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Rucaparib

(Synonyms: AG014699; PF-01367338)
50 Cited Publications
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Based on 50 publication(s) in Google Scholar

Rucaparib (AG014699) is an orally active, potent inhibitor of PARP proteins (PARP-1, PARP-2 and PARP-3) with a Ki of 1.4 nM for PARP1. Rucaparib is a modest hexose-6-phosphate dehydrogenase (H6PD) inhibitor. Rucaparib has the potential for castration-resistant prostate cancer (CRPC) research.

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  • Pureza: 99.96%
  • No. CAS: 283173-50-2
  • Fòrmula: C19H18FN3O
  • Peso molecular:323.36
  • Almacenamiento:
    Powder   -20°C, 3 years , 4°C, 2 years ; In solvent   -80°C, 6 months , -20°C, 1 month
  • Rucaparib Chemical Structure
    Rucaparib Chemical Structure
  • Experimental Validation Results for Rucaparib
  • Experimental Validation Results for Rucaparib
  • Experimental Validation Results for Rucaparib
  • Experimental Validation Results for Rucaparib
  • Experimental Validation Results for Rucaparib
No. CAS: 283173-50-2
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Cell Proliferation/Viability AssayFlow CytometryIn Vivo Efficacy Study
  • Cell Proliferation/Viability Assay
  • Flow Cytometry
  • Cell Proliferation/Viability Assay
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  • Rucaparib Chemical Structure
    Rucaparib Chemical Structure
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  • 1/16

    Rucaparib purchased from MedChemExpress. Usage Cited in: Nat Commun. 2025 Jun 2;16(1):5126. [Abstract]

    Customer Validation
     Treatment of MYCN-amplified SK-N-BE(2)C, KELLY, NGP, and CHP-212 or MYCN non-amplified SH-SY5Y neuroblastoma cells expressing) LINE-1 or MYCN targeting sgRNA with Cas9D10A-mRNA (7.5, 15, or 30 nM; increase in concentration marked by black triangle) without or with the PARP inhibitor, Rucaparib (10 µM). Inhibition of PARP1 in the presence of Cas9D10A is protective, as indicated in the reduced cell-killing efficacy of Cas9D10A at 3-days post-treatment (n = 3). PARP1 inhibition only had a modest effect on cell killing in KELLY and CHP-212 cells. A modest reduction in cell viability in SH-SY5Y cells in the presence of the PARP inhibitor is likely due to non-specific toxicity. Data are presented as mean ± s.d. normalized relative to viability of cells expressing AAVS1 targeting sgRNA treated with Cas9D10A.

  • 1/16

    Rucaparib purchased from MedChemExpress. Usage Cited in: Nat Commun. 2025 Jun 2;16(1):5126. [Abstract]

    Customer Validation
     Representative histograms of flow cytometric cell cycle analysis of SK-N-BE(2)C cells supplemented with PARP inhibitors at their respective IC50. SK-N-BE(2)C cells were incubated with Rucaparib (10 µM) or Olaparib (10 µM) in the absence of Cas9D10A and monitored for abberations in cell cycle progression at 1-, 2-, and 3-days (n = 3).

  • 1/16

    Rucaparib purchased from MedChemExpress. Usage Cited in: Sci Adv. Sci Adv. 2025 Apr 25;11(17):eadu0847. [Abstract]

    Customer Validation
     Cell viability assays in LNCaP and 22Rv1 cells treated with BSJ-5-63 for 2 days, PARPis [olaparib (Ola), Rucaparib (Ruca; 3 μM), niraparib (Nira), or talazoparib (Tala)] for 7 days, or sequential combination where BSJ-5-63 was removed after 2 days and followed by PARPi treatment for additional 5 days. Data represent means ± SEM (n = 3).

  • 1/16

    Rucaparib purchased from MedChemExpress. Usage Cited in: Sci Transl Med. 2021 May 26;13(595):eabe8226. [Abstract]

    Customer Validation
     Viability of enz-resistant LAPC4 cells treated with Rucaparib (RUCA, 10-40 μM). Cells were treated with 100 nM cortisol with 10 μM Enzalutamide (enz) combined with the indicated drugs for 5 days and assayed using CellTiter-Glo. Viability is normalized to Ctrl.

  • 1/16

    Rucaparib purchased from MedChemExpress. Usage Cited in: Sci Transl Med. 2021 May 26;13(595):eabe8226. [Abstract]

    Customer Validation
     Rucaparib (RUCA, 150 mg/kg; oral gavage BID, 5 days on, 2 days off) and the inhibitory effect of Enzalutamide (Enz) on xenograft growth in the F, VCaP and H, LAPC4 mouse xenograft models.

  • Rucaparib