717for the metabolism of PCPE. If this is true, our experiments raise the questions as to whether the substance excreted in the urine and characterized as "pregnanediol" by the Klopper method is actually 5P-pregnan-3~, 2 0 a-diol or alternatively, whether the "pregnanediol" measured originates from PCPE or arises from endogenous sources under the influence of PCPE. To answer these points, the metabolism of isotopically labeled PCPE must be studied in animals as well as in humans.Summary. Progesterone and its 3-cyclopentyl enol ether (PCPE) have been compared in a battery of biological tests. Orally or intraperitoneally administered PCPE was respectively l/SOth and 1/20th as active as subcutaneously injected progesterone in the Clauberg test. Oral doses of PCPE, 10-20 times those of subcutaneous progesterone were unable to maintain pregnancy in ovariectomized rats. Three to four times as much "pregnanediol" was detected in the urine of rabbits following oral administration of progesterone than a comparable dose of PCPE. Orally or intraperitoneally administered PCPE at doses 20-40 times those of effective doses of progesterone failed to potentiate the anesthetic effect of a subhypnotic dose of sodium hexobarbital. These data demonstrate that PCPE and progesterone have a markedly different biological profile and cast serious doubt on the possibility that biologically active amounts of PCPE are converted to and/or metabolized in the same way as progesterone, as claimed by others. Our data strongly support the view that if any transformation of PCPE to progesterone occurs, the likeliest site of this conversion is the gut.
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