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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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.

  • 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.

    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.

  • 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 NUjUZ|I6TnWwY4Tpc44hSXO|YYm= MYOwMlEwOS93MECvNVAxOCCwTR?= NVX0N3p5cW6qaXLpeJMhWEGUUDDhZ5Rqfmm2eTDheEB{fGG{dHnu[{Bkd26lZYLueJJifGmxbjDv[kA2ODBibl2= NUf4cVhzOjVzMki0OVU>
BT474 NHHIOYNIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NH\yZ|A2ODBibl2= MmDKNVDjiJNzNdMg[C=> NVPR[Fg3emWmdXPld{Bk\WyuIHfyc5d1cCCrbjD0bIUh\m:3cjDsbY5meyCjbnSgd4lodmmoaXPhcpRtgQ>? M3HOOVI2OTJ6NEW1
SKBR3 MljnS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? Mn[0OVAxKG6P Mn7tNVDjiJNzNdMg[C=> MoPzdoVlfWOnczDj[YxtKGe{b4f0bEBqdiC2aHWg[o92eiCuaX7ld{BidmRic3nncolncWOjboTsfS=> MVyyOVEzQDR3NR?=
AU565 NFv1ToJIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MlrpOVAxKG6P MlHlNVDjiJNzNdMg[C=> MV\y[YR2[2W|IHPlcIwh\3Kxd4ToJIlvKHSqZTDmc5VzKGyrbnXzJIFv\CC|aXfubYZq[2GwdHz5 NVLvV41ROjVzMki0OVU>
EFM192A NHnhRpJIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NFHMepE2ODBibl2= NYP2ZXc2OTEkgKOxOeKh\A>? M4q0e5Jm\HWlZYOgZ4VtdCCpcn;3eIghcW5idHjlJIZwfXJibHnu[ZMh[W6mIIPp[45q\mmlYX70cJk> M3q1TFI2OTJ6NEW1
MDA-MB-231 NYH5cVh1TnWwY4Tpc44hSXO|YYm= MorsNVAwOjBxNECg{txO NWnnS4tQOjRiaB?= MXPpcoNz\WG|ZYOgdE1CU1RibHX2[Yx{KGmwIHGg[I9{\S2mZYDlcoRmdnRibXHucoVz M3XRSVI1PDJyMUWy
MDA-MB-231 M{K0TWNmdGxiVnnhZoltcXS7IFHzd4F6 Ml;PNE4yNTRyIN88US=> NIThfpMzPCCq M4L6R2lEPTEkgJm95qCKOTdwN{hCpO69VQ>? MnXCNlQ1OjBzNUK=
MDA-MB-231 NH7SUZVCeG:ydH;zbZMhSXO|YYm= MXexNE8zOC92MDFOwG0> MVmyOEBp NE\TV4hqdmS3Y3XzJIFxd3C2b4Ppd{Bld3OnIHTldIVv\GWwdHz5 M1nyOFI1PDJyMUWy
MDA-MB-231 MXvHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? Mn3tNVAwOjBxNECg{txO M2C5O|I1KGh? NYHaTlJv[myxY3vzJINmdGxiY4njcIUheHKxZ4Lld5Nqd25iaX6gS|IwVSCyaHHz[S=> NGewNoszPDR{MEG1Ni=>
H460 M1fP[Gdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NYD5fHVvPDByIH7N NELwdnMzPMLiaB?= NYT3W2VrcW6lcnXhd4V{KGOnbHz1cIFzKHKjZHnvd4Vve2m2aY\peJk> M3:xZ|I1PDFzNkGx
A549  MUPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NEPic|Q1ODBibl2= MWSyOOKhcA>? MX\pcoNz\WG|ZYOgZ4VtdHWuYYKgdoFlcW:|ZX7zbZRqfmm2eR?= NHLmR24zPDRzMU[xNS=>
DT40 M3jt[Wdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NX7DXHRxUUN3ME2yNUBvVQ>? MorCNlQ{PTZ6MUO=
DU145 NHPsU21Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MnOzTWM2OD1zODDuUS=> NX;hZVJzOjR|NU[4NVM>
COLO704 M3\XVmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MXPJR|UxRTJwNUKgxtEhOC54NzFOwG0> MmW3NlM4Ojl2MEK=
OVMANAb MlS0S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M{LidWlEPTB;Mj61PEDDuSByLkO4JO69VQ>? M{S3eVI{PzJ7NECy
OV177 M4m3UWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NID2Tm9KSzVyPUKuO|ghyrFiMD63NUDPxE1? M3f0flI{PzJ7NECy
