| Indication | Used in the treatment of Cushing's syndrome. It is normally used in short-term treatment until permanent therapy is possible. |
| Pharmacodynamics | Trilostane blocks an enzyme involved in the production of several steroids including cortisol. Inhibiting this enzyme inhibits the production of cortisol. In Cushing's syndrome, the adrenal gland overproduces steroids. Although steroids are important for various functions of the body, too much can cause problems. Trilostane reduces the amount of steroids produced by the adrenal gland. This product was withdrawn from the U.S. market in April 1994. |
| Mechanism of action | Trilostane produces suppression of the adrenal cortex by inhibiting enzymatic conversion of steroids by 3-beta-hydroxysteroid dehydrogenase/delta 5,4 ketosteroid isomerase, thus blocking synthesis of adrenal steroids. |
| Absorption | Not Available |
| Volume of distribution | Not Available |
| Protein binding | Not Available |
| Metabolism | Hepatic. |
| Route of elimination | Not Available |
| Half life | 8 hours. |
| Clearance | Not Available |
| Toxicity | Symptoms of overdose include darkening of skin, drowsiness or tiredness, loss of appetite, mental depression, skin rash, and/or vomiting. |