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

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

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

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

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

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

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

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

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

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