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Zytiga

Generic Name: Abiraterone Acetate
Class: Antineoplastic Agents
Chemical Name: (3β)-17-(3-Pyridinyl)-16-dien-3-ol-androsta-5 acetate(ester)
Molecular Formula: C26H33NO2
CAS Number: 154229-18-2

Medically reviewed by Drugs.com. Last updated on May 4, 2020.

Introduction

Antineoplastic agent; inhibitor of 17α-hydroxylase/C17,20-lyase (CYP17).1 5 6 10 13

Uses for Zytiga

Prostate Cancer

In combination with prednisone for the treatment of metastatic castration-resistant prostate cancer.1 4 18 20 21 22 25 Efficacy determined based on substantially prolonged overall survival and radiographic progression-free survival in 2 randomized, double-blind, placebo-controlled phase 3 studies (COU-AA-301 and COU-AA-302).1 4 18 20 21 22 25

In combination with prednisone for the treatment of high-risk metastatic castration-sensitive prostate cancer.1 23 24 Efficacy determined based on substantially prolonged overall survival compared with placebo in men with metastatic castration-sensitive prostate cancer and ≥2 high-risk factors associated with poor prognosis in the LATITUDE study.1

Zytiga Dosage and Administration

General

  • Use concurrently with a gonadotropin-releasing hormone (GnRH) analog unless patient has undergone bilateral orchiectomy.1

  • Increasing the corticosteroid dosage before, during, and after stressful situations may be indicated to prevent adrenocortical insufficiency.1 (See Adrenocortical Insufficiency under Cautions.)

  • Women who are or may be pregnant should not handle abiraterone acetate tablets without protection (e.g., gloves).1 (See Fetal/Neonatal Morbidity and Mortality under Cautions.)

Administration

Oral Administration

Administer orally once daily on an empty stomach; consume no food for at least 2 hours before or 1 hour after a dose.1 18 (See Food under Pharmacokinetics.)

Administer tablets whole with water; do not chew or crush.1

Dosage

Available as abiraterone acetate; dosage expressed in terms of the salt.1

Adults

Prostate Cancer
Metastatic Castration-resistant Prostate Cancer
Oral

1 g once daily in combination with prednisone 5 mg orally twice daily.1

Avoid concomitant use of potent CYP3A4 inducers; if concomitant use cannot be avoided, increase dosing frequency of abiraterone acetate from once daily to twice daily (e.g., from 1 g once daily to 1 g twice daily).1

Metastatic Castration-sensitive Prostate Cancer
Oral

1 g once daily in combination with prednisone 5 mg orally once daily.1

Avoid concomitant use of potent CYP3A4 inducers; if concomitant use cannot be avoided, increase dosing frequency of abiraterone acetate from once daily to twice daily (e.g., from 1 g once daily to 1 g twice daily).1

Dosage Modification for Toxicity
Hepatic Toxicity

For ALT and/or AST elevations >5 times ULN or total bilirubin elevations >3 times ULN, interrupt dosing until liver function test results return to baseline or until ALT and AST return to ≤2.5 times ULN and total bilirubin returns to ≤1.5 times ULN, and then resume at a reduced dosage of 750 mg once daily.1

If hepatic toxicity recurs on dosage of 750 mg daily, interrupt dosing until liver function test results return to baseline or until ALT and AST return to ≤2.5 times ULN and total bilirubin returns to ≤1.5 times ULN, and then resume at a reduced dosage of 500 mg once daily.1

If hepatic toxicity recurs on dosage of 500 mg daily, discontinue abiraterone.1

In patients reinitiating therapy, measure serum aminotransferases and bilirubin at least every 2 weeks for 3 months and then monthly thereafter.1 (See Hepatic Toxicity under Cautions.)

For ALT elevations >3 times ULN with total bilirubin elevations >2 times ULN in the absence of biliary obstruction or other causes, permanently discontinue abiraterone.1

Special Populations

Hepatic Impairment

Mild preexisting hepatic impairment (Child-Pugh class A): No dosage adjustment required.1

Moderate preexisting hepatic impairment (Child-Pugh class B): 250 mg once daily.1 Monitor serum aminotransferases and bilirubin at baseline, every week for the first month of therapy, every 2 weeks during the second and third months, and then monthly thereafter.1 If elevations in ALT and/or AST to >5 times ULN or in total bilirubin to >3 times ULN occur, permanently discontinue abiraterone.1 (See Pharmacokinetics and also see Hepatic Toxicity under Cautions.)

