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A substantial number of patients with gout has been shown to produce excessive amounts of uric acid (1-4). This overproduction has been demonstrated by the excretion of greater than normal amounts of uric acid in the urine, or an excessive incorporation of isotopically labeled glycine into urinary uric acid. The present day treatment of tophaceous gout consists primarily in the administration of uricosuric agents to increase the renal excretion of the uric acid formed, with use of colchicine, ACTH gel, or phenylbutazone for management of the acute attacks. Control of the production of uric acid has been of necessity confined to limiting the purine and protein content of the diet (5). A logical approach to the treatment of those patients who overproduce uric acid would be to inhibit the excessive production by pharmacologic agents. In recent years several compounds have been reported to interfere with purine biosynthesis. Two such compounds, azaserine (o-diazoacetyl-L-serine) and 6-diazo-5-oxo-L-norleucine (DON), have been shown to suppress the forma

SUPPRESSION OF URIC ACID SYNTHESIS IN THE GOUTY HUMAN BY THE USE OF 6-DIAZO-5-OXO-L-NORLEUCINE*