Rucaparib, an inhibitor of poly(adenosine diphosphate [ADP]-ribose) polymerase (PARP), is an antineoplastic agent.1
Rucaparib is used for the maintenance treatment of adults with deleterious germline or somatic BRCA -mutated recurrent epithelial ovarian, fallopian tube, or primary peritoneal cancer who are in complete or partial response to platinum-based chemotherapy.1 The drug has been designated an orphan drug by FDA for the treatment of this cancer.7
This indication is based principally on the results of a randomized, double-blind, placebo-controlled, phase 3 study (ARIEL3).1, 15 Patients with high-grade recurrent epithelial ovarian, fallopian tube, or primary peritoneal cancer previously treated with at least 2 platinum-based chemotherapy regimens were enrolled if they were in partial or complete response to their most recent platinum-based chemotherapy.1, 15 A total of 564 patients were randomized (stratified by best response to last platinum chemotherapy, time to progression after the penultimate platinum chemotherapy, and homologous recombination repair [HRR] mutation status) in a 2:1 ratio to receive either rucaparib 600 mg orally twice daily or placebo within 8 weeks following completion of the last dose of platinum-based chemotherapy.1, 15 Treatment was continued until disease progression or unacceptable toxicity occurred.1
The primary endpoint of the ARIEL3 study was investigator-assessed progression-free survival according to Response Evaluation Criteria in Solid Tumors (RECIST).1, 15 Efficacy results were based on the subgroup of patients with tumor BRCA mutation (germline or somatic).1 Among the 196 patients in the trial with a BRCA mutation, the median age was 58 years in those receiving rucaparib and 59 years in those receiving placebo; 84% of patients were white and all patients had a baseline Eastern Cooperative Oncology Group (ECOG) performance status of 0 or 1.1 Thirty percent of patients had a somatic BRCA mutation; the remaining 70% had a germline BRCA mutation.1 All patients had received at least 2 prior platinum-based chemotherapies (range: 2-5).1 Thirty-three percent were in complete response to their most recent therapy.1 The progression-free interval to penultimate platinum regimen was 6-12 months in 41% of patients and >12 months in 59%.1 Approximately one-third (32%) of patients had measurable disease at baseline.1 A total of 22 and 17% of patients in the rucaparib and placebo groups, respectively, had previously received bevacizumab.1
Patients with a tumor BRCA mutation who received rucaparib had a substantially longer median progression-free survival than those who received placebo (16.6 versus 5.4 months).1 At a median follow-up of 28.1 months, median progression-free survival-2 (an exploratory endpoint defined as the time to second event of disease progression or death from any cause) was 26.8 and 18.4 months with rucaparib and placebo, respectively.32 Similar results were observed at a median follow-up of 77 months, with a median progression-free survival-2 of 26.1 and 18.4 months observed with rucaparib and placebo, respectively.32 Median overall survival was 45.9 months among patients treated with rucaparib and 47.8 months among patients receiving placebo.1, 32
For recurrent ovarian cancer, the American Society of Clinical Oncology (ASCO) states that PARP inhibitor monotherapy may be used for second-line or greater maintenance treatment in PARP inhibitor-naïve patients with epithelial ovarian cancer who have responded to platinum-based regimens, regardless of BRCA mutation status.33 PARP inhibitor options include olaparib, rucaparib, and niraparib, with treatment continued until disease progression or toxicity.33 In December 2022, the labeled use for rucaparib maintenance therapy was restricted to patients with a tumor BRCA mutation only, based on final overall survival data from the ARIEL3 trial.36
Rucaparib was previously labeled for use in the treatment of patients with BRCA -mutated epithelial ovarian, fallopian tube, or primary peritoneal cancer after treatment with 2 or more chemotherapies; however, this use was removed from the labeling in June 2022 based on the results of the ARIEL4 trial, which found a decrease in overall survival with rucaparib compared to chemotherapy.33, 35