Severe preexisting hepatic impairment (Child-Pugh class C): Use not recommended.1 (See Hepatic Impairment under Cautions.)

Renal Impairment

No dosage adjustment required.1

Geriatric Patients

No dosage adjustment required.1

Cautions for Zytiga

Contraindications

  • No known contraindications.1

Warnings/Precautions

Excessive Mineralocorticoid Activity

Mineralocorticoid excess occurs secondary to CYP17 blockade by abiraterone; commonly manifested as hypertension, hypokalemia, and fluid retention.1 9 10 12 14 Concomitant glucocorticoid administration may reduce severity and incidence of these adverse effects.5 7 8 9 10 12 14

Monitor at least monthly for hypertension, hypokalemia, and fluid retention.1 Control BP and correct hypokalemia before and during treatment.1

Closely monitor patients with a history of cardiovascular disease or underlying medical condition that might be compromised by increased BP, hypokalemia, or fluid retention (e.g., heart failure, recent MI, ventricular arrhythmia).1

Safety not established in patients with left ventricular ejection fraction <50% or NYHA class II–IV heart failure.1

Adrenocortical Insufficiency

Adrenocortical insufficiency reported following interruption of daily corticosteroid regimen and/or during periods of infection or stress.1

Use with caution and monitor for manifestations of adrenocortical insufficiency, especially following prednisone dosage reduction or discontinuance or when patient is subjected to unusual stress.1 Consider possible need for increased corticosteroid dosage before, during, and after stressful situations.1

Symptoms of mineralocorticoid excess may mask manifestations of adrenocortical insufficiency; perform appropriate tests to confirm diagnosis of adrenocortical insufficiency if clinically indicated.1

Hepatic Toxicity

ALT or AST elevations of >5 times ULN reported in 6% of patients, generally during the initial 3 months of therapy.1 No fatalities reported.1

Elevations in liver function test results reported more frequently in patients with preexisting ALT or AST elevations than in patients with normal baseline values.1

Monitor serum aminotransferase and bilirubin concentrations at baseline, every 2 weeks for the first 3 months of therapy, and then monthly thereafter.1 In patients with moderate preexisting hepatic impairment, monitor serum aminotransferase and bilirubin concentrations at baseline, every week for the first month of therapy, every 2 weeks during the second and third months, and then monthly thereafter.1 (See Dosage Modification for Toxicity under Dosage and Administration.)

More frequent monitoring is indicated if aminotransferase or bilirubin concentrations rise above pretreatment levels.1 Evaluate liver function tests promptly if manifestations suggestive of hepatotoxicity develop.1

Treatment-related Mortality and Fractures

Increased mortality and fractures reported in patients with asymptomatic or mildly symptomatic castration-resistant prostate cancer metastatic to bone receiving abiraterone in combination with prednisone (or prednisolone) and radium Ra 223 dichloride; abiraterone is not currently FDA-labeled for use in combination with prednisone (or prednisolone) and radium Ra 223 dichloride.1

In a clinical trial, fractures (28.6 versus 11.4%) and death (38.5 versus 35.5%) occurred more frequently in patients receiving abiraterone in combination with prednisone (or prednisolone) and radium Ra 223 dichloride compared with those receiving abiraterone in combination with prednisone (or prednisolone).1 Treatment groups were unblinded based on recommendations of an independent data monitoring board.1

Patients should not receive abiraterone in combination with prednisone (or prednisolone) and radium Ra 223 dichloride outside of a clinical trial.1

Fetal/Neonatal Morbidity and Mortality

May cause fetal harm and potential loss of pregnancy.1 Safety and efficacy not established in females.1 If used during pregnancy or if patient becomes pregnant, apprise of potential fetal hazard and potential risk for loss of pregnancy.1

Women who are or may be pregnant should not handle abiraterone acetate tablets without protection (e.g., gloves).1

Men with female partners of reproductive potential should use effective methods of contraception during therapy and for 3 weeks following discontinuance of the drug.1

Infertility

Based on animal studies, abiraterone may impair male fertility.1

Specific Populations

Pregnancy

May cause fetal harm and potential loss of pregnancy.1 (See Fetal/Neonatal Morbidity and Mortality under Cautions.)

