite of phenacetin), caffeine, and other related drugs individua

7 gs such as ibuprofen amide, moclobemide, and phenacetin, demonstrates the industrial potential of our

8                Moving one methylene group of phenacetin from the O-alkyl group to the N-acyl moiety i

9                      The prototype substrate phenacetin is oxidized to an acetol as well as the O-dea

10 of the test compounds over time (benzocaine, phenacetin, metribuzin, phenytoin, thiacloprid, valproic

11 kcat and Km values for 7-ethoxyresorufin and phenacetin O-deethylation and the (in vitro) activation

12 ch reactions did not show a burst for either phenacetin O-deethylation or formation of the acetol, a

13 ecular kinetic deuterium isotope effects for phenacetin O-deethylation were 2-3.

14 ates of 7-ethoxyresorufin O-deethylation and phenacetin O-deethylation were in accord with those expe

15 thylations, diclofenac 4'-hydroxylation, and phenacetin O-deethylation.

16            For benzocaine, valproic acid and phenacetin several transformation products (TPs) were ob

17 bination products that contained aspirin and phenacetin (used by three patients with SICK), which are