Rucaparib (AG-014699,PF-01367338) phosphate

Catalog No.S1098

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

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.

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In DMSO USD 134 In stock
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6 Customer Reviews

  • 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) phosphate 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) phosphate 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) phosphate 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) phosphate 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) phosphate purchased from Selleck.

    in vivo suppression of PAR formation by the PARP inhibitor AG-014699 upon induction of DNA damage

    Primary 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) phosphate purchased from Selleck.

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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.
PARP [1]
(Cell-free assay)
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]

Cell Data
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
BT-474 Mn;OSpVv[3Srb36gRZN{[Xl? M3f4UFAvOS9zL{WwNE8yODByIH7N MoC1bY5pcWKrdIOgVGFTWCCjY4Tpeol1gSCjdDDzeIFzfGmwZzDjc45k\XKwdILheIlwdiCxZjC1NFAhdk1? NUPuOGJTOjVzMki0OVU>
BT474 MXHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NXfJVZBVPTByIH7N M1PoOVEx6oDVMUZCpIQ> NGfyeGpz\WS3Y3XzJINmdGxiZ4Lve5RpKGmwIITo[UBnd3W{IHzpcoV{KGGwZDDzbYdvcW[rY3HueIx6 Ml\pNlUyOjh2NUW=
SKBR3 MkfzS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NEPU[Yo2ODBibl2= NXnndmZJOTEkgKOxOeKh\A>? MUHy[YR2[2W|IHPlcIwh\3Kxd4ToJIlvKHSqZTDmc5VzKGyrbnXzJIFv\CC|aXfubYZq[2GwdHz5 M3nI[lI2OTJ6NEW1
AU565 M2T2T2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NE\SWo42ODBibl2= M3zlXlEx6oDVMUZCpIQ> NIO4fnJz\WS3Y3XzJINmdGxiZ4Lve5RpKGmwIITo[UBnd3W{IHzpcoV{KGGwZDDzbYdvcW[rY3HueIx6 M2LqblI2OTJ6NEW1
EFM192A MUDHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MmTpOVAxKG6P NH;INoEyOOLCk{G1xsBl MXvy[YR2[2W|IHPlcIwh\3Kxd4ToJIlvKHSqZTDmc5VzKGyrbnXzJIFv\CC|aXfubYZq[2GwdHz5 MUKyOVEzQDR3NR?=
MDA-MB-231 MofWSpVv[3Srb36gRZN{[Xl? MojoNVAwOjBxNECg{txO NHfwUlAzPCCq NHTVWoNqdmO{ZXHz[ZMheC2DS2SgcIV3\Wy|IHnuJIEh\G:|ZT3k[ZBmdmSnboSgcYFvdmW{ M4XTclI1PDJyMUWy
MDA-MB-231 MorsR4VtdCCYaXHibYxqfHliQYPzZZk> M4nPclAvOS12MDFOwG0> M3vybFI1KGh? MXfJR|Ux6oDLPfMAjVE4Njd5wrFOwG0> NWjo[|F5OjR2MkCxOVI>
MDA-MB-231 MXTBdI9xfG:|aYOgRZN{[Xl? MVSxNE8zOC92MDFOwG0> MkPDNlQhcA>? MX3pcoR2[2W|IHHwc5B1d3OrczDkc5NmKGSncHXu[IVvfGy7 M4TlZ|I1PDJyMUWy
MDA-MB-231 MlnRS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MUCxNE8zOC92MDFOwG0> MYiyOEBp M3ziWYJtd2OtczDj[YxtKGO7Y3zlJJBzd2e{ZYPzbY9vKGmwIFeyM20heGijc3W= NI\kPG8zPDR{MEG1Ni=>
H460 NXLHRmd[T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NGTXT4Y1ODBibl2= M{TvfFI1yqCq MVHpcoNz\WG|ZYOgZ4VtdHWuYYKgdoFlcW:|ZX7zbZRqfmm2eR?= NYj5WVVtOjR2MUG2NVE>
A549  MXLHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NV3h[WsxPDByIH7N MnHSNlTDqGh? MlzMbY5kemWjc3XzJINmdGy3bHHyJJJi\Gmxc3Xud4l1cX[rdIm= MV6yOFQyOTZzMR?=
DT40 MWrHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MoXaTWM2OD1{MTDuUS=> NHXtXmEzPDN3NkixNy=>
DU145 NFrpbI5Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M1;CSmlEPTB;MUigcm0> MmP2NlQ{PTZ6MUO=
COLO704 NFnwNolIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NXnCc29zUUN3ME2yMlUzKMLzIECuOlch|ryP Mlv5NlM4Ojl2MEK=
OVMANAb MW\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MmTjTWM2OD1{LkW4JOKyKDBwM{ig{txO MU[yN|czQTRyMh?=
OV177 NYD6[JpbT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NXPtfHhiUUN3ME2yMlc5KMLzIECuO|Eh|ryP NUiyO3l{OjN5Mkm0NFI>
OAW28 NXLRZWxUT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M4jZSmlEPTB;Mz62NUDDuSByLkK4JO69VQ>? NH\5W3czOzd{OUSwNi=>
OVCAR3 NWrxflFtT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M3rHbGlEPTB;Mz63OEDDuSByLkSwJO69VQ>? NHeyTJIzOzd{OUSwNi=>
PEO14 NHfzTGNIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M4PiS2lEPTB;Mz64OEDDuSByLke2JO69VQ>? NFHFco0zOzd{OUSwNi=>
A2780 M33aRWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MUjJR|UxRTNwOUSgxtEhOC5{NTFOwG0> NX3hbVltOjN5Mkm0NFI>
