Sodium aurothiomalate is most probably not an inhibitor or inducer of CYP enzymes.

Aurothiomalate is used in the management of active progressive rheumatoid arthritis and progressive juvenile chronic arthritis especially if polyarticular or seropositive.

In vitro data indicates that polymorphonuclear leukocytes (PMN) metabolise thiocyanate to cyanide, which in turn converts aurothiomalate to aurocyanide (dicyanogold(I)) which inhibits the functions of PMN and other cells (Graham 1994). Aurothiomalate is mainly excreted in the urine with smaller amounts in the faeces (SPC). Half-life elimination is initially around 5-6 days and then 10-35 days (Legemiddelhåndboka), but after a course of treatment, gold may be found in the urine for up to a year or more owing to its presence in the deep body compartments (SPC). In a study 24-hour urinary ALA and PBG were measured prior to and ten weeks after the beginning of gold injections. These in vivo data may indicate that aurothiomalate does not affect hem metabolism (Herrick 1999). No drug-drug interactions with sodium aurothiomalate as a perpetrator are observed (Interaksjoner and Interaktionsdatabasen), which may indicate that sodium aurothiomalate is not an inhibitor or inducer of CYP enzymes.

Aurothiomalate is listed to have been associated with acute attacks of porphyria (Moore 1997).