Rucaparib is used for the treatment of adults with deleterious germline or somatic BRCA -mutated metastatic castration-resistant prostate cancer previously treated with androgen receptor-directed therapy and a taxane-based chemotherapy.1 The accelerated approval of rucaparib for this indication is based on objective response rate and duration of response.1 Continued approval for this indication may be contingent on verification and description of clinical benefit of rucaparib in confirmatory studies.1 An FDA-approved companion diagnostic test is required to confirm the presence of mutations in the BRCA genes ( BRCA1 and/or BRCA2 ) prior to initiation of rucaparib therapy.1
The current indication for rucaparib in the treatment of adults with deleterious germline or somatic BRCA -mutated metastatic castration-resistant prostate cancer previously treated with androgen receptor-directed therapy and taxane-based chemotherapy is based principally on the results of a single-arm, open label, phase 2 trial (TRITON2).1, 23 The TRITON2 trial enrolled 115 adult men with BRCA -mutated metastatic castration-resistant prostate cancer who had evidence of disease progression after 1-2 lines of antiandrogen therapy for prostate cancer and 1 prior taxane-based regimen for castration-resistant prostate cancer.1, 23 Patients were required to continue receiving a gonadotropin-releasing hormone (GnRH) analog if they had not undergone bilateral orchiectomy.1, 23 All patients received rucaparib 600 mg orally twice daily until disease progression or unacceptable toxicity occurred.1, 23 The primary measure of efficacy was objective response rate, assessed by independent radiology review according to modified RECIST/Prostate Cancer Working Group 3 criteria.1, 23
The primary efficacy population consisted of 62 patients with measurable disease at baseline.1, 23 In the primary efficacy population, the median age was 73 years (range: 52-88 years); 73% were white, and 98% had an ECOG performance status of 0 or 1.1 All patients received a prior taxane chemotherapy and at least 1 prior antiandrogen; 34% received 2 prior antiandrogen therapies and 2% received 3 prior antiandrogen therapies.1 Most patients received prior therapy with enzalutamide (71.3%) and abiraterone acetate (64.3%).23 Lung and liver metastases were present in 18 and 21%, respectively, of patients at baseline, while 24% had metastases to lymph nodes only.1 Approximately one-half (40%) of patients had 10 or more bone lesions at baseline.1 BRCA mutations were detected in all patients via central plasma, central tissue, or local testing; 66% had a somatic BRCA mutation and 85% had a BRCA2 mutation.1
The median independent radiologic review-assessed overall response rate was 44% in the primary efficacy population, with 11.3% achieving complete response and 32.3% achieving partial response.1, 23 Overall response rates were similar in patients with germline or somatic BRCA mutations.1 Analyses based on relevant patient and disease characteristics suggested similar overall response rates across all subgroups.23 The median duration of response was not evaluable at the time of analysis, but ranged from 1.7 months to greater than 24 months.1
At the time of final analysis in TRITON2, 172 patients with BRCA -mutated disease were enrolled.37 All patients were evaluable for overall survival, and 81 patients were evaluable by independent radiology review for objective response and radiographic progression-free survival.37 The median overall survival was 17.2 months for patients with a BRCA mutation, and the median radiographic progression-free survival was 10.7 months among evaluable patients.37 The objective response rate among evaluable patients was 46%.37 Complete response, partial response, and stable disease were observed in 9.9, 36, and 42% of evaluable patients with BRCA -mutated disease, respectively.37 For subgroups with BRCA1 and BRCA2 alterations, the objective response rates with rucaparib were 30 and 48%, respectively.37
Available guidelines from the American Urological Association (AUA) recommend offering a PARP inhibitor to patients with confirmed or suspected deleterious germline or somatic homologous recombination repair (HRR) gene-mutated (including BRCA -mutated) metastatic castration-resistant prostate cancer following prior treatment with enzalutamide or abiraterone acetate, and/or a taxane-based chemotherapy.34 For patients unable to take PARP inhibitors, platinum-based chemotherapy is an alternative.34
Rucaparib camsylate is administered orally twice daily.1 The drug may be given without regard to meals.