KURAMOCHIb M1rQPGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NYDnV3dJUUN3ME20MlM1KMLzIECuNlkh|ryP NInFbW8zOzd{OUSwNi=>
TOV21G NGK4eJlIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NX\NPIMxUUN3ME21MlA4KMLzIEGuN|Ah|ryP NF7MPFQzOzd{OUSwNi=>
KK MofoS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M1vwXGlEPTB;Nj6xOUDDuSBzLkSyJO69VQ>? M1\oZ|I{PzJ7NECy
RMUGS NGHBVZhIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= Mlj4TWM2OD15LkCzJOKyKDFwOEOg{txO NF\VS2IzOzd{OUSwNi=>
PEO6 MX3Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MVzJR|UxRTdwME[gxtEhOC55NDFOwG0> NHz2bWgzOzd{OUSwNi=>
OVCA429 NGXVenZIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MkP2TWM2OD16LkK5JOKyKDFwNkSg{txO M3LyRlI{PzJ7NECy
OV167 MV\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MoKyTWM2OD16LkOzJOKyKDFwMUig{txO M1fRfVI{PzJ7NECy
OVCAR5 M1L4bGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NGXHUWhKSzVyPUmuOVAhyrFiMj61PUDPxE1? M{j6Z|I{PzJ7NECy
EFO21 NFfuVVRIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NE\5NG9KSzVyPUmuPVIhyrFiMT64O{DPxE1? MVyyN|czQTRyMh?=
ES2 M3v3UWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NInkUWZKSzVyPUGwMlEzKMLzIEGuNlMh|ryP NWPPR2VNOjN5Mkm0NFI>
Tyk-nu NHvVenhIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M3fXVGlEPTB;MUCuNlAhyrFiMT6xNkDPxE1? MVeyN|czQTRyMh?=
CAOV3 Mo[wS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M3jNb2lEPTB;MUCuN|chyrFiMD64O{DPxE1? MlPiNlM4Ojl2MEK=
OV207 MnHxS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MXvJR|UxRTF{LkK3JOKyKDBwM{Kg{txO NGnZSpozOzd{OUSwNi=>
HEY Mlv0S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M3W2XGlEPTB;MUOuNFEhyrFiMD63OUDPxE1? NFjZbG4zOzd{OUSwNi=>
DOV13 M3\mWmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NFm4blFKSzVyPkG1JO69VQ>? Ml3ENlM4Ojl2MEK=
EFO27 M1HSSmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NGPCToNKSzVyPkG1JO69VQ>? M{jH[|I{PzJ7NECy
HEY C2 MlzNS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NGXodYRKSzVyPkG1JO69VQ>? NVS4eZBoOjN5Mkm0NFI>
KOC-7cc NF[xSmdIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M37TdGlEPTB-MUWg{txO NV\lZWRIOjN5Mkm0NFI>
MCASb M{P1[2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M2PtNmlEPTB-MUWg{txO NEP3OmszOzd{OUSwNi=>
OAW42 M4fZO2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MU\JR|UxRjF3IN88US=> MV[yN|czQTRyMh?=
OV2008 MVLHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NVfG[4RHUUN3ME6xOUDPxE1? NWjxSVM6OjN5Mkm0NFI>
OV90 NHn1V25Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MYHJR|UxRjF3IN88US=> NG\sVHAzOzd{OUSwNi=>
OVCA420b NYPqVHBwT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M{P4R2lEPTB-MUWg{txO NWH5fnBJOjN5Mkm0NFI>
OVCA432 NYjjbI9MT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MX3JR|UxRjF3IN88US=> NGjveZAzOzd{OUSwNi=>
PEA2 M{e0OWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NILmbG1KSzVyPkG1JO69VQ>? NFSzWpAzOzd{OUSwNi=>
SKOV3 NIT1[ZRIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MXjJR|UxRjF3IN88US=> M3PmUVI{PzJ7NECy
TOV112D MnfaS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M1LRcVAuOyEQvF2= M2f1[2lEPTB-MUWg{txO NXexOY81OjN5Mkm0NFI>
C4-2 MmTUS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NW\xbpFuOC1|IN88US=> M1nBeFE1KGR? MVnEUXNQ NXzVbpA{\GWlcnXhd4V{KGOxbH;ufUBvfW2kZYKg[I9{\SCmZYDlcoRmdnSueR?= NYjUVoN{OjN3NkWyOFQ>
PC3 NGjYTIZIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NEG3VYgxNTNizszN NHH3eoUyPCCm NVvZSI9TTE2VTx?= M{XxdIRm[3KnYYPld{Bkd2yxbomgcpVu[mW{IHTvd4Uh\GWyZX7k[Y51dHl? NVHu[XByOjN3NkWyOFQ>
DU145 NHzxd2VIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MkO1NE0{KM7:TR?= M3HW[|E1KGR? MlPhSG1UVw>? NFHZSmZl\WO{ZXHz[ZMh[2:ub375JI52dWKncjDkc5NmKGSncHXu[IVvfGy7 M2G4elI{PTZ3MkS0
VCaP  NUfITmxxT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NV3kSZEzOC1|IN88US=> MoezNVQh\A>? NVLIUFVITE2VTx?= MknQ[IVkemWjc3XzJINwdG:weTDueY1j\XJiZH;z[UBl\XCnbnTlcpRtgQ>? NIX2fGIzOzV4NUK0OC=>
LNCaP  NGfDXVNIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MlzGNE0{KM7:TR?= NGWxXZkyPCCm NUPy[ZZ5TE2VTx?= Mlyw[IVkemWjc3XzJINwdG:weTDueY1j\XJiZH;z[UBl\XCnbnTlcpRtgQ>? MmDQNlM2PjV{NES=
Cal-51 NGLzXXRE\WyuIG\pZYJqdGm2eTDBd5NigQ>? NGizbnJKSzVyPUiuOkDPxE1? M1yzdVIzPjd6MU[x

