August 1955

The Effect of Intravenous Demecolcine (Colcemid) on Acute Gout

Author Affiliations

San Francisco

From the Rheumatic Disease Study Group, Department of Pharmacology and Therapeutics, Stanford University School of Medicine.

AMA Arch Intern Med. 1955;96(2):153-156. doi:10.1001/archinte.1955.00250130027003

In 1950 Šantavý and Reichstein 1 reported the isolation of several previously unknown alkaloids from the meadow saffron (Colchicum autumnale), the source of colchicine. Subsequently the pharmacological properties of these alkaloids were investigated by Schär, Loustalot, and Gross,2 and one of the compounds, demecolcine, was found to have an antimitotic effect equivalent to that of colchicine in fibroblast cultures and considerably less toxicity in laboratory animals. Structurally, demecolcine differs from colchicine in the replacement of the acetyl group at the nitrogen by a methyl radical (Fig.).

Formulas of colchicine (left) and demecolcine (desacetylmethylcolcine) (right).

Extensive laboratory study by Schär, Loustalot, and Gross demonstrated that, in all animal species, demecolcine is considerably less toxic than colchicine. In mice, for example, the intravenous lethal dose of demecolcine is as much as 40 times greater than that of colchicine. Paradoxically, in mice demecolcine is about six times more toxic orally than intravenously

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