Lactation

Not known whether distributed into milk, affects milk production, or affects nursing infants; safety and efficacy not established in females.1

Pediatric Use

Safety and efficacy not established.1

Geriatric Use

No overall differences in safety and efficacy relative to younger adults, but increased sensitivity cannot be ruled out.1 27

Hepatic Impairment

Systemic exposure may be increased and clearance may be decreased.1 (See Absorption: Special Populations and Elimination: Special Populations, under Pharmacokinetics.)

Dosage adjustment and careful monitoring of hepatic function required in patients with moderate hepatic impairment (Child-Pugh class B).1 (See Hepatic Impairment under Dosage and Administration.)

Not recommended in patients with severe hepatic impairment (Child-Pugh class C).1

Renal Impairment

Pharmacokinetics not altered by end-stage renal disease requiring hemodialysis.1 (See Absorption: Special Populations, under Pharmacokinetics.)

Common Adverse Effects

Combination therapy with prednisone (twice daily) in patients with metastatic castration-resistant prostate cancer: Fatigue,1 joint swelling or discomfort,1 edema,1 4 muscle discomfort,1 constipation,1 diarrhea,1 hot flush,1 hypertension,1 4 cough,1 insomnia,1 contusion,1 upper respiratory tract infection,1 urinary tract infection,1 dyspnea,1 dyspepsia,1 nasopharyngitis,1 hematuria,1 hypertriglyceridemia,1 hyperglycemia,1 elevated ALT and/or AST concentrations,1 lymphopenia,1 hypernatremia,1 hypokalemia,1 hypophosphatemia.1

Combination therapy with prednisone (once daily) in patients with high-risk metastatic castration-sensitive prostate cancer: Hypertension,1 hypokalemia,1 lymphopenia,1 elevated ALT and/or AST concentrations,1 hot flush.1

Interactions for Zytiga

Abiraterone is a potential inhibitor of CYP isoenzymes 1A2, 2D6, and 2C8 and, to a lesser extent, CYP isoenzymes 2C9, 2C19, and 3A4/5.1 Abiraterone is a substrate of CYP3A4 in vitro.1

Neither abiraterone acetate nor abiraterone is a substrate of P-glycoprotein (P-gp) in vitro at clinically relevant concentrations; abiraterone acetate inhibits P-gp.1

In vitro, abiraterone and its major metabolites are inhibitors of organic anion transport protein (OATP) 1B1.1

Drugs Affecting Hepatic Microsomal Enzymes

Potent CYP3A4 inhibitors: No clinically meaningful effect on systemic exposure of abiraterone.1 (See Specific Drugs under Interactions.)

Potent CYP3A4 inducers: Possible decreased serum concentrations of abiraterone.1 18 Avoid concomitant use; if concomitant use cannot be avoided, increase dosing frequency of abiraterone from once daily to twice daily (e.g., from 1 g once daily to 1 g twice daily).1 If potent CYP3A4 inducer is discontinued, resume prior dose and frequency of abiraterone.1 (See Specific Drugs under Interactions.)

Drugs Metabolized by Hepatic Microsomal Enzymes

Substrates of CYP2D6: Possible increased serum concentrations of CYP2D6 substrate drug and possible toxicity.1 18 Avoid concomitant use of abiraterone and CYP2D6 substrates with a narrow therapeutic index.1 15 If concomitant use cannot be avoided, consider dosage reduction of the CYP2D6 substrate drug and use with caution.1 15 (See Specific Drugs under Interactions.)

Substrates of CYP2C8: Possible increased serum concentrations of CYP2C8 substrate drug and possible toxicity.1 If concomitant use of abiraterone and CYP2C8 substrates with a narrow therapeutic index is necessary, closely monitor for signs of toxicity of the CYP2C8 substrate drug.1 (See Specific Drugs under Interactions.)