... Click to View More Cell Line Experimental Data

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]


Kinase Assay:[1]
+ Expand

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.
Cell Research:[4]
+ Expand
  • 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.
    (Only for Reference)
Animal Research:[4]
+ Expand
  • 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.
    (Only for Reference)

Solubility (25°C)

In vitro DMSO 84 mg/mL (199.35 mM)
Water slightly soluble or insoluble
Ethanol slightly soluble or insoluble
In vivo Add solvents individually and in order:
30% propylene glycol, 5% Tween 80, 65% D5W
30 mg/mL

* 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 Information

Molecular Weight 421.36


CAS No. 459868-92-9
Storage powder
in solvent
Synonyms N/A

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Clinical Trial Information

NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT02975934 Recruiting Metastatic Castration Resistant Prostate Cancer Clovis Oncology, Inc.|Foundation Medicine January 2017 Phase 3
NCT02986100 Recruiting Solid Tumor Clovis Oncology, Inc. November 2016 Phase 1
NCT02952534 Recruiting Metastatic Castration Resistant Prostate Cancer Clovis Oncology, Inc.|Foundation Medicine November 2016 Phase 2
NCT02855944 Recruiting Ovarian Cancer|Epithelial Ovarian Cancer|Fallopian Tube Cancer|Peritoneal Cancer Clovis Oncology, Inc.|Foundation Medicine September 2016 Phase 3
NCT02740712 Recruiting Neoplasms Clovis Oncology, Inc. March 2016 Phase 1
NCT02505048 Recruiting Metastatic Breast Cancer UNICANCER|Clovis Oncology, Inc.|Fondation ARC March 2016 Phase 2

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID