Molecular Weight(MW): 421.36
Rucaparib (AG-014699, PF-01367338) is an inhibitor of PARP with Ki of 1.4 nM for PARP1 in a cell-free assay, also showing binding affinity to eight other PARP domains. Phase 3.
Cited by 14 Publications
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For anchorage dependent clonogenic assays, HER2+ breast cancer BT474 cells were seeded at low density in 6-well plates and allowed to adhere overnight. The next day, olaparib and rucaparib were added at the indicated concentrations. Media and drugs were replenished every three days. After 10-15 days, depending on cell proliferation rate, cells were fixed and stained with crystal violet. Images and graphs indicate the results compared to control condition. Data are mean ± S.D. n.s.: non-significant, ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001.
Eur J Cancer 2014 50(15), 2725-34. Rucaparib (AG-014699,PF-01367338) purchased from Selleck.
Total cell extracts of BT-474 cells treated with increasing concentrations of olaparib or rucaparib were subjected to western blot analysis for PARP-1 and poly ADP-ribose (PAR) expression. β-tubulin was used as loading control. Representative images from two separate experiments are shown.
Eur J Cancer 2014 50(15), 2725-34. Rucaparib (AG-014699,PF-01367338) purchased from Selleck.
purified PARP-1 and His-XPA were incubated alone ( lane 7 ), with activated PARP-1 (addition of activated DNA and NAD＋, lane 8 ), or in the presence of the PARP inhibitor AG-014699 (lane 9 ). Following the various treatments, His-XPA was pulled down ( IP ) from each sample using cobalt-conjugated magnetic beads.
J Biol Chem 2012 287, 39824-33. Rucaparib (AG-014699,PF-01367338) purchased from Selleck.
Three sensitive and three resistant cell lines were treated for 24 h with 0.02% DMSO (negative control) or 10 uM rucaparib. Serving as positive control were cells fixed 30 min after exposure to 2 Gy IR. Image acquisition was performed with a confocal microscope (Leica TCS SP2) using the 100X objective and a 2X optical zoom and oil immersion. Red: γH2AX foci. Green: RAD51 foci. *P < 0.05 **P < 0.01 ***P < 0.001. Fluorescence microscopy images of DAPI-stained rucaparib-sensitive (HN4) and rucaparib-resistant (SAS) HNC cell lines treated with DMSO, 2 Gy or 10 uM rucaparib for 24 h.
Oral Oncol 2014 50(9), 825-31. Rucaparib (AG-014699,PF-01367338) purchased from Selleck.
Antitumor effects of transfecting of INPP4B gene combined with PARP inhibitor treatment on PC3 cells. (A) The change of cell number and shape under the microscope. (B) The viability of PC3 cells measured using CCK-8. (C) The cell cycle phase distribution of PC3 detected by flow cytometry. (D) Apoptosis of PC3 cells detected using annexin V-FITC/PI staining. (Asterisks denote statistical significance between Lenti-INPP4B+PARP inhibitor and Lenti-INPP4B and PARP inhibitor treatment, *P<0.05).
Urol Oncol 2014 32(5), 720-6. Rucaparib (AG-014699,PF-01367338) purchased from Selleck.
in vivo suppression of PAR formation by the PARP inhibitor AG-014699 upon induction of DNA damagePrimary human lung fibroblast cells (MRC-5) were pre-treated with the indicated concentration of the PARP inhibitor AG-014699 for two hours. Oxidative DNA damage was induced by 500 µM H2O2 for 10 min and cellular PARP activity was measured by immuno-staining of poly(ADP)-ribose (PAR) (right panels). The in vivo effect of PARP inhibition was compared to cells without DNA damage induction and inhibitor (control) and H2O2-treated cells without inhibitor.
Average nuclear PAR staining intensities of more than 50 cells were statistically analysed by Kruskal-Wallis and the post-hoc Dunn’s Multiple Comparison tests (left panel). Asterisks indicate highly significant (p<1%) differences to H2O2-treated cells without PARP inhibitor. Thick horizontal bars mark medians and error bars the interquartile range.