Substrates of CYP1A2: Pharmacokinetic interaction not observed to date.1

Specific Drugs

Drug or Food

Interaction

Comments

Antimycobacterials, rifamycins (e.g., rifabutin, rifampin, rifapentine)

Possible decreased abiraterone concentrations1 18

Rifampin: Decreased mean systemic exposure of abiraterone by 55%1

Avoid concomitant use1

If concomitant use cannot be avoided, increase dosing frequency of abiraterone from once daily to twice daily (e.g., from 1 g once daily to 1 g twice daily); resume prior dose and frequency when potent CYP3A4 inducer is discontinued1

Carbamazepine

Possible decreased abiraterone concentrations1 18

Avoid concomitant use1

If concomitant use cannot be avoided, increase dosing frequency of abiraterone from once daily to twice daily (e.g., from 1 g once daily to 1 g twice daily); resume prior dose and frequency when potent CYP3A4 inducer is discontinued1

Dextromethorphan

Increased peak concentrations and AUC of dextromethorphan1 2

Ketoconazole

No clinically meaningful effect on systemic exposure of abiraterone1

Phenobarbital

Possible decreased abiraterone concentrations1 18

Avoid concomitant use1

If concomitant use cannot be avoided, increase dosing frequency of abiraterone from once daily to twice daily (e.g., from 1 g once daily to 1 g twice daily); resume prior dose and frequency when potent CYP3A4 inducer is discontinued1

Phenytoin

Possible decreased abiraterone concentrations1 18

Avoid concomitant use1

If concomitant use cannot be avoided, increase dosing frequency of abiraterone from once daily to twice daily (e.g., from 1 g once daily to 1 g twice daily); resume prior dose and frequency when potent CYP3A4 inducer is discontinued1

Pioglitazone

Increased systemic exposure to pioglitazone, a CYP2C8 substrate, by 46%1

If concomitant use with CYP2C8 substrates with a narrow therapeutic index is necessary, closely monitor for toxicity of the CYP2C8 substrate drug1

Theophylline

No change in systemic exposure of single-dose theophylline1

Thioridazine

Possible increased thioridazine concentrations1 15 18

Avoid concomitant use; if concomitant use cannot be avoided, consider thioridazine dosage reduction and use with caution1 15

Zytiga Pharmacokinetics

Absorption

Bioavailability

Systemic exposure is dose proportional over a dose range of 250 mg to 1 g;1 however, systemic exposure does not substantially increase when dose is doubled from 1 g to 2 g.1

Abiraterone acetate is a prodrug that is converted in vivo to abiraterone; peak plasma abiraterone concentrations are attained about 2 hours after abiraterone acetate dose.1 5 13

Food

Food increases systemic exposure.1 8 13

Oral administration of a single 1-g dose of abiraterone acetate with a low-fat or high-fat meal increases abiraterone AUC by approximately fivefold or tenfold, respectively, and increases peak plasma concentrations by approximately sevenfold or 17-fold, respectively.1

When a single dose of abiraterone acetate is administered 2 hours after or 1 hour before a medium-fat meal, abiraterone AUC increases by approximately sevenfold or 1.6-fold, respectively.1

Systemic exposure is similar following administration of abiraterone acetate for 7 days with a low-fat meal or ≥2 hours after or 1 hour before a meal, but increases approximately twofold when administered with a high-fat meal.1

Special Populations

In patients with mild (Child-Pugh class A) or moderate (Child-Pugh class B) hepatic impairment, AUC is increased 1.1- or 3.6-fold, respectively, compared with individuals with normal hepatic function.1

In patients with severe hepatic impairment (Child-Pugh class C), AUC is increased approximately sevenfold and free fraction of the drug is increased twofold compared with individuals with normal hepatic function.1 (See Distribution: Special Populations, in Pharmacokinetics.)

Distribution

Plasma Protein Binding

>99% (mainly albumin and α1-acid glycoprotein).1

Special Populations

In patients with severe hepatic impairment (Child-Pugh class C), plasma protein binding of drug is decreased.1 (See Absorption: Special Populations, in Pharmacokinetics.)

Elimination

Metabolism

Abiraterone acetate is hydrolyzed to abiraterone (active metabolite), most likely by esterases in non-CYP-dependent pathways.1 Further metabolized to 2 inactive sulfate conjugates, abiraterone sulfate (formed by SULT2A1, a sulfotransferase that catalyzes sulfate conjugation of dehydroepiandrosterone [DHEA] and other steroids) and N-oxide abiraterone sulfate (formed by CYP3A4 and SULT2A1).1 19

Elimination Route

Excreted in feces (88%), mainly as abiraterone acetate (55%) and abiraterone (22%), and in urine (5%).1

Half-life

Approximately 12 hours.1

Special Populations

Mean half-life in patients with mild or moderate hepatic impairment is approximately 18 hours or 19 hours, respectively.1

In patients with end-stage renal disease requiring hemodialysis, pharmacokinetic parameters were similar to those in individuals with normal renal function.1

