Rucaparib Phosphate

- Overview
  - Rucaparib phosphate is the phosphate salt of Rucaparib. It is a Poly(ADP-ribose) polymerase (PARP) inhibitor. PARP inhibitors have proven to have anti-cancer activity.
    
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    Background
    
    PARP inhibitors prevent the synthesis of poly-ADP ribose by impinging on the downstream DNA repair processes.
- Properties
  - CAS Number
    
    459868-92-9
    
    Molecular Formula
    
    C19H18FN3O • H3PO4
    
    Molecular Weight
    
    431.36
    
    Appearance
    
    Off-white to yellow solid
    
    Solubility
    
    DMSO
    
    Other Properties
    
    Source: synthetic
    Purity Level: ≥98% by HPLC
    
    Storage
    
    -20°C
    
    * For research use only
- Applications
  - Application Description
    
    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-tumor 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 the first study with 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)