Darolutamide, a nonsteroidal antiandrogen, is an antineoplastic agent.1, 2, 3
Nonmetastatic Castration-resistant Prostate Cancer
Darolutamide is used for the treatment of nonmetastatic castration-resistant prostate cancer (nmCRPC) in adults; patients treated with darolutamide should also receive a gonadotropin-releasing hormone (GnRH) agonist or antagonist concurrently or have had a bilateral orchiectomy.1, 2
Darolutamide has been shown to prolong metastasis-free survival in patients with nmCRPC.1, 2 The drug was evaluated in a randomized, double-blind, placebo-controlled, phase 3 study (ARAMIS) in 1509 patients with nmCRPC at high risk for metastasis (i.e., prostate-specific antigen [PSA] doubling time of 10 months or less despite continuous androgen deprivation therapy).1, 2, 3 Patients were randomized to receive either darolutamide (600 mg twice daily) or placebo; androgen deprivation therapy was continued in all patients.1 Patients were stratified by PSA doubling time and use of bone resorption inhibitors.1 Treatment was continued until disease progression or unacceptable toxicity occurred or the patient withdrew from the study.1 The primary measure of efficacy was metastasis-free survival.1 The median age of patients enrolled in the study was 74 years; 9% of patients were 85 years of age or older.1 Nearly half of patients (42%) had undergone prior surgery or radiation therapy of the prostate; 73% had a Gleason score of 7 or higher, 73% had received prior treatment with a nonsteroidal antiandrogen (66% had received bicalutamide and 13% had received flutamide), and all had an Eastern Cooperative Oncology Group (ECOG) performance status of 0 or 1.1, 2 Patients with a history of seizures or with conditions predisposing to seizures were not excluded.1, 2 At a median follow-up of 17.9 months, median metastasis-free survival was substantially longer in darolutamide-treated patients compared with those receiving placebo (40.4 and 18.4 months, respectively).1, 2 Results of a subgroup analysis (based on PSA doubling time, baseline PSA concentration, number of prior hormonal therapies, use of bone resorption inhibitors, regional nodal disease, Gleason score, age, race, ECOG performance status, and geographic region) suggested that the drug's effect on metastasis-free survival was consistent across subgroups.1, 2 Time to pain progression and time to initiation of cytotoxic chemotherapy were delayed in patients receiving darolutamide compared with those receiving placebo.1 Deterioration of health-related quality of life measures was significantly delayed with use of darolutamide compared to placebo.15 At the end of the initial study, patients continued open-label treatment.16 After a median follow-up time of 29 months, overall survival at 3 years was 83% with darolutamide and 77% with placebo.16 The risk of death was reduced by 31% with darolutamide treatment compared to placebo.16
According to a joint guideline from the American Urological Association (AUA) and the Society of Urologic Oncology (SUO), the decision to add an androgen receptor antagonist to androgen deprivation therapy (ADT) in patients with nonmetastatic castration-resistant prostate cancer is dependent on metastatic risk.3016 The risk of metastasis is determined by the time to doubling of PSA levels.3016 If the PSA doubling time is 10 months or less, metastatic risk is high and the guideline recommends use of either apalutamide, darolutamide, or enzalutamide in addition to ADT.3016 Continuation of ADT with observation is recommended for patients who have a PSA doubling time greater than 10 months as risk of metastasis is considered to be lower in such patients.16
Metastatic Castration-sensitive Prostate Cancer
Darolutamide is used for the treatment of metastatic castration-sensitive prostate cancer (mCSPC) as monotherapy or in combination with docetaxel in adults; patients treated with darolutamide should also receive a gonadotropin-releasing hormone (GnRH) agonist or antagonist concurrently or have had a bilateral orchiectomy1, 17, 18
