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Inhibition of Cholesterol Biosynthesis in Hyperlipemic Subjects

BERNARD A. SACHS, MD; LILA WOLFMAN, BA

Arch Intern Med. 1965;116(3):366-372.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

THE QUEST for the ideal inhibitor of cholesterol biosynthesis continues. To date, the clinical use of such inhibitors has disclosed definite disadvantages which include the accumulation in serum of triglycerides ¹ or a precursor sterol, 24-dehydrocholesterol (desmosterol).^2,3 The theoretically ideal inhibitor would be free of these disadvantages and would have its specific site of inhibition between β-hydroxy-β-methyl-glutaryl CoA and mevalonic acid. This has been suggested as the inhibition point in the negative feedback control of cholesterol synthesis by dietary cholesterol.⁴ The synthetic structural analog of cholesterol, 20,25-diazacholestenol dihydrochloride (SC-12937; 20,25-diazacholesterol) (Fig 1), was found to have its primary site of action at this enzymatic step and produced marked falls in serum cholesterol levels in experimental animals.⁵ Therefore, the compound was administered over a prolonged period of time to 13 patients with severe disorders of lipid metabolism and their serum lipids were studied.

Materials and Methods

The subjects . . . [Full Text PDF of this Article]

Author Affiliations
NEW YORK

From the Endocrine Service, Medical Division, Mantefiore Hospital and Medical Center. Head, Endocrine Service (Dr. Sachs) and Research Assistant (Miss Wolfman).

Footnotes
Received for publication Dec 2, 1964; accepted Jan 27, 1965.

Reprint requests to Montefiore Hospital and Medical Center, 210th St and Bainbridge Ave, New York 67, NY (Dr. Sachs).

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