If a dose of rucaparib is missed or vomited, the next dose should be taken at the regularly scheduled time. Vomited doses should not be replaced.1, 10
Store tablets at 20-25°C (excursions permitted between 15-30°C).1
Dosage of rucaparib camsylate is expressed in terms of rucaparib.1
The recommended adult dosage of rucaparib for the maintenance treatment of deleterious germline and/or somatic BRCA -mutated recurrent epithelial ovarian, fallopian tube, or primary peritoneal cancer in complete or partial response to platinum-based chemotherapy is 600 mg (two 300-mg tablets) orally twice daily (total daily dose of 1200 mg).1 Therapy should be continued until disease progression or unacceptable toxicity occurs.1
The recommended adult dosage of rucaparib for the treatment of deleterious germline or somatic BRCA -mutated metastatic castration-resistant prostate cancer previously treated with androgen receptor-directed therapy and a taxane-based chemotherapy is 600 mg (two 300-mg tablets) twice daily (total daily dose of 1200 mg).1 Therapy should be continued until disease progression or unacceptable toxicity occurs.1
Patients should receive concurrent therapy with a GnRH analog, unless they have had a bilateral orchiectomy.1
Dosage Modification for Toxicity
If adverse reactions occur, interruption of therapy or dosage reduction of rucaparib should be considered.1 If a reduction from 600 mg twice daily is necessary, the recommended dosage is 500 mg twice daily.1 If a dosage reduction from 500 mg twice daily is necessary, the recommended dosage is 400 mg twice daily.1 If further dosage reduction is necessary, the dosage should be reduced to 300 mg twice daily.1
The manufacturer states that no dosage adjustment is necessary in patients with mild or moderate hepatic impairment (total bilirubin concentration not exceeding 3 times the upper limit of normal [ULN] or AST concentrations exceeding the ULN).1
There are no data in patients with severe hepatic impairment (total bilirubin exceeding 3 times the ULN with any AST concentration); the manufacturer provides no specific dosage recommendations for such patients.1, 6
The manufacturer states that no dosage adjustment is necessary in patients with mild or moderate renal impairment (creatinine clearance 30-89 mL/minute).1 Rucaparib has not been studied in patients with severe renal impairment (creatinine clearance less than 30 mL/minute), including in those receiving dialysis, and the manufacturer provides no specific dosage recommendations for such patients.1, 6
The manufacturer makes no specific dosage recommendations for geriatric patients.1
Myelodysplastic Syndrome/Acute Myeloid Leukemia
In clinical studies, myelodysplastic syndrome (MDS) and acute myeloid leukemia (AML) were reported in 32 of 1594 patients (2%) receiving rucaparib.1 Of these, 14 occurred during treatment or during the 28-day safety follow-up (0.9%).1 The duration of rucaparib use prior to the diagnosis of MDS/AML ranged from less than 2 months to approximately 72 months.1 All of these patients received previous chemotherapy with platinum-containing agents and/or other DNA-damaging antineoplastic agents.1
In the ARIEL3 study, in patients with germline and/or somatic BRCA mutations, MDS/AML was observed in 9 of 129 patients (7%) receiving rucaparib and in 4 of 66 patients (6%) receiving placebo.1 The duration of rucaparib use in patients who developed secondary MDS/cancer therapy-related AML ranged from 1.2—4.7 years.1
In the TRITON2 study, MDS/AML was not observed in patients with metastatic castration-resistant prostate cancer regardless of homologous recombination deficiency (HRD) mutation.1