OAW28 NYW3S2pXT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NHnpXlJKSzVyPUOuOlEhyrFiMD6yPEDPxE1? NWiyVmh4OjN5Mkm0NFI>
OVSAHO M1;sT2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NGLocY9KSzVyPUOuOlQhyrFiMD6zN{DPxE1? MmjoNlM4Ojl2MEK=
PEO14 NH64OYlIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MoHuTWM2OD1|Lki0JOKyKDBwN{[g{txO NGPwdGwzOzd{OUSwNi=>
A2780 MmXnS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M1e0bGlEPTB;Mz65OEDDuSByLkK1JO69VQ>? M4npZlI{PzJ7NECy
KURAMOCHIb M2i2d2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MlKyTWM2OD12LkO0JOKyKDBwMkmg{txO MVWyN|czQTRyMh?=
TOV21G MXjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M3fYTGlEPTB;NT6wO{DDuSBzLkOwJO69VQ>? M3fJU|I{PzJ7NECy
OVISE Mny0S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M4X5R2lEPTB;NT62PEDDuSByLkKzJO69VQ>? NV;Yb|BHOjN5Mkm0NFI>
KK MYfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NGDo[pZKSzVyPU[uNVUhyrFiMT60NkDPxE1? Mnq3NlM4Ojl2MEK=
RMUGS NFT5R41Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M33GcmlEPTB;Nz6wN{DDuSBzLkizJO69VQ>? NX;mRpllOjN5Mkm0NFI>
PEO6 M{DL[Wdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MmjhTWM2OD15LkC2JOKyKDBwN{Sg{txO MXOyN|czQTRyMh?=
OVCA429 NGLITVFIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MWDJR|UxRThwMkmgxtEhOS54NDFOwG0> NUX0R2h{OjN5Mkm0NFI>
OV167 MUPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MWLJR|UxRThwM{OgxtEhOS5zODFOwG0> M3H6[lI{PzJ7NECy
RMG1 MlyzS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MkTGTWM2OD17LkOyJOKyKDJwM{[g{txO NX[weoZuOjN5Mkm0NFI>
OVCAR5 NHqyW5VIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M3:2fmlEPTB;OT61NEDDuSB{LkW5JO69VQ>? NIjFVI8zOzd{OUSwNi=>
EFO21 Mm\SS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M2rSN2lEPTB;OT65NkDDuSBzLki3JO69VQ>? NWnGd3Q1OjN5Mkm0NFI>
ES2 NUH1S25IT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M1TKNmlEPTB;MUCuNVIhyrFiMT6yN{DPxE1? NF3Jb2QzOzd{OUSwNi=>
Tyk-nu NIezUXpIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MXLJR|UxRTFyLkKwJOKyKDFwMUKg{txO MXiyN|czQTRyMh?=
CAOV3 MVrHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? Mk[yTWM2OD1zMD6zO{DDuSByLki3JO69VQ>? MlvBNlM4Ojl2MEK=
OV207 M3;Y[Gdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M3HZcmlEPTB;MUKuNlchyrFiMD6zNkDPxE1? MXWyN|czQTRyMh?=
HEY M13mOGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NXvTbWd1UUN3ME2xN{4xOSEEsTCwMlc2KM7:TR?= MU[yN|czQTRyMh?=
DOV13 MVLHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NGfScmdKSzVyPkG1JO69VQ>? M4W1R|I{PzJ7NECy
EFO27 MlvQS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M4PUfWlEPTB-MUWg{txO M{C1d|I{PzJ7NECy
HEY C2 NWrk[XBDT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M{jWTmlEPTB-MUWg{txO MXqyN|czQTRyMh?=
KOC-7cc M2jMWWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M1;UVGlEPTB-MUWg{txO M4PzU|I{PzJ7NECy
MCASb NETK[I1Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M1PaNGlEPTB-MUWg{txO NHWyb|QzOