"Oct. 24, 2012 -- It is not a desired discussion for the doctor, and certainly not for the patient. But an overwhelming majority of people with advanced cancer are under the impression that the chemotherapy they are receiving will cure their disea"...
LYSODREN (mitotane) can best be described as an adrenal cytotoxic agent, although it can cause adrenal inhibition, apparently without cellular destruction. Its biochemical mechanism of action is unknown. Data are available to suggest that the drug modifies the peripheral metabolism of steroids as well as directly suppressing the adrenal cortex. The administration of LYSODREN (mitotane) alters the extra-adrenal metabolism of cortisol in man; leading to a reduction in measurable 17-hydroxy corticosteroids, even though plasma levels of corticosteroids do not fall. The drug apparently causes increased formation of 6-β-hydroxycortisol.
Data in adrenal carcinoma patients indicate that about 40% of oral LYSODREN (mitotane) is absorbed and approximately 10% of administered dose is recovered in the urine as a water-soluble metabolite. A variable amount of metabolite (1 to 17%) is excreted in the bile and the balance is apparently stored in the tissues.
Following discontinuation of LYSODREN (mitotane) , the plasma terminal half-life has ranged from 18 to 159 days. In most patients blood levels become undetectable after 6 to 9 weeks. Autopsy data have provided evidence that LYSODREN (mitotane) is found in most tissues of the body; however, fat tissues are the primary site of storage. LYSODREN (mitotane) is converted to a water-soluble metabolite.
No unchanged LYSODREN (mitotane) has been found in urine or bile.
Last reviewed on RxList: 3/12/2009
This monograph has been modified to include the generic and brand name in many instances.
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