Monitor CBC at baseline and then monthly in patients receiving rucaparib.1 Do not initiate rucaparib therapy until hematologic toxicity caused by previous chemotherapy has resolved to grade 1 or less.1 If prolonged hematologic toxicity (greater than 4 weeks) occurs during therapy, withhold rucaparib or administer at a reduced dosage, and monitor CBC weekly until recovery to grade 1 or less occurs.1 If hematologic toxicity persists for more than 4 weeks following dosage modification or if MDS/AML is suspected, refer patient to a hematologist for further evaluation, including bone marrow analysis and cytogenetic testing of a blood sample.1 If MDS/AML is confirmed, rucaparib should be discontinued.1
Fetal/Neonatal Morbidity and Mortality
Based on its mechanism of action and animal findings, rucaparib may cause fetal harm.1 Embryotoxicity (i.e., postimplantation loss) was observed in pregnant rats receiving rucaparib at exposure levels equivalent to approximately 0.04 times the human exposure at the recommended rucaparib dosage.1
The manufacturer recommends verifying pregnancy status prior to initiation of rucaparib, and females of reproductive potential should be advised to use effective contraceptive methods during rucaparib therapy and for 6 months after discontinuance of the drug.1 Males with female partners of reproductive potential or partners who are pregnant should be advised to use effective contraception while receiving rucaparib and for 3 months after discontinuance of therapy.1 Male patients should not donate sperm while receiving rucaparib and for 3 months after discontinuance of therapy.1 If rucaparib is used during pregnancy or if the patient becomes pregnant while receiving the drug, the patient should be apprised of the potential risk to the fetus and the potential risk for loss of the pregnancy.1
Rucaparib may cause fetal harm if administered to pregnant women based on its mechanism of action and animal findings.1
Verification of pregnancy status prior to initiation of rucaparib therapy is recommended.1
It is not known whether rucaparib is distributed into milk.1 Because of the potential for serious adverse reactions to rucaparib in breast-fed infants, women should be advised to discontinue breast-feeding during rucaparib therapy.1 Women may begin breast-feeding 2 weeks after discontinuance of therapy.1 The effects of the drug on breast-feeding infants or on milk production are unknown.1
Females and Males of Reproductive Potential
Rucaparib can cause fetal harm when administered during pregnancy.1
Pregnancy testing is recommended for females of reproductive potential prior to initiation of rucaparib.1 Effective contraception is recommended for females of reproductive potential during treatment with rucaparib and for 6 months following the last dose.1
Advise male patients with female partners of reproductive potential or partners who are pregnant to use an effective method of contraception while receiving rucaparib and for 3 months following discontinuance.1 Advise male patients to avoid donating sperm while receiving rucaparib and for 3 months following the last dose.1
Safety and efficacy of rucaparib have not been established in pediatric patients.1
In clinical studies evaluating rucaparib in women with ovarian cancer, 41% of patients were 65 years of age or older and 10% were 75 years of age or older.1 In clinical studies evaluating rucaparib in men with metastatic castration-resistant prostate cancer, 77% of patients were 65 years of age or older and 33% were 75 years of age or older.1
No major differences in safety were observed between geriatric patients and younger adults with ovarian cancer or metastatic castration-resistant prostate cancer.1
In pharmacokinetic population analyses, age did not have a clinically important effect on systemic exposure to rucaparib.1
Mild hepatic impairment (total bilirubin less than the upper limit of normal [ULN] with AST greater than ULN, or total bilirubin 1-1.5 times ULN with any AST) did not have a clinically meaningful effect on rucaparib pharmacokinetics.1 Systemic exposure to rucaparib was increased by 45% in patients with moderate hepatic impairment (total bilirubin concentration 1.5—3 times the ULN with any AST) when compared to patients with normal hepatic function.1 No dosage modification is recommended for patients with mild to moderate hepatic impairment.1