Darolutamide has been shown to prolong overall survival in patients with mCSPC.1 The drug was evaluated in a multicenter, double-blind, placebo-controlled clinical trial (ARASENS) in 1306 patients with mCSPC.1, 18 Patients were randomized 1:1 to receive 600 mg darolutamide orally twice daily or matching placebo, concomitantly with 75 mg/m2 of docetaxel for 6 cycles.1, 18 All patients received a GnRH analog concurrently or had a bilateral orchiectomy.1, 18 Treatment with darolutamide or placebo continued until symptomatic progressive disease, change of antineoplastic therapy, or unacceptable toxicity.1, 18 Patients with regional lymph node involvement only (M0) were excluded from the study; patients were stratified by extent of disease (non-regional lymph nodes metastases only (M1a), bone metastases with or without lymph node metastases (M1b) or visceral metastases with or without lymph node metastases or with or without bone metastases (M1c) and by alkaline phosphatase level (< or ≥ upper limit of normal) at study entry.1 The median age of patients was 67 years (range 41-89) and 17% of patients were 75 years of age or older.1 In this study, 78% of patients had a Gleason score of ≥8 at diagnosis, 71% of patients had an ECOG performance status score of 0, and 29% of patients had an ECOG performance status score of 1.1 The study population included 86% with de novo disease and 13% with recurrent disease.1
The major efficacy outcome measure was overall survival (OS).1, 18 Treatment with darolutamide with docetaxel resulted in a risk of death that was 32.5% lower than seen in the placebo group.1, 18
In a multicenter, double-blind, placebo-controlled clinical trial (ARANOTE), 669 patients with high- or low-volume mCSPC were randomized 2:1 to receive 600 mg darolutamide orally twice daily or matching placebo.1, 17 All patients received a GnRH agonist or antagonist concurrently or had a bilateral orchiectomy.1, 17 Treatment with darolutamide or placebo continued until symptomatic progressive disease, change of antineoplastic therapy, or unacceptable toxicity, death, or study withdrawal.1, 17 The median age of patients was 70 years (range 43-93) and 29% of patients were 75 years of age or older; 56% were White, 31% Asian, and 10% Black.1 In this study, 68% of patients had a Gleason score of ≥8 at diagnosis, 50% of patients had an ECOG performance status score of 0, and 47% of patients had an ECOG performance status score of 1.1 The study population included 71% with high volume disease and 29% with low volume disease.1
The major efficacy outcome measure was radiographic progression-free survival; an additional efficacy outcome was OS.1, 17 Treatment with darolutamide plus ADT significantly improved radiographic progression-free survival, reducing the risk of progression or death by 46% as compared to placebo plus ADT.1, 17 Results regarding OS were suggestive of benefit with darolutamide as compared to placebo but were not significant.1, 17
The American Urological Association (AUA) and the Society of Urologic Oncology (SUO) published updated guidelines in 2023 for the management of advanced prostate cancer.3016 The guidelines state that in selected patients with de novo mCSPC, clinicians should offer ADT in combination with docetaxel and either abiraterone acetate plus prednisone or darolutamide.3016
Darolutamide is administered orally twice daily with food.1 Tablets should be swallowed whole.1
If a dose of darolutamide is missed, the missed dose should be taken as soon as it is remembered.1 A missed dose may be taken together with the next scheduled dose; patients should resume the regular twice daily dosing schedule thereafter.1
Store darolutamide tablets at 20-25°C (excursions permitted between 15-30°C).1
Nonmetastatic Castration-resistant Prostate Cancer
For the treatment of nonmetastatic castration-resistant prostate cancer, the recommended adult dosage of darolutamide is 600 mg twice daily.1 Continue until disease progression or unacceptable toxicity occurs.1
Metastatic Castration-sensitive Prostate Cancer
For the treatment of metastatic castration-sensitive prostate cancer as monotherapy or in combination with docetaxel, the recommended adult dosage of darolutamide is 600 mg twice daily.1
