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Dr. Mary-Ellen Taplin, from the Dana-Farber Cancer Institute, on Abiraterone Acetate's Mechanism of Action
Mary-Ellen Taplin, MD, associate professor of Medicine at Harvard Medical School and the Dana-Farber Cancer Institute, describes the mechanism of action for the oral androgen biosynthesis inhibitor abiraterone acetate (Zytiga), which is approved for treating men with castration-resistant prostate cancer.
The agent abiraterone acetate prevents testosterone production through a mechanism of action that is unique from previous androgen deprivation therapies such as leuprolide and Zoladex. The agent inhibits the CYP17A1 enzyme, a rate-limiting enzyme implicated in androgen biosynthesis that is created primarily by the testicles but also within the adrenal glands and the prostate cancer itself. Blocking this enzyme prevents the conversion of pregnenolone and progesterone into testosterone precursors, such as dehydroepiandrosterone (DHEA) and androstenedione.
This mechanism of action establishes a more complete inhibition of circulating testosterone. Abiraterone acetate is unique in blocking the adrenal glands and prostatic testosterone production. Other agents only block production at the level of the testicles.