Rucaparib Camsylate

1859053-21-6

C19H18FN3O ∙ C10H16O4S

555.66

Light yellow to off-white solid

DMSO (2 mg/ml)

Source: Synthetic
Purity Level: ≥98% by HPLC

-20°C

Cancer Applications: Mutations in BRCA1 and BRCA2 (BRCA1/2), components of the homologous recombination DNA repair pathway, are associated with hereditary breast and ovarian cancers. The anti-cancer activity of Rucaparib was studied in human cancer cell lines carrying a mutated BRCA1/2. Nine human cell lines were studied in vitro: Nonmutated BRCA1/2 (MCF7, MDA-MB-231, HCC1937-BRCA1 [breast cancer] and OSEC-2 [ovarian surface epithelial], mutated BRCA1 (MDA-MB-436, and HCC1937 [breast cancer], mutated BRCA2 (CAPAN-1 [ pancreatic cancer]), heterozygous for BRCA2 (OSEC-1 [ovarian cancer], epigenetically silenced BRCA1 (UACC3199 [breast cancer], and CHO cell lines (parental AA8, XRCC3 mutated IRS 1SF). Rucaparib induced double-strand breaks in all cell lines (Drew et al, 2011). The effectiveness of Rucaparib can be enhanced with radiation.
In prostate cancer cell lines (PC3, LNCaP, DU145, and VCaP) the compound radiosensitized the cells, allowing a low dose of radiation over a longer period to enhance DNA damage. LNCaPa and VCaP showed a maximum sensitivity to the compound, followed by PC3 and C4-2 cells (Chatterjee et al, 2013).
In neuroblastoma cell lines (SK-N-BE(2c), the combination of Rucaparib with radiation reduced the X-radiation dose required to achieve 50% cell kill. It is likely that the mechanism of radiosensitisation entails the accumulation of unrepaired radiation-induced DNA damage (Nile et al, 2016). By combining Rucaparib with radiation, it was possible to reduce the X-radiation dose (or 131I-meta-iodobenzylguanidine activity concentration) required to achieve 50% cell kill in neuroblastoma SK-N-BE(2c) cell lines. It is likely that the mechanism of radiosensitisation entails the accumulation of unrepaired radiation-induced DNA damage (Nile et al, 2016).