When used in combination with docetaxel, administer the first of 6 cycles of docetaxel within 6 weeks after the start of darolutamide treatment.1 Refer to docetaxel prescribing information for additional dosing information, including dosage modifications.1
Continue treatment until disease progression or unacceptable toxicity occurs, even if a cycle of docetaxel is delayed, interrupted, or discontinued.1
Dosage Modification for Toxicity
If an intolerable or grade 3 or greater adverse effect occurs, interrupt darolutamide therapy or reduce dosage to 300 mg twice daily until symptoms improve.1 Resume dosage of 600 mg twice daily when the adverse reaction returns to baseline.1 Dosage reduction below 300 mg twice daily is not recommended.1
The recommended dosage of darolutamide in patients with moderate hepatic impairment (Child-Pugh class B) is 300 mg twice daily.1 No initial dosage adjustment is necessary in patients with mild hepatic impairment (Child-Pugh class A).1 Pharmacokinetics of darolutamide have not been established in patients with severe hepatic impairment (Child-Pugh class C).1
The recommended dosage of darolutamide in patients with severe renal impairment (estimated glomerular filtration rate [eGFR] of 15-29 mL/minute per 1.73 m2) not receiving hemodialysis is 300 mg twice daily.1 No initial dosage adjustment is necessary in patients with mild or moderate renal impairment (eGFR of 30-89 mL/minute per 1.73 m2).1 Pharmacokinetics of darolutamide have not been established in patients with end-stage renal disease (eGFR of less than 15 mL/minute per 1.73 m2).1
The manufacturer makes no special dosage recommendations for geriatric patients; most patients (88%) in the principal efficacy study were 65 years of age or older.1
Ischemic heart disease, including fatalities, have been reported in patients receiving darolutamide.1 In a pooled analysis (ARAMIS and ARANOTE) of patients with nonmetastatic castration-resistant prostate cancer (nmCRPC), ischemic heart disease occurred in 3.4% of patients receiving darolutamide and 2.2% of patients receiving placebo, including Grade 3-4 events in 1.4% and 0.3% of the respective groups.1 Ischemic events led to death in 0.4% of patients receiving darolutamide and 0.4% of patients receiving placebo.1 In a randomized study of patients with metastatic castration-sensitive prostate cancer (mCSPC; ARASENS), ischemic heart disease occurred in 3.2% of patients receiving darolutamide with docetaxel and 2% of patients receiving placebo with docetaxel, including grade 3-4 events in 1.3% and 1.1% of the respective treatment groups.1 Ischemic events led to death in 0.3% of patients receiving darolutamide with docetaxel and 0% of patients receiving placebo with docetaxel.1
Monitor for signs and symptoms of ischemic heart disease.1 Optimize management of cardiovascular risk factors, such as hypertension, diabetes, or dyslipidemia.1 Discontinue darolutamide for Grade 3 or 4 ischemic heart disease.1
Seizures have been reported in patients receiving darolutamide.1
In a pooled analysis (ARAMIS and ARANOTE) of patients with nmCRPC, grade 1-3 seizures occurred in 0.2% of patients receiving darolutamide.1 Seizures occurred from 261 to 665 days after initiation of darolutamide.1
In a study in patients with mCSPC (ARASENS), seizures occurred in 0.8% of patients receiving darolutamide with docetaxel, including two Grade 3 events.1 Seizures occurred from 38 to 1754 days after initiation of darolutamide.1
It is unknown whether anti-epileptic medications will prevent seizures with darolutamide.1 Advise patients of the risk of developing a seizure while receiving darolutamide and of engaging in any activity where sudden loss of consciousness could cause harm to themselves or others.1 Consider discontinuation of darolutamide in patients who develop a seizure during treatment.1
Fetal/Neonatal Morbidity and Mortality
Darolutamide may cause fetal harm and potential loss of pregnancy in humans based on its mechanism of action.1 Safety and efficacy of darolutamide have not been established in females.1
Males with female partners of reproductive potential should use effective methods of contraception during darolutamide therapy and for 1 week after the last dose of the drug.1
Based on its mechanism of action, darolutamide can cause fetal harm and potential loss of pregnancy if administered to pregnant women.1
