Difference between revisions of "Rucaparib (Rubraca)"
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=General information= | =General information= | ||
| − | Class/mechanism: PARP inhibitor. Rucaparib inhibits activity of the poly (ADP-ribose) polymerase (PARP) enzymes--including PARP-1, PARP-2, and PARP-3--and interferes with PARP-mediated DNA repair. PARP inhibitor cytotoxicity is believed to involve formation of PARP-DNA complexes, DNA damage, apotosis, and cell death. This cytotoxicity was observed to have increased cytotoxicity in cells with mutations in BRCA1, BRCA2, and other DNA repair genes.<ref name="insert">[ | + | Class/mechanism: PARP inhibitor. Rucaparib inhibits activity of the poly (ADP-ribose) polymerase (PARP) enzymes--including PARP-1, PARP-2, and PARP-3--and interferes with PARP-mediated DNA repair. PARP inhibitor cytotoxicity is believed to involve formation of PARP-DNA complexes, DNA damage, apotosis, and cell death. This cytotoxicity was observed to have increased cytotoxicity in cells with mutations in BRCA1, BRCA2, and other DNA repair genes.<ref name="insert">[https://clovisoncology.com/media/1094/rubraca-prescribing-info.pdf Rucaparib (Rubraca) package insert]</ref><ref>[[Media:Rucaparib.pdf | Rucaparib (Rubraca) package insert (locally hosted backup)]]</ref><ref>[http://rubraca.com/ Rubraca manufacturer's website]</ref><ref>[https://www.cancer.gov/publications/dictionaries/cancer-drug?cdrid=594405 Rucaparib phosphate at NCI Drug Dictionary]</ref> |
<br>Route: PO | <br>Route: PO | ||
<br>Extravasation: n/a | <br>Extravasation: n/a | ||
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==Patient drug information== | ==Patient drug information== | ||
| − | *[ | + | *[https://clovisoncology.com/media/1094/rubraca-prescribing-info.pdf Rucaparib (Rubraca) package insert]<ref name="insert" /> |
==History of changes in FDA indication== | ==History of changes in FDA indication== | ||
Revision as of 22:08, 11 September 2019
General information
Class/mechanism: PARP inhibitor. Rucaparib inhibits activity of the poly (ADP-ribose) polymerase (PARP) enzymes--including PARP-1, PARP-2, and PARP-3--and interferes with PARP-mediated DNA repair. PARP inhibitor cytotoxicity is believed to involve formation of PARP-DNA complexes, DNA damage, apotosis, and cell death. This cytotoxicity was observed to have increased cytotoxicity in cells with mutations in BRCA1, BRCA2, and other DNA repair genes.[1][2][3][4]
Route: PO
Extravasation: n/a
For conciseness and simplicity, HemOnc.org currently will focus on treatment regimens and not list information such as: renal/hepatic dose adjustments, metabolism (including CYP450), excretion, monitoring parameters (although this will be considered for checklists), or manufacturer. Instead, for the most current information, please refer to your preferred pharmacopeias such as Micromedex, Lexicomp, UpToDate (courtesy of Lexicomp), or the prescribing information.[1]
Diseases for which it is used
Patient drug information
History of changes in FDA indication
- 12/19/2016: FDA granted accelerated approval "for treatment of patients with deleterious BRCA mutation (germline and/or somatic) associated advanced ovarian cancer who have been treated with two or more chemotherapies."
- 4/6/2018: FDA approved "for the maintenance treatment of recurrent epithelial ovarian, fallopian tube, or primary peritoneal cancer who are in a complete or partial response to platinum-based chemotherapy."
Also known as
- Code names: CO-338, AG-014699, PF-0136738
- Brand name: Rubraca