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SUMMARY In dogs treated intravenously or orally with sodium pantothenate, the principal urinary metabolite has been identified provisionally as the vitamin ester β-glucuronide; 0-5 per cent of an oral dose is excreted in the urine as unchanged pantothenic acid, all in the first 24 h, and up to 40 per cent as the ester β-glucuronide in 7 days. Small amounts of the ester β-glucuronide are detectable in the urine, voided 2 months after dosing. In comparison, rats excrete 25 per cent of the dose in the 7-day urine as unchanged pantothenic acid, but no ester glucuronide was detected. Thus, dogs and rats show a species difference both in the metabolic pathway of pantothenic acid and in the rate of excretion of the vitamin and its metabolites. Excretion of pantothen [ 14 C]ic acid in the urine of dogs, treated 2 months earlier with pantothen [ 14 C]ate, was brought about by the administration of a massive dose of unlabelled pantothenate.