It is not known whether darolutamide or its metabolites are distributed into human milk.1 The effects of darolutamide on nursing infants or on milk production also are not known.1
Female and Males of Reproductive Potential
Males with female partners of reproductive potential should use effective methods of contraception during darolutamide therapy and for 1 week after the last dose of the drug.1
Based on animal studies, darolutamide may impair fertility in males of reproductive potential.1 Darolutamide was associated with tubular dilation of the testes, hypospermia, and atrophy of the seminal vesicles, testes, prostate gland, and epididymides in rats and dogs at exposure levels approximately 0.6 and 1 times the human exposure, respectively.1
Safety and efficacy of darolutamide have not been established in pediatric patients.1
In the ARAMIS study, 88% of patients were 65 years of age or older, and 49% were 75 years of age or older.1 In the ARANOTE study, 74% of patients were 65 years of age or older, and 30% were 75 years of age or older.1 In the ARASENS study, 63% of patients were 65 years of age and over, and 16% were 75 years of age and over.1 No overall differences in safety or efficacy were observed between geriatric patients and younger adults in both studies.1
Exposure to darolutamide in individuals with moderate hepatic impairment (Child-Pugh class B) is increased about 1.9-fold compared with individuals with normal hepatic function.1
Pharmacokinetics of darolutamide have not been established in patients with severe hepatic impairment (Child-Pugh class C).1
Exposure to darolutamide in individuals without cancer with severe renal impairment (estimated glomerular filtration rate [eGFR] of 15-29 mL/minute per 1.73 m2) not receiving dialysis is increased about 2.5-fold compared with those with normal renal function.1
Pharmacokinetics of darolutamide have not been established in patients with end-stage renal disease (eGFR of less than 15 mL/minute per 1.73 m2).1
Adverse effects reported in ≥10% of patients with nmCRPC and mCSPC administered darolutamide, with a ≥2% increase over placebo, include increased AST, decreased neutrophil count, increased bilirubin, fatigue, and increased ALT.1
Adverse effects reported ≥10% of patients with mCSPC receiving darolutamide in combination with docetaxel, with a ≥2% increase over placebo, include constipation, rash, decreased appetite, hemorrhage, increased weight, and hypertension.1 The most common laboratory abnormalities (≥30%) in these patients include anemia, hyperglycemia, decreased lymphocyte count, decreased neutrophil count, increased AST, increased ALT, and hypocalcemia.1
Darolutamide is metabolized principally by cytochrome P-450 (CYP) isoenzyme 3A4; the drug also is metabolized by uridine diphosphate-glucuronosyltransferase (UGT) 1A9 and UGT1A1.1, 3, 10
In vitro, darolutamide is an inducer of CYP3A4 and an inhibitor of P-glycoprotein (P-gp) and breast cancer resistance protein (BCRP); darolutamide also inhibits organic anion transport protein (OATP) 1B1 and OATP1B3 in vitro.1, 3
Darolutamide did not inhibit the major CYP enzymes 1A2, 2A6, 2B6, 2C8, 2C9, 2C19, 2D6, 2E1, and 3A4 or transporters, including multidrug resistance protein 2 (MRP2), bile salt export pump (BSEP), organic anion transporters (OATs), organic cation transporters (OCTs), multidrug and toxin extrusion transporters (MATEs), OATP2B1, and sodium taurocholate co-transporting polypeptide (NTCP), at clinically relevant concentrations.1
Drugs Affecting Hepatic Microsomal Enzymes and Efflux Transport Systems
Inhibitors of CYP3A4 and Efflux Transport Systems
Concomitant use of darolutamide with drugs that are combined P-gp and strong CYP3A4 inhibitors increases exposure of darolutamide and may increase the risk of darolutamide adverse effects.1 Concomitant use of the combined P-gp and strong CYP3A4 inhibitor itraconazole (200 mg twice daily) with darolutamide (single 600-mg dose) increased the mean area under the concentration-time curve (AUC) and peak plasma concentration of darolutamide by 1.7- and 1.4-fold, respectively.1, 10
