Newborn infants with glutaric aciduria type II are initially treated with IM or IV riboflavin. In cases responsive to riboflavin, the urinary organic acid profile is progressively normalized, except for ethylmalonic acid which is greatly increased over its initial value. For a tentative explanation of this phenomenon, a mild glutaric aciduria was induced in weanling rats with chlorpromazine, a structural analog of riboflavin. In these animals, riboflavin, partially corrected the aciduria, except for ethylmalonic acid and n-butyrylglycine which were increased. These two metabolites are predominant in rats given inhibitors of butyryl-CoA dehydrogenase, suggesting that massive doses of riboflavin could inhibit this enzyme by a still unknown mechanism. This is the first study of organic aciduria in chlorpromazine-treated rats.