Rucaparib (AG-014699,PF-01367338)

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.

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Rucaparib (AG-014699,PF-01367338) Chemical Structure

Rucaparib (AG-014699,PF-01367338) Chemical Structure
Molecular Weight: 421.36

Validation & Quality Control

Customer Product Validation(6)

Quality Control & MSDS

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Rucaparib (AG-014699,PF-01367338) is available in the following compound libraries:

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Product Description

Biological Activity

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.
Targets PARP [1]
(Cell-free assay)
IC50 1.4 nM(Ki)
In vitro 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. [1] [2] 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. [3] Rucaparib inhibits PARP-1 activity by 97.1% at a concentration of 1 μM in permeabilised D283Med cells. [4]
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. [4] 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. [5]
Features The first PARP inhibitor used in clinical trials combined with temozolomide.

Protocol(Only for Reference)

Kinase Assay: [1]

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.
Inhibition of PARP activity Inhibition of PARP activity in 5 × 103 D283Med cells is measured using various concentrations of Rucaparib (0-1 μM), compared with DMSO-only. Maximally stimulated PARP activity is measured in samples of permeabilised cells by immunologica

Cell Assay: [4]

Cell lines D425Med, D283Med and D384Med cells
Concentrations 0.4 μM
Incubation Time 3 or 5 days
Method Medulloblastoma cell lines are seeded in 96-well plates at a density of 1 × 103, 3 × 103 and 3 × 103, respectively. At 24 hours (D384Med) or 48 hours (D283Med and D425Med) after seeding, the cells are exposed to various concentrations of temozolomide in the presence or absence of 0.4 μM Rucaparib. After 3 days (D425Med and D384Med) or 5 days (D283Med) of culture, cell viability is evaluated by a XTT cell proliferation kit assay. Cell growth is expressed as a percentage in relation to DMSO or 0.4 μM Rucaparib-alone controls. The concentration of temozolomide, alone or in combination with Rucaparib that inhibited growth by 50% (GI50) is calculated. The potentiation factor 50 (PF50) is defined as the ratio of the GI50 of temozolomide in the presence of Rucaparib to the GI50 of temozolomide alone.

Animal Study: [4]

Animal Models CD-1 nude mice bearing established D283Med xenografts
Formulation Normal saline
Dosages 1 mg/kg
Administration One or four daily by i.p.

Conversion of different model animals based on BSA (Value based on data from FDA Draft Guidelines)

SpeciesMouseRatRabbitGuinea pigHamsterDog
Weight (kg)
Body Surface Area (m2)0.0070.0250.
Km factor36128520
Animal A (mg/kg) = Animal B (mg/kg) multiplied by  Animal B Km
Animal A Km

For example, to modify the dose of resveratrol used for a mouse (22.4 mg/kg) to a dose based on the BSA for a rat, multiply 22.4 mg/kg by the Km factor for a mouse and then divide by the Km factor for a rat. This calculation results in a rat equivalent dose for resveratrol of 11.2 mg/kg.

Rat dose (mg/kg) = mouse dose (22.4 mg/kg) ×  mouse Km(3)  = 11.2 mg/kg
rat Km(6)


[1] Thomas HD, et al. Mol Cancer Ther, 2007, 6(3), 945-956.

[2] Kotz, J. SciBX 5(13); doi:10.1038/scibx.2012.323.

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Clinical Trial Information( data from, updated on 2015-08-29)

NCT Number Recruitment Conditions Sponsor
Start Date Phases
NCT02505048 Not yet recruiting Metastatic Breast Cancer UNICANCER|Clovis Oncology, Inc.|Fondation ARC July 2015 Phase 2
NCT02042378 Active, not recruiting Pancreatic Cancer|Pancreatic Ductal Adenocarcinoma Clovis Oncology, Inc. April 2014 Phase 2
NCT01968213 Recruiting Ovarian Cancer|Fallopian Tube Cancer|Peritoneal Cancer Clovis Oncology, Inc. January 2014 Phase 3
NCT01891344 Recruiting Ovarian Cancer|Epithelial Ovarian Cancer|Fallopian Tube Cancer|Peritoneal Cancer Clovis Oncology, Inc.|Foundation Medicine September 2013 Phase 2
NCT01482715 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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Chemical Information