The pharmacokinetic profile of rucaparib has not been established in patients with severe hepatic impairment (total bilirubin concentration exceeding 3 times the ULN and any AST).1, 6
Mild to moderate renal impairment (creatinine clearance ≥30 mL/minute) does not have clinically important effects on rucaparib pharmacokinetics.1 No dosage modification is recommended in patients with mild to moderate renal impairment.1
The pharmacokinetics of rucaparib have not been established in patients with severe renal impairment (creatinine clearance 15—29 mL/minute) or end-stage renal disease (creatinine clearance <15 mL/minute).1, 6 Rucaparib has not been studied in patients receiving dialysis.1
Adverse effects reported in 10% or more of patients receiving rucaparib for ovarian cancer include nausea, fatigue/asthenia, vomiting, anemia, dysgeusia, AST/ALT elevation, decreased appetite, diarrhea, thrombocytopenia, neutropenia, increased blood creatinine, dyspnea, dizziness, dyspepsia, photosensitivity reactions, and leukopenia.1
Adverse effects reported in 20% or more of patients receiving rucaparib for metastatic castration-resistant prostate cancer include fatigue/asthenia, nausea, anemia, AST/ALT elevation, decreased appetite, rash, constipation, thrombocytopenia, vomiting, and diarrhea.1
Rucaparib is metabolized principally by cytochrome P-450 (CYP) isoenzyme 2D6 and, to a lesser extent, by CYP1A2 and 3A4.1 Drug interaction studies indicate that rucaparib inhibits CYP isoenzymes 1A2, 2C19, 2C9, and 3A.1 In vitro studies indicate that rucaparib is an inhibitor of CYP isoenzymes 2C8 and 2D6 as well as uridine diphosphate-glucuronosyltransferase (UGT) 1A1.1, 6 In vitro, rucaparib induces CYP1A2.1
In vitro, rucaparib is an inhibitor of organic anion transporting polypeptide (OATP) 1B1, OATP1B3, organic anion transporter (OAT) 1, OAT3, organic cation transporter (OCT) 1, OCT2, multidrug and toxic compound extrusion (MATE) 1, MATE2K, and multidrug resistance protein (MRP) 4.1 The drug does not inhibit MRP2, MRP3, or bile salt export pump (BSEP).1
In vitro studies indicate that rucaparib is a substrate of the efflux transporters P-glycoprotein (P-gp) and breast cancer resistance protein (BCRP), but is not a substrate for OAT1, OAT3, OCT2, OATP1B1, or OATP1B3.1
Drugs Metabolized by Hepatic Microsomal Enzymes
Concomitant use of rucaparib with CYP1A2, 3A, 2C9, or 2C19 substrates may result in increased systemic exposure and possible toxicity of the substrate drug.1 When rucaparib was administered concomitantly with caffeine (CYP1A2 substrate), midazolam (CYP3A4 substrate), warfarin (CYP2C9 substrate), and omeprazole (CYP2C19 substrate), AUC of the substrates increased by 2.6-, 1.4-, 1.5-, and 1.6-fold, respectively; peak plasma concentrations of each substrate drug increased by 1.1-fold or less.1
Concomitant administration of rucaparib with an oral contraceptive containing ethinyl estradiol and levonorgestrel (CYP3A substrates) resulted in increased exposure to ethinyl estradiol and levonorgestrel by 1.4 and 1.6-fold, respectively.1
If concomitant administration of CYP1A2, 3A, 2C9, and 2C19 substrates with rucaparib is unavoidable and minimal concentration changes of the substrate could result in serious adverse effects, the substrate dosage should be reduced in accordance with prescribing information.1 If rucaparib is co-administered with warfarin, consider increasing the frequency of international normalized ratio (INR) monitoring.1
Drugs Affected by Efflux Transport Systems
When rucaparib was administered concomitantly with digoxin (a P-gp substrate), AUC increased by 1.2-fold.1