Patients receiving darolutamide with a drug that is a combined P-gp and strong CYP3A4 inhibitor should be monitored more frequently for darolutamide toxicity, and the dosage of darolutamide should be modified as needed.1
Inducers of CYP3A4 and Efflux Transport Systems
Concomitant use of darolutamide with drugs that are combined P-gp and moderate or strong CYP3A4 inducers decreases exposure of darolutamide and may decrease darolutamide activity.1 Concomitant use of the P-gp and strong CYP3A4 inducer rifampin (600 mg once daily) with darolutamide (single 600-mg dose) decreased the mean AUC and peak plasma concentration of darolutamide by 72 and 52%, respectively.1, 10 Concomitant use of moderate CYP3A4 inducers with darolutamide is expected to decrease darolutamide exposure by 36-58%.1
Concomitant use of darolutamide with combined P-gp and moderate or strong CYP3A4 inducers should be avoided.1
Drugs Metabolized by Hepatic Microsomal Enzymes
Concomitant use of darolutamide (600 mg twice daily) and the sensitive CYP3A4 substrate midazolam (single 1-mg dose) decreased the mean AUC and peak plasma concentration of midazolam by 29 and 32%, respectively.1, 10 These effects were not considered clinically important.1, 10
Drugs Affected by Breast Cancer Resistance Protein and Organic Anion Transport Protein
Concomitant use of darolutamide with drugs that are BCRP, OATP1B1, and/or OATP1B3 substrates increases exposure of the substrate and may increase the risk of substrate-related toxicity.1
Concomitant use of darolutamide (600 mg twice daily) and the BCRP, OATP1B1, and OATP1B3 substrate rosuvastatin (single 5-mg dose) increased the mean AUC and peak plasma concentration of rosuvastatin by approximately fivefold.1, 10 No clinically important effects on the pharmacokinetics of darolutamide were observed.10 In the principal efficacy study evaluating darolutamide (ARAMIS), approximately 30% of patients received concomitant antilipemic therapy with a statin that was a BCRP substrate.11 In this subset of patients, elevations in serum creatinine, aminotransferase, and bilirubin concentrations were observed more frequently in those receiving darolutamide compared with those receiving placebo.3, 11
Concomitant use of darolutamide with BCRP substrates should be avoided when possible.1 If concomitant use cannot be avoided, patients should be monitored more frequently for adverse effects; the manufacturer's prescribing information for the BCRP substrate should be consulted and dosage reduction of the BCRP substrate should be considered.1
Concomitant use of darolutamide with OATP1B1 or OATP1B3 substrates requires close monitoring for adverse reactions of these drugs and may require dosage reduction while taking darolutamide.1 The manufacturer's prescribing information for the OATP1B1 or OATP1B3 substrate should be consulted.1
Concomitant use of darolutamide and docetaxel resulted in no clinically important effects on the pharmacokinetics of docetaxel in metastatic castration-sensitive prostate cancer (mCSPC) patients.1 There were no clinically important effects on the pharmacokinetics of darolutamide, when used in combination with docetaxel.1
Drugs Affected by P-glycoprotein Transport
Concomitant use of darolutamide (600 mg twice daily) with the P-gp substrate dabigatran etexilate (single 75-mg dose) did not result in clinically important effects on the pharmacokinetics of dabigatran.1, 10
Darolutamide, a nonsteroidal antiandrogen, is an antineoplastic agent.1, 2, 3 The drug competitively inhibits androgen binding to androgen receptors;1, 3, 6 its mechanism of action is similar to those of enzalutamide and apalutamide (nonsteroidal antiandrogens structurally unrelated to darolutamide).6, 8, 13 Darolutamide inhibits nuclear translocation of the androgen receptor, interaction of the androgen receptor with DNA, and androgen receptor-mediated gene transcription.1, 3, 9, 13 Compared with enzalutamide and apalutamide,2, 8, 9 darolutamide appears to cross the blood-brain barrier to a negligible or lesser extent and to have less affinity for γ-aminobutyric acid type A (GABAA) receptors in preclinical models, which has theoretical implications for a potentially improved CNS adverse effect profile (e.g., decreased risk of seizures).2, 6, 8, 9, 13 Darolutamide inhibited tumor growth in vitro and decreased tumor volume in xenograft models of castration-resistant prostate cancer in mice.1, 3