Dr. David Schrmann from University of Base. Rucaparib (AG-014699,PF-01367338) purchased from Selleck.
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2. For more details, such as half maximal inhibitory concentrations (IC50s) and working concentrations of each inhibitor, please click on the link of the inhibitor of interest.
3. "+" indicates inhibitory effect. Increased inhibition is marked by a higher "+" designation.
4. Orange "√" refers to compounds which do inhibitory effects on the related isoform, but without specific value.
|Description||Rucaparib (AG-014699, PF-01367338) is an inhibitor of PARP with Ki of 1.4 nM for PARP1 in a cell-free assay, also showing binding affinity to eight other PARP domains. Phase 3.|
|Features||The first PARP inhibitor used in clinical trials combined with temozolomide.|
Rucaparib is a potent inhibitor of purified full-length human PARP-1 and shows higher inhibition of cellular PARP in LoVo and SW620 cells. Besides, Rucaparib binds detectably to eight other PARP domains, including PARP2, 3, 4, 10, 15, 16, TNKS1 and TNKS2.   The radio-sensitization by Rucaparib is due to downstream inhibition of activation of NF-κB, and is independent of SSB repair inhibition. Rucaparib could target NF-κB activated by DNA damage and overcome toxicity observed with classical NF-κB inhibitors without compromising other vital inflammatory functions.  Rucaparib inhibits PARP-1 activity by 97.1% at a concentration of 1 μM in permeabilised D283Med cells. 
|In vivo||Rucaparib is not toxic but significantly enhances temozolomide-induced TGD in the DNA repair protein-competent D384Med xenografts. Pharmacokinetics studies also show that Rucaparib is detected in the brain tissue, which indicates that Rucaparib has potential in intra-cranial malignancy therapy.  Rucaparib significantly potentiates the cytotoxicity of topotecan and temozolomide in NB-1691, SH-SY-5Y, and SKNBE (2c) cells. Rucaparib enhances the antitumor activity of temozolomide and indicates complete and sustained tumor regression in NB1691 and SHSY5Y xenografts. |
Ki Determination:Inhibition of human full-length recombinant PARP-1 by [32P]NAD+ incorporation is measured. The [32P]ADP-ribose incorporated into acid insoluble material is quantified using a PhosphorImager. Ki is calculated by nonlinear regression analysis.
-  Thomas HD, et al. Mol Cancer Ther, 2007, 6(3), 945-956.
-  Kotz, J. SciBX 5(13); doi:10.1038/scibx.2012.323.
-  Hunter JE, et al. Oncogene, 2012, 31(2), 251-264.
|In vitro||DMSO||84 mg/mL (199.35 mM)|
|In vivo||30% propylene glycol, 5% Tween 80, 65% D5W||30 mg/mL|
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Clinical Trial Information
|NCT Number||Recruitment||Conditions||Sponsor/Collaborators||Start Date||Phases|
|NCT02740712||Recruiting||Neoplasms||Clovis Oncology, Inc.||March 2016||Phase 1|
|NCT02505048||Not yet recruiting||Metastatic Breast Cancer||UNICANCER|Clovis Oncology, Inc.|Fondation ARC||March 2016||Phase 2|
|NCT02042378||Completed||Pancreatic Cancer|Pancreatic Ductal Adenocarcinoma||Clovis Oncology, Inc.||April 2014||Phase 2|
|NCT01968213||Active, not recruiting||Ovarian Cancer|Fallopian Tube Cancer|Peritoneal Cancer||Clovis Oncology, Inc.||January 2014||Phase 3|
|NCT01891344||Active, not recruiting||Ovarian Cancer|Epithelial Ovarian Cancer|Fallopian Tube Cancer|Peritoneal Cancer||Clovis Oncology, Inc.|Foundation Medicine||September 2013||Phase 2|
|NCT01482715||Active, not recruiting||Ovarian Cancer|Fallopian Tube Cancer|Peritoneal Cancer|Advanced Solid Tumor With Evidence of Germline or Somatic BRCA||Clovis Oncology, Inc.||November 2011||Phase 1|Phase 2|
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