Fenoxaprop-p-ethyl (FE), 2-[4-[(6-chloro-2-benzoxazolyl)oxy]phenoxy] propanoate, ethyl ester (R), is an aryloxyphenoxypropionate herbicide for postemergence control of annual and perennial grasses in paddy fields; its site of action is acetyl-coenzyme A carboxylase (ACCase), an enzyme in fatty acids biosynthesis. The possible mechanism(s) of resistance to FE in a resistant biotype of Echinochloa phyllopogon was examined, namely, absorption, translocation, and metabolism of FE and ACCase susceptibility to fenoxaprop acid (FA). Studies of the in vitro inhibition of ACCase discounted any differential active site sensitivity as the basis of resistance to FE. There were differences in absorption rates between biotypes from 3 to 48 h after application (HAA). Biotypes did not differ in either the amounts or the rates of FE translocated; 98% of applied [14C]FE remaining in the treated leaf. However, there was a good correlation between the rate of herbicide metabolism and the plant resistance. The R biotype produced 5-fold less FA and approximately 2-fold more nontoxic (polar) metabolites 48 HAA than the S biotype. Moreover, the higher rate of GSH conjugation in the resistant biotype as compared to the susceptible one indicates that GSH and cysteine conjugation is the major mechanism of resistance of the R biotype against FE toxicity.