In castration-resistant prostate cancer, alterations in androgen receptor signaling (e.g., androgen receptor gene mutation or amplification, androgen receptor overexpression) have been shown to result in persistence of androgen receptor signaling and to contribute to disease progression despite castrate levels of androgens.5, 6, 7, 13 Resistance to conventional antiandrogens (e.g., bicalutamide, flutamide, nilutamide) in castration-resistant prostate cancer has been associated with paradoxical agonistic effects of these drugs and continued androgen receptor signaling.13 Unlike these conventional antiandrogens but similar to other second generation antiandrogens (e.g., enzalutamide, apalutamide), darolutamide does not exhibit agonistic activity in cells that overexpress the androgen receptor.5, 13, 14 In addition to inhibition of wild-type androgen receptors, darolutamide also has demonstrated inhibition of mutant androgen receptors known to trigger bicalutamide, enzalutamide, and apalutamide antagonist-to-agonist switch.3, 6, 9, 12
Darolutamide exhibits nearly dose-proportional exposure over a dose range of 100-700 mg.1 Following oral administration of a single 600-mg dose, peak plasma concentration is attained in approximately 4 hours.1 Absolute bioavailability of a 300-mg dose of darolutamide administered orally under fasted conditions is approximately 30%; bioavailability increases 2 to 2.5-fold when administered with food.1, 8 Steady-state concentrations of darolutamide are achieved after 2-5 days of repeated dosing with food, and the accumulation ratio is approximately 2-fold.1 Darolutamide is metabolized principally by cytochrome P-450 (CYP) isoenzyme 3A4 to form its major active metabolite, keto-darolutamide.1, 3, 10 Keto-darolutamide has been shown to have activity similar to that of the parent drug in vitro;1 however, its contribution to the overall pharmacologic effect of the drug in vivo is expected to be minor, owing to its small unbound fraction (0.2%).3, 10 Uridine diphosphate-glucuronosyltransferase (UGT) enzymes 1A9 and 1A1 also contribute to the metabolism of darolutamide.1, 3 Darolutamide and keto-darolutamide are 92 and 99.8% bound, respectively, to plasma proteins, mainly albumin.1, 3 The half-life of both darolutamide and keto-darolutamide is approximately 20 hours.1 Following oral administration of a single radiolabeled dose of darolutamide, 63.4% of the dose was recovered in urine (7% as unchanged drug) and 32.4% was recovered in feces (30% as unchanged drug).1
Additional Information
The American Society of Health-System Pharmacists, Inc. represents that the information provided in the accompanying monograph was formulated with a reasonable standard of care, and in conformity with professional standards in the field. Readers are advised that decisions regarding use of drugs are complex medical decisions requiring the independent, informed decision of an appropriate health care professional, and that the information contained in the monograph is provided for informational purposes only. The manufacturer's labeling should be consulted for more detailed information. The American Society of Health-System Pharmacists, Inc. does not endorse or recommend the use of any drug. The information contained in the monograph is not a substitute for medical care. For further information on the handling of antineoplastic agents, see the ASHP Guidelines on Handling Hazardous Drugs at http://www.ahfsdruginformation.com.
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.
Darolutamide can only be obtained through designated specialty pharmacies.4 Contact the manufacturer or consult the Nubeqa specialty pharmacy network ([Web]) for specific information.4
Routes | Dosage Forms | Strengths | Brand Names | Manufacturer |
|---|---|---|---|---|
Oral | Tablets, film-coated | 300 mg | Nubeqa® |
AHFS® Drug Information. © Copyright, 1959-2026, Selected Revisions July 10, 2026. American Society of Health-System Pharmacists, Inc., 4500 East-West Highway, Suite 900, Bethesda, MD 20814.
