Rucaparib in Ovarian Cancer: Extending the Use of PARP Inhibitors in the Recurrent Disease

Abstract

Rucaparib is a potent inhibitor of poly (ADP-ribose) polymerase (PARP) PARP1, PARP2 and PARP3, and to a lesser extent, PARP4, PARP10, PARP12, PARP15 and PARP16. Study 10 and ARIEL2 evaluated the use of rucaparib as treatment in patients with recurrent high-grade ovarian carcinoma and resulting in approval of rucaparib for patients with both germline and somatic BRCA mutation. Data from the Phase III trial ARIEL3 led to approval in platinum-sensitive disease as maintenance. This article reviews the efficacy, safety, pharmacokinetics and pharmacodynamics of rucaparib as well as future and ongoing trials.

Keywords::

• BRCA mutated ovarian cancer
• company tests
• ovarian cancer
• ovarian cancer maintenance treatment
• PARP
• platinum sensitive ovarian cancer
• poly (ADP-ribose) polymerase inhibitors
• rucaparib

Acknowledgements

The authors want to thank P Morello for assistance in manuscript preparation.

Financial & competing interests disclosure

R Coleman is supported by CPRIT RP120214, the Ann Rife Cox Chair in Gynecology, Judy Reis/Albert Pisani and the MD Anderson ovarian cancer research fund. R Coleman has clinical research funding from Merck, AstraZeneca/Medimmune, Genentech/Roche, Novartis, Clovis Oncology, Abbvie and Janssen pharmaceuticals. Other parts of this work are supported by R35 CA209904, the Frank McGraw Memorial Chair in Cancer Research, the American Cancer Society Research Professor Award and the Blanton-Davis Ovarian Cancer Research Program. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

No writing assistance was utilized in the production of this manuscript.

Additional information

Funding

R Coleman is supported by CPRIT RP120214, the Ann Rife Cox Chair in Gynecology, Judy Reis/Albert Pisani and the MD Anderson ovarian cancer research fund. R Coleman has clinical research funding from Merck, AstraZeneca/Medimmune, Genentech/Roche, Novartis, Clovis Oncology, Abbvie and Janssen pharmaceuticals. Other parts of this work are supported by R35 CA209904, the Frank McGraw Memorial Chair in Cancer Research, the American Cancer Society Research Professor Award and the Blanton-Davis Ovarian Cancer Research Program. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed. No writing assistance was utilized in the production of this manuscript.