Stability

Storage

Oral

Tablets

20–25°C (may be exposed to 15–30°C).1

Actions

  • Abiraterone acetate is a prodrug of abiraterone, a potent, selective, and irreversible inhibitor of 17α-hydroxylase/C17,20-lyase (CYP17), an enzyme expressed in adrenal glands, testes, and prostate tumor.1 5 6 10 12 13 CYP17 inhibition results in suppression of androgen production.10 12

  • 17α-Hydroxylase catalyzes conversion of pregnenolone and progesterone to their 17α-hydroxy derivatives; C17,20-lyase catalyzes conversion of these 17α-hydroxy derivatives to DHEA and androstenedione, respectively.1 6 10 12 DHEA and androstenedione are androgenic precursors of testosterone.1 6 10 12

  • Abiraterone is tenfold to 30-fold more potent than ketoconazole (a nonspecific CYP inhibitor and weak inhibitor of CYP17) in its inhibition of CYP17.5 9

  • CYP17 inhibition can result in increased mineralocorticoid synthesis.3

Advice to Patients

  • Importance of taking prednisone as directed to minimize adverse effects of abiraterone.1 If a dose of abiraterone or prednisone is missed, take the next dose at the regularly scheduled time; importance of advising clinician if more than one daily dose of abiraterone is missed.1

  • For patients currently receiving gonadotropin-releasing hormone (GnRH) agonist therapy, importance of continuing this therapy during abiraterone therapy.1

  • Risk of increased abiraterone exposure and adverse effects if the drug is taken with food.1 Importance of swallowing abiraterone acetate tablets whole with water and consuming no food for at least 2 hours before or 1 hour after a dose.1

  • Risk of peripheral edema, hypertension, and hypokalemia (with potential to cause QT-interval prolongation or torsades de pointes).1 Importance of patients informing their clinician if dizziness, palpitations, tachycardia, feelings of faintness or lightheadedness, headache, confusion, leg pain, muscle weakness, or peripheral edema occurs.1

  • Risk of adrenocortical insufficiency.1 Importance of patients informing their clinician if symptoms of adrenocortical insufficiency occur.1

  • Risk of severe hepatotoxicity and importance of liver function test monitoring.1 Importance of patients immediately informing their clinician if jaundice, dark urine, or severe nausea or vomiting occurs.1

  • Increased risk of treatment-related mortality and fractures in patients receiving abiraterone acetate in combination with prednisone (or prednisolone) and radium Ra 223 dichloride.1 Use of abiraterone acetate in combination with prednisone (or prednisolone) and radium Ra 223 dichloride is not recommended outside of a clinical trial.1 (See Treatment-related Mortality and Fractures under Cautions.)

  • Importance of advising patients that abiraterone may cause fetal harm and potential loss of pregnancy; it is not known whether the drug distributes into semen.1 Necessity of advising men to use an effective contraceptive method during sexual encounters with women of reproductive potential; these contraceptive measures are required during and for 3 weeks after discontinuance of abiraterone therapy.1 Importance of advising patients that women who are or may be pregnant should not handle abiraterone acetate tablets without protection (e.g., gloves).1

  • Importance of informing clinicians of existing or contemplated concomitant therapy, including prescription and OTC drugs and herbal supplements, as well as any concomitant illnesses.1

  • Importance of informing patients of other important precautionary information.1 (See Cautions.)

Preparations

Excipients in commercially available drug preparations may have clinically important effects in some individuals; consult specific product labeling for details.

Please refer to the ASHP Drug Shortages Resource Center for information on shortages of one or more of these preparations.

Abiraterone Acetate

Routes

Dosage Forms

Strengths

Brand Names

Manufacturer

Oral

Tablets

250 mg

Zytiga

Janssen Biotech

Tablets, film-coated

500 mg

Zytiga

Janssen Biotech

AHFS DI Essentials™. © Copyright 2020, Selected Revisions May 4, 2020. American Society of Health-System Pharmacists, Inc., 4500 East-West Highway, Suite 900, Bethesda, Maryland 20814.

