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33 1 c H 3 -p = c H 3 H I 2 hr., and was greater at 3 hr. than at 2 hr. This delayed onset of activity follo~ing intravenous administration as compared to oral administration was consistent with a hypothesis that the liver was necessaiy for activity, since a higher concentration of I would be available for metabolism following absorption and transport to the liver via the portal vein after oral administration. These observations and the fact that I was inactive in rats previously treated with P-diethylaminoethyl diphenylpropylacetate hydrochloride4 (11), an agent which inhibits certain microsomal enzyme pathways of drug metabolism in vivo and in vitro,5suggested an active metabolite. Studies were undertaken, therefore, to establish vhether the urine of animals treated with I contained an active metabolite and if so, to isolate and identify it.

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