Rucaparib (AG014699) acetate is an orally active, potent inhibitor of PARP proteins (PARP-1, PARP-2 and PARP-3) with a K_i of 1.4 nM for PARP1. Rucaparib acetate is a modest hexose-6-phosphate dehydrogenase (H6PD) inhibitor. Rucaparib acetate has the potential for castration-resistant prostate cancer (CRPC) research^[1][2][3][4].

Rucaparib (AG014699) acetate is a possible N-demethylation metabolite of AG14644^[1].
Rucaparib (0.1, 1, 10, 100 μM; 24 hours) acetate is cytotoxic and has the LC₅₀ being 5 μM in Capan-1 (BRCA2 mutant) cells and only 100 nM in MX-1 (BRCA1 mutant) cells^[2].
The radio-sensitization by Rucaparib acetate is due to downstream inhibition of activation of NF-κB, and is independent of SSB repair inhibition. Rucaparib acetate can target NF-κB activated by DNA damage and overcome toxicity observed with classical NF-κB inhibitors without compromising other vital inflammatory functions^[5].
Rucaparib acetate inhibits PARP-1 activity by 97.1% at a concentration of 1 μM in permeabilised D283Med cells^[6].

Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.

Rucaparib (AG014699) acetate and AG14584 significantly increase Temozolomide toxicity. Rucaparib (1 mg/kg) acetate significantly increases Temozolomide-induced body weight loss. Rucaparib (0.1 mg/kg) acetate esults in a 50% increase in the temozolomide-induced tumor growth delay^[1].
Rucaparib (10 mg/kg for i.p. or 50, 150 mg/kg for p.o.; daily for 5 days per week for 6 weeks) acetate significantly inhibits the growth of the tumor, and there is one complete tumor regression and two persistent partial regressions^[2].
Rucaparib (150 mg/kg; p.o.; once per week for 6 weeks or three times per week for 6 weeks) acetate has greatest antitumor effect with three complete regressions^[2].
Rucaparib acetate enhances the antitumor activity of temozolomide and indicates complete and sustained tumor regression in NB1691 and SHSY5Y xenografts^[6].

Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.

383.42

C₂₁H₂₂FN₃O₃

773059-23-7

瑞卡帕布醋酸盐；鲁卡帕尼醋酸盐

Room temperature in continental US; may vary elsewhere.

Please store the product under the recommended conditions in the Certificate of Analysis.

• [1]. Thomas HD, et al. Preclinical selection of a novel poly(ADP-ribose) polymerase inhibitor for clinical trial. Mol Cancer Ther, 2007, 6(3), 945-956.

  [2]. J Murray, et al. Tumour cell retention of rucaparib, sustained PARP inhibition and efficacy of weekly as well as daily schedules. Br J Cancer. 2014 Apr 15;110(8):1977-84.

  [3]. Matt Shirley, et al. Rucaparib: A Review in Ovarian Cancer. Target Oncol. 2019 Apr;14(2):237-246.

  [4]. Jianneng Li, et al. Hexose-6-phosphate dehydrogenase blockade reverses prostate cancer drug resistance in xenograft models by glucocorticoid inactivation. Sci Transl Med. 2021 May 26;13(595):eabe8226.

  [5]. Hunter JE, et al. NF-κB mediates radio-sensitization by the PARP-1 inhibitor, AG-014699. Oncogene, 2012, 31(2), 251-264.

  [6]. Daniel RA, et al. Inhibition of poly(ADP-ribose) polymerase-1 enhances temozolomide and topotecan activity against childhood neuroblastoma. Clin Cancer Res, 2009, 15(4), 1241-1249.