References

1. Janssen Biotech Inc. Zytiga (abiraterone acetate) tablets prescribing information. Horsham, PA; 2019 Jun.

2. US Food and Drug Administration. Center for Drug Evaluation and Research. Application number 202379orig1s000: Clinical pharmacology and biopharmaceutics review(s). From FDA website. http://www.accessdata.fda.gov/drugsatfda_docs/nda/2011/202379Orig1s000ClinPharmR.pdf

3. US Food and Drug Administration. Center for Drug Evaluation and Research: Application number 202379: Summary review for abiraterone. From FDA website. http://www.accessdata.fda.gov/drugsatfda_docs/nda/2011/202379Orig1s000SumR.pdf

4. de Bono JS, Logothetis CJ, Molina A et al. Abiraterone and increased survival in metastatic prostate cancer. N Engl J Med. 2011; 364:1995-2005. http://www.ncbi.nlm.nih.gov/pubmed/21612468?dopt=AbstractPlus http://www.pubmedcentral.nih.gov/picrender.fcgi?tool=pmcentrez&artid=3471149&blobtype=pdf

5. Reid AH, Attard G, Danila DC et al. Significant and sustained antitumor activity in post-docetaxel, castration-resistant prostate cancer with the CYP17 inhibitor abiraterone acetate. J Clin Oncol. 2010; 28:1489-95. http://www.ncbi.nlm.nih.gov/pubmed/20159823?dopt=AbstractPlus http://www.pubmedcentral.nih.gov/picrender.fcgi?tool=pmcentrez&artid=2849770&blobtype=pdf

6. Salem M, Garcia JA. Abiraterone acetate, a novel adrenal inhibitor in metastatic castration-resistant prostate cancer. Curr Oncol Rep. 2011; 13:92-6. http://www.ncbi.nlm.nih.gov/pubmed/21243537?dopt=AbstractPlus

7. Attard G, Reid AH, A’Hern R et al. Selective inhibition of CYP17 with abiraterone acetate is highly active in the treatment of castration-resistant prostate cancer. J Clin Oncol. 2009; 27:3742-8. http://www.ncbi.nlm.nih.gov/pubmed/19470933?dopt=AbstractPlus http://www.pubmedcentral.nih.gov/picrender.fcgi?tool=pmcentrez&artid=3535569&blobtype=pdf

8. Attard G, Reid AH, Yap TA et al. Phase I clinical trial of a selective inhibitor of CYP17, abiraterone acetate, confirms that castration-resistant prostate cancer commonly remains hormone driven. J Clin Oncol. 2008; 26:4563-71. http://www.ncbi.nlm.nih.gov/pubmed/18645193?dopt=AbstractPlus

9. Attard G, Richards J, de Bono JS. New strategies in metastatic prostate cancer: targeting the androgen receptor signaling pathway. Clin Cancer Res. 2011; 17:1649-57. http://www.ncbi.nlm.nih.gov/pubmed/21372223?dopt=AbstractPlus http://www.pubmedcentral.nih.gov/picrender.fcgi?tool=pmcentrez&artid=3513706&blobtype=pdf

10. Massard C, Fizazi K. Targeting continued androgen receptor signaling in prostate cancer. Clin Cancer Res. 2011; 17:3876-83. http://www.ncbi.nlm.nih.gov/pubmed/21680543?dopt=AbstractPlus

11. Heinlein CA, Chang C. Androgen receptor in prostate cancer. Endocr Rev. 2004; 25:276-308. http://www.ncbi.nlm.nih.gov/pubmed/15082523?dopt=AbstractPlus

12. Molina A, Belldegrun A. Novel therapeutic strategies for castration resistant prostate cancer: inhibition of persistent androgen production and androgen receptor mediated signaling. J Urol. 2011; 185:787-94. http://www.ncbi.nlm.nih.gov/pubmed/21239012?dopt=AbstractPlus

13. Ryan CJ, Smith MR, Fong L et al. Phase I clinical trial of the CYP17 inhibitor abiraterone acetate demonstrating clinical activity in patients with castration-resistant prostate cancer who received prior ketoconazole therapy. J Clin Oncol. 2010; 28:1481-8. http://www.ncbi.nlm.nih.gov/pubmed/20159824?dopt=AbstractPlus http://www.pubmedcentral.nih.gov/picrender.fcgi?tool=pmcentrez&artid=2849769&blobtype=pdf

14. Danila DC, Morris MJ, de Bono JS et al. Phase II multicenter study of abiraterone acetate plus prednisone therapy in patients with docetaxel-treated castration-resistant prostate cancer. J Clin Oncol. 2010; 28:1496-501. http://www.ncbi.nlm.nih.gov/pubmed/20159814?dopt=AbstractPlus http://www.pubmedcentral.nih.gov/picrender.fcgi?tool=pmcentrez&artid=3040042&blobtype=pdf