Download Rucaparib (AG-014699,PF-01367338) SDF
Molecular Weight (MW) 421.36


CAS No. 459868-92-9
Storage 3 years -20℃powder
6 months-80℃in solvent
Synonyms N/A
Solubility (25°C) * In vitro DMSO 84 mg/mL (199.35 mM)
Water <1 mg/mL (<1 mM)
Ethanol <1 mg/mL (<1 mM)
In vivo 30% propylene glycol, 5% Tween 80, 65% D5W 30 mg/mL
* <1 mg/ml means slightly soluble or insoluble.
* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.
Chemical Name 8-fluoro-5-(4-((methylamino)methyl)phenyl)-3,4-dihydro-2H-azepino[5,4,3-cd]indol-1(6H)-one phosphoric acid

Customer Product Validation (6)

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Source Eur J Cancer 2014 50(15), 2725-34. Rucaparib (AG-014699,PF-01367338) purchased from Selleck
Method Clonogenic assays
Cell Lines BT474 cells
Concentrations 500, 1000 nM
Incubation Time 10-15 days
Results Rucaparib significantly reduced clonogenic growth and PAR production at the concentration of 300 nM, and the effect was greater at a higher concentration of 1000 nM. Of note, pharmacokinetic data from a phase I trial suggest that these are clinically achievable plasma concentrations.

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Source Eur J Cancer 2014 50(15), 2725-34. Rucaparib (AG-014699,PF-01367338) purchased from Selleck
Method Western blot
Cell Lines BT-474 cells
Concentrations 0.01-1000 nM
Incubation Time 6 h
Results It tested the drug rucaparib, which target PARP. It decided to test two different PARP inhibitors to reasonably study whether effects on cell growth were class-dependent instead of drug dependent. It confirmed that rucaparib inhibited PARP activity, as assayed by western blot of its product (poly ADP-ribose (PAR) levels), at starting concentrations of 500 nM of rucaparib.

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Source J Biol Chem 2012 287, 39824-33. Rucaparib (AG-014699,PF-01367338) purchased from Selleck
Method Western Blotting
Cell Lines HaCaT cells
Concentrations 1 μM
Incubation Time 30 min
Results preincubation of purified PARP-1 with AG-014699, a potent PARP inhibitor , prior to PARP-1 activation led to decreased associa-tion between PARP-1 and XPA.

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Source Oral Oncol 2014 50(9), 825-31. Rucaparib (AG-014699,PF-01367338) purchased from Selleck
Method Fluorescence assay
Cell Lines HN4, SAS cells
Concentrations 10 uM
Incubation Time 24 h
Results For treatment with positive control (2 Gy IR), we found this to be the case. In sensitive cell lines, the median foci formation decreased and conversely, RAD51 foci formation in resistant cell lines increased after exposure to 2 Gy.

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Source Urol Oncol 2014 32(5), 720-6. Rucaparib (AG-014699,PF-01367338) purchased from Selleck
Method CCK-8, flow cytometry, annexin V-FITC/PI staining
Cell Lines PC3 cells
Concentrations 10 uM
Incubation Time 24-48 h
Results The number of PC3 cells decreased significantly and the shape of PC3 cells became irregular after treatment with transfecting INPP4B gene combined with AG014699 treatment compared with single treatment (A). Next, it tested the proliferation of PC3 cells under the combined treatment. Compared with control, which combined with AG014699, the vitality of cells was 49.85%?.30%, 26.30%?.81%, and 9.72%?.10% after 24, 36, and 48 hours. Significant growth inhibition could be observed upon combination than transfection of INPP4B gene and AG014699 given separately (P<0.05) (B). Then the cell cycle distribution was detected. Transfection of INPP4B gene combined with AG014699 treatment caused a G1 arrest (C). Finally, we analyzed cell apoptosis, finding that compared with AG014699 alone, combination with transfection of INPP4B gene did not result in any further significant increase apoptosis rate (D).

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Source Dr. David Schrmann from University of Base. Rucaparib (AG-014699,PF-01367338) purchased from Selleck
Method Kruskal-Wallis and the post-hoc Dunn’s Multiple Comparison tests, immuno-staining
Cell Lines Primary human lung fibroblast cells (MRC-5)
Concentrations 0-1 μM
Incubation Time 2 h

Product Use Citation (14)

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