1. Bayer HealthCare Pharmaceuticals Inc. Nubeqa® (darolutamide) tablets prescribing information. Whippany, NJ; 2026 Feb.
2. Fizazi K, Shore N, Tammela TL et al. Darolutamide in Nonmetastatic, Castration-Resistant Prostate Cancer. N Engl J Med . 2019; 380:1235-1246. [PubMed 30763142]
3. Food and Drug Administration. Center for Drug Evaluation and Research. Application number: 212099Orig1s000: Multi-discipline review. From FDA website. [Web]
4. Bayer. Resources for you and your practice: Nubeqa specialty pharmacy network. Nubeqa® Healthcare Professional Site. [Web]
5. Gupta E, Guthrie T, Tan W. Changing paradigms in management of metastatic Castration Resistant Prostate Cancer (mCRPC). BMC Urol . 2014; 14:55. [PubMed 25062956]
6. Crona DJ, Whang YE. Androgen Receptor-Dependent and -Independent Mechanisms Involved in Prostate Cancer Therapy Resistance. Cancers (Basel) . 2017; 9 [PubMed 28604629]
7. Karantanos T, Corn PG, Thompson TC. Prostate cancer progression after androgen deprivation therapy: mechanisms of castrate resistance and novel therapeutic approaches. Oncogene . 2013; 32:5501-11. [PubMed 23752182]
8. Massard C, Penttinen HM, Vjaters E et al. Pharmacokinetics, Antitumor Activity, and Safety of ODM-201 in Patients with Chemotherapy-naive Metastatic Castration-resistant Prostate Cancer: An Open-label Phase 1 Study. Eur Urol . 2016; 69:834-40. [PubMed 26463318]
9. Bastos DA, Antonarakis ES. Darolutamide For Castration-Resistant Prostate Cancer. Onco Targets Ther . 2019; 12:8769-8777. [PubMed 31695432]
10. Zurth C, Koskinen M, Fricke R et al. Drug-Drug Interaction Potential of Darolutamide: In Vitro and Clinical Studies. Eur J Drug Metab Pharmacokinet . 2019; 44:747-759. [PubMed 31571146]
11. Shore N, Zurth C, Fricke R et al. Evaluation of Clinically Relevant Drug-Drug Interactions and Population Pharmacokinetics of Darolutamide in Patients with Nonmetastatic Castration-Resistant Prostate Cancer: Results of Pre-Specified and Post Hoc Analyses of the Phase III ARAMIS Trial. Target Oncol . 2019; 14:527-539. [PubMed 31571095]
12. Rice MA, Malhotra SV, Stoyanova T. Second-Generation Antiandrogens: From Discovery to Standard of Care in Castration Resistant Prostate Cancer. Front Oncol . 2019; 9:801. [PubMed 31555580]
13. Rathkopf D, Scher HI. Androgen receptor antagonists in castration-resistant prostate cancer. Cancer J . 2013 Jan-Feb; 19:43-9. [PubMed 23337756]
14. Tucci M, Zichi C, Buttigliero C et al. Enzalutamide-resistant castration-resistant prostate cancer: challenges and solutions. Onco Targets Ther . 2018; 11:7353-7368. [PubMed 30425524]
15. Smith MR, Shore N, Tammela TL, et al. Darolutamide and health-related quality of life in patients with non-metastatic castration-resistant prostate cancer: an analysis of the phase III ARAMIS trial. Eur J Cancer. 2021;154:138-146. doi: 10.1016/j.ejca.2021.06.010.
16. Fizazi K, Shore N, Tammela TL, et al. ARAMIS Investigators. Nonmetastatic, castration-resistant prostate cancer and survival with d arolutamide. N Engl J Med. 2020;383(11):1040-1049. doi: 10.1056/NEJMoa2001342.
17. Saad F, Vjaters E, Shore N, et al. Darolutamide in combination with androgen-deprivation therapy in patients with metastatic hormone-sensitive prostate cancer from the Phase III ARANOTE trial. J Clin Oncol. 2024;42:4271-81.
18. Smith MR, Hussain M, Saad F, et al for the ARASENS trial investigators. Darolutamide and survival in metastatic, hormone-sensitive prostate cancer. N Engl J Med. 2022;386:1132-42.
3016. Lowrance WT, Dreicer R, Jarrard DF, et. al. Updates to Advanced Prostate Cancer: AUA/SUO Guideline (2023). J Urol. 2023; 209:1082-90. doi: 10.1097/JU.0000000000001376