15. Janssen. Titusville, NJ: Personal communication.

16. US Food and Drug Administration. Center for Drug Evaluation and Research. Application number 202379orig1s000: Medical review(s). From FDA website. http://www.accessdata.fda.gov/drugsatfda_docs/nda/2011/202379Orig1s000MedR.pdf

17. Lilja JJ, Kivistö KT, Neuvonen PJ. Duration of effect of grapefruit juice on the pharmacokinetics of the CYP3A4 substrate simvastatin. Clin Pharmacol Ther. 2000; 68:384-90. http://www.ncbi.nlm.nih.gov/pubmed/11061578?dopt=AbstractPlus

18. . Abiraterone acetate (Zytiga) for metastatic castration-resistant prostate cancer. Med Lett Drugs Ther. 2011; 53:63-4. http://www.ncbi.nlm.nih.gov/pubmed/21836546?dopt=AbstractPlus

19. Thomae BA, Eckloff BW, Freimuth RR et al. Human sulfotransferase SULT2A1 pharmacogenetics: genotype-to-phenotype studies. Pharmacogenomics J. 2002; 2:48-56. http://www.ncbi.nlm.nih.gov/pubmed/11990382?dopt=AbstractPlus

20. Ryan CJ, Smith MR, de Bono JS et al. Abiraterone in metastatic prostate cancer without previous chemotherapy. N Engl J Med. 2013; 368:138-48. http://www.ncbi.nlm.nih.gov/pubmed/23228172?dopt=AbstractPlus

21. Rathkopf DE, Smith MR, de Bono JS et al. Updated interim efficacy analysis and long-term safety of abiraterone acetate in metastatic castration-resistant prostate cancer patients without prior chemotherapy (COU-AA-302). Eur Urol. 2014; 66:815-25. http://www.ncbi.nlm.nih.gov/pubmed/24647231?dopt=AbstractPlus

22. Ryan CJ, Smith MR, Fizazi K et al. Abiraterone acetate plus prednisone versus placebo plus prednisone in chemotherapy-naive men with metastatic castration-resistant prostate cancer (COU-AA-302): final overall survival analysis of a randomised, double-blind, placebo-controlled phase 3 study. Lancet Oncol. 2015; 16:152-60. http://www.ncbi.nlm.nih.gov/pubmed/25601341?dopt=AbstractPlus

23. Fizazi K, Tran N, Fein L et al. Abiraterone plus Prednisone in Metastatic, Castration-Sensitive Prostate Cancer. N Engl J Med. 2017; 377:352-360. http://www.ncbi.nlm.nih.gov/pubmed/28578607?dopt=AbstractPlus

24. Fizazi K, Tran N, Fein L et al. Abiraterone acetate plus prednisone in patients with newly diagnosed high-risk metastatic castration-sensitive prostate cancer (LATITUDE): final overall survival analysis of a randomised, double-blind, phase 3 trial. Lancet Oncol. 2019; 20:686-700. http://www.ncbi.nlm.nih.gov/pubmed/30987939?dopt=AbstractPlus

25. Fizazi K, Scher HI, Molina A et al. Abiraterone acetate for treatment of metastatic castration-resistant prostate cancer: final overall survival analysis of the COU-AA-301 randomised, double-blind, placebo-controlled phase 3 study. Lancet Oncol. 2012; 13:983-92. http://www.ncbi.nlm.nih.gov/pubmed/22995653?dopt=AbstractPlus

26. Logothetis CJ, Basch E, Molina A et al. Effect of abiraterone acetate and prednisone compared with placebo and prednisone on pain control and skeletal-related events in patients with metastatic castration-resistant prostate cancer: exploratory analysis of data from the COU-AA-301 randomised trial. Lancet Oncol. 2012; 13:1210-7. http://www.ncbi.nlm.nih.gov/pubmed/23142059?dopt=AbstractPlus

27. Mulders PF, Molina A, Marberger M et al. Efficacy and safety of abiraterone acetate in an elderly patient subgroup (aged 75 and older) with metastatic castration-resistant prostate cancer after docetaxel-based chemotherapy. Eur Urol. 2014; 65:875-83. http://www.ncbi.nlm.nih.gov/pubmed/24099659?dopt=AbstractPlus

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