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The possibility of reducing elevated blood cholesterol levels with agents that inhibit endogenous biosynthesis of cholesterol is an attractive one, since dietary treatment is sometimes difficult to achieve and almost always difficult to maintain. Some of the theoretical aspects of such an approach have been outlined (3, 4), and the feasibility of the approach has been established in experimental animals. For example, it has been shown that A4-cholestenone, a potent inhibitor of cholesterol biosynthesis (5), can indeed lower levels of blood cholesterol (3, 6). Unfortunately, the feeding of A4-cholestenone in man and animals leads to accumulation of dihydrocholesterol in the serum (7) and this latter compound is known to be itself atherogenic (8). Certain other inhibitory substances have been explored but either have proved to be relatively ineffective (9, 10) or have not yet been adequately tested clinically (11, 12). In 1959 Blohm, MacKenzie, Kariya and Laughlin at the William S. Merrell Company reported their finding of a new inhibitor of cholesterol synthesis, MER-29 (1[p-,8-diethylaminoethoxy) phenyl] -1(p-tolyl) -2(p-chlorophenyl) ethanol). Their studies indicated that the compound blocked synthesis at some point subsequent to the formation of lanosterol (13) and that serum and tissue levels of cholesterol were reduced in experimental animals (14). Animal studies in this laboratory demonstrated the accumulation of desmosterol (24-dehydrocholesterol) in the tissues of MER29-treated animals, and a series of isotopic studies established that the major site of action of the drug was at the last step in cholesterol biosynthesis-namely, in the reduction of desmosterol to

EFFECTS OF TRIPARANOL (MER-29) ON CHOLESTEROL BIOSYNTHESIS AND ON BLOOD STEROL LEVELS IN MAN*