Concomitant administration of rosuvastatin (BCRP substrate) with rucaparib resulted in no clinically meaningful effects on rosuvastatin concentrations.1
Concomitant administration of rucaparib with proton-pump inhibitors did not have a clinically meaningful effect on systemic exposure to rucaparib.1, 6
Rucaparib camsylate, an inhibitor of mammalian poly(adenosine diphosphate [ADP]-ribose) polymerase (PARP) enzymes, including PARP-1, PARP-2, and PARP-3, is an antineoplastic agent.1 PARP enzymes are involved in normal cellular homeostasis, including DNA transcription, cell cycle regulation, and DNA repair.1, 6
In vitro studies have demonstrated that rucaparib-induced cytotoxicity may involve inhibition of PARP enzymatic activity and increased formation of PARP-DNA complexes, which result in DNA damage, apoptosis, and cancer cell death.1 PARP inhibitors, such as rucaparib, appear to be selective for tumor cells that harbor certain homologous recombination deficiencies, including those harboring BRCA1 and BRCA2 mutations.1, 8, 9 Rucaparib reduced tumor growth of xenograft models of human cancer (with or without deficiencies in BRCA) in mice.1
Following oral administration, the mean absolute bioavailability of rucaparib is 36% (range: 30-45%).1 Rucaparib exhibits linear, time-independent, dose-proportional pharmacokinetics over the dosage range of 240-840 mg twice daily.1, 6, 10 Following oral administration at the recommended dosage, the median time to peak plasma concentrations of rucaparib is 1.9 hours.1 Repeated twice-daily administration of rucaparib resulted in 3.5- to 6.2-fold mean rucaparib accumulation (based on AUC).1, 6 Administration of rucaparib (single 600-mg dose) with a high-fat meal (800—1000 kcal with 500—600 kcal from fat) in patients with solid tumors decreased the rate but only modestly increased the extent of absorption; time to peak plasma concentration was delayed by 2.5 hours, and peak plasma concentration and AUC were increased by 20 and 38%, respectively, relative to fasted conditions.1, 6 Rucaparib is metabolized principally by cytochrome P-450 (CYP) isoenzyme 2D6 and, to a lesser extent, by CYP1A2 and 3A4.1 Genetic polymorphisms of CYP2D6 (i.e., poor, intermediate, or ultrarapid metabolizer) or CYP1A2 (i.e., hyperinducers) do not substantially affect systemic exposure to rucaparib at steady state.1, 6 In vitro, rucaparib is 70% bound to plasma proteins at therapeutic concentrations.1 Following oral administration of a single radiolabeled dose of rucaparib, unchanged rucaparib accounted for 64% of the radioactivity in plasma.1 Oxidation, N -demethylation, N -methylation, and glucuronidation were the major metabolic pathways for rucaparib.1 Rucaparib accounted for 45 and 95% of the radioactivity recovered in urine and feces, respectively. The mean terminal half-life of the drug is 26 hours.1
Data from population pharmacokinetic analyses indicate that age (20—86 years), race (white, Black, Asian), sex, body weight (41—171 kg), and CYP2D6 or CYP1A2 genetic polymorphisms do not have clinically important effects on systemic exposure to rucaparib.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.
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.
Distribution of rucaparib is restricted.3 Contact manufacturer or consult the Rubraca® Healthcare Provider website ([Web]) for specific availability information.3
Routes | Dosage Forms | Strengths | Brand Names | Manufacturer |
|---|---|---|---|---|
Oral | Tablets, film-coated | 200 mg (of rucaparib) | Rubraca® | pharma& |
250 mg (of rucaparib) | Rubraca® | pharma& | ||
300 mg (of rucaparib) | Rubraca® | pharma& |
AHFS® Drug Information. © Copyright, 1959-2026, Selected Revisions May 10, 2024. American Society of Health-System Pharmacists, Inc., 4500 East-West Highway, Suite 900, Bethesda, MD 20814.
1. pharma&. Rubraca® (rucaparib) tablets prescribing information. Vienna, Austria; 2023 Sept.
3. pharma&. Rubraca® (rucaparib) healthcare provider website. Undated. Accessed 2024 Feb 23. [Web]
6. Food and Drug Administration. Center for Drug Evaluation and Research. Application number 209115Orig1s000: Multi-discipline review. From FDA website. [Web]
7. Food and Drug Administration. Search orphan drug designations and approvals. From FDA website. Accessed 2021 Jun 30. [Web]
8. Kaufman B, Shapira-Frommer R, Schmutzler RK et al. Olaparib monotherapy in patients with advanced cancer and a germline BRCA1/2 mutation. J Clin Oncol . 2015; 33:244-50. [PubMed 25366685]
9. Reinbolt RE, Hays JL. The role of PARP inhibitors in the treatment of gynecologic malignancies. Front Oncol . 2013; 3:237. [PubMed 24098868]
10. Kristeleit R, Shapiro GI, Burris HA et al. A Phase I-II Study of the Oral PARP Inhibitor Rucaparib in Patients with Germline BRCA1/2-Mutated Ovarian Carcinoma or Other Solid Tumors. Clin Cancer Res . 2017; [PubMed 28264872]
15. Coleman RL, Oza AM, Lorusso D et al. Rucaparib maintenance treatment for recurrent ovarian carcinoma after response to platinum therapy (ARIEL3): a randomised, double-blind, placebo-controlled, phase 3 trial. Lancet . 2017; 390:1949-1961. [PubMed 28916367]
18. Ledermann JA, Oza AM, Lorusso D et al. Rucaparib for patients with platinum-sensitive, recurrent ovarian carcinoma (ARIEL3): post-progression outcomes and updated safety results from a randomised, placebo-controlled, phase 3 trial. Lancet Oncol . 2020; 21:710-722. [PubMed 32359490]
23. Abida W, Patnaik A, Campbell D et al. Rucaparib in Men With Metastatic Castration-Resistant Prostate Cancer Harboring a BRCA1 or BRCA2 Gene Alteration. J Clin Oncol . 2020; 38:3763-3772. [PubMed 32795228]
31. Tew WP, Lacchetti C, Ellis A et al. PARP Inhibitors in the Management of Ovarian Cancer: ASCO Guideline. J Clin Oncol . 2020; 38:3468-3493. [PubMed 32790492]
32. Coleman R, Oza A, Lorusso D, et al. Overall survival results from ARIEL3: a phase 3 randomised, double-blind study of rucaparib vs placebo following response to platinum-based chemotherapy for recurrent ovarian cancer. Int J Gynecol Cancer . 2022;32(suppl 2): A226.
33. Tew W, Lacchetti C, Kohn E. Poly(ADP-Ribose) polymerase inhibitors in the management of ovarian cancer: ASCO guideline rapid recommendation update. J Clin Oncol . 2022;40(33):3878-3883.
34. Lowrance W, Breau R, Chou R, et al. Updates to advanced prostate cancer: AUA/AUO guideline (2023). J Urol . 2023;209:1082-1090.
35. Oza A, Lisyanskaya A, Fedenko A, et al. Overall survival results from ARIEL4: a phase III study assessing rucaparib vs chemotherapy in patients with advanced, relapsed ovarian carcinoma and a deleterious BRCA1/2 mutation. Ann Oncol . 2022;33(S7):S780.
36. Clovis Oncology. Important Prescribing Information. 12 Dec 2022. Accessed 2023 Nov 5. Available at: http://www.rubracahcp.com/wp-content/themes/rubracahcp/temp-landing-assets/pdf/DearHealthcareProviderDec2022.pdf
37. Abida W, Campbell D, Patnaik A, et al. Rucaparib for the treatment of metastatic castration-resistant prostate cancer associated with a DNA damage repair gene alteration: final results from the phase 2 TRITON2 study. Eur Urol . 2023;84:321-330.