A review of the absorption, distribution, metabolism and excretion of ticrynafen (tienilic acid) in 8 animal species, including man, is presented. Although some species effects are apparent, ticrynafen absorption is essentially complete following oral administration. The compound is extensively bound to plasma proteins, primarily albumin. Consequently, tissue concentrations are generally lower than plasma concentrations. Plasma and whole body clearance of ticrynafen is rapid due both to metabolism and to extensive renal excretion of the compound and its metabolites. Male/female differences in renal excretion occur, with a subsequent effect on ticrynafen metabolism. Ticrynafen is an inhibitor of reabsorption of sodium and uric acid by the kidney. This inhibitory effect, within the renal tubular lumen, accounts for its diuretic and uricosuric activity and could account for its antihypertensive activity, although a direct effect has also been claimed. Ticrynafen is also a classical example of a competitive inhibitor of organic acid transport in the kidney and other organs. Much of the drug-drug interaction involving ticrynafen is understandable due to its effect on transport. However, potentiation of anticoagulant activity appears to involve some direct effects upon warfarin metabolism although ticrynafen, in general, is not an enzyme inducer or inhibitor. Toxicity of ticrynafen is low in all animal species.