Abiraterone starves prostate cancer cells of the hormones they need to grow. It does this by blocking a key enzyme involved in producing androgens (male hormones like testosterone), cutting off hormone supply from multiple sources in the body. The drug is used to treat metastatic prostate cancer, both in earlier hormone-sensitive stages and in later castration-resistant stages where the cancer has found ways to keep growing despite standard hormone therapy.
The Enzyme Abiraterone Targets
Prostate cancer cells rely on androgens to fuel their growth. Even after surgical removal of the testicles or drug-based suppression of testicular function, the body still produces androgens in two other places: the adrenal glands (small organs on top of the kidneys) and within the tumor itself. Abiraterone shuts down androgen production at all these sites by blocking an enzyme called CYP17A1, which plays an essential role in converting cholesterol into testosterone and its more potent form, DHT.
Beyond CYP17A1, research published in Clinical Cancer Research shows that abiraterone also inhibits a second enzyme required for DHT synthesis. This enzyme is needed regardless of whether androgens are being made from adrenal building blocks or assembled from scratch inside the tumor. By hitting both enzymes, abiraterone attacks androgen production through multiple pathways simultaneously, making it harder for cancer cells to find an alternative fuel source.
From Pill to Active Drug
What you actually swallow is abiraterone acetate, a prodrug that the body must convert into its active form, abiraterone. This conversion happens remarkably fast. In laboratory testing with human liver tissue, the transformation was nearly complete within 20 seconds. The process works through simple enzyme-driven hydrolysis (splitting off a chemical group), not through the liver’s usual drug-processing machinery. Once converted, abiraterone circulates and reaches androgen-producing tissues throughout the body.
Why It’s Taken With a Steroid
Abiraterone is always prescribed alongside a low-dose steroid, typically prednisone. This pairing isn’t optional, and the reason comes down to how the adrenal glands respond when their hormone-producing pathway gets blocked.
When abiraterone shuts down CYP17A1 in the adrenal glands, it doesn’t just stop androgen production. It also disrupts the production of cortisol, the body’s main stress hormone. The brain detects the cortisol drop and responds by signaling the adrenal glands to work harder. This overcompensation pushes production down an alternative pathway, generating excess mineralocorticoids, hormones that regulate salt and water balance. The result can be high blood pressure, low potassium levels, and fluid retention. Taking a low dose of prednisone replaces just enough cortisol to keep the brain from sending those overdrive signals, preventing the mineralocorticoid buildup before it starts.
Food Has a Major Effect on Absorption
Abiraterone is one of the most food-sensitive cancer drugs available. Taking it with a meal can increase the amount absorbed into the bloodstream by up to 10-fold compared to taking it on an empty stomach. That sounds like it might be helpful, but the spike is unpredictable and varies depending on what and how much you eat. This makes dosing unreliable and raises the risk of side effects. For this reason, abiraterone should be taken on an empty stomach, with no food for at least two hours before and one hour after the dose.
How Well It Works
The landmark trial that led to abiraterone’s approval, called COU-AA-301, enrolled nearly 1,200 men with metastatic castration-resistant prostate cancer whose disease had progressed after chemotherapy. After a median follow-up of about 20 months, men taking abiraterone plus prednisone lived a median of 15.8 months compared to 11.2 months for those on prednisone alone. That translates to a 26% reduction in the risk of death. These results were highly statistically significant and established abiraterone as a standard treatment for advanced prostate cancer.
Since then, abiraterone’s use has expanded. It is now approved for metastatic castration-sensitive prostate cancer as well, meaning it can be started earlier in the disease course before the cancer becomes resistant to standard hormone suppression. A newer combination pairs abiraterone with a DNA-repair-targeting drug for patients whose tumors carry specific BRCA gene mutations.
Monitoring During Treatment
Because abiraterone affects steroid hormone pathways broadly, liver function needs regular monitoring. The recommended schedule is blood tests every two weeks for the first three months, then monthly after that. These tests check for elevations in liver enzymes that could signal the liver is under stress. Most elevations are mild and manageable, but catching them early allows your medical team to adjust the dose or pause treatment if needed.
Blood pressure and potassium levels also require ongoing attention due to the mineralocorticoid effects described above. Even with prednisone on board, some degree of fluid retention, blood pressure changes, or potassium drops can still occur. Regular monitoring catches these shifts early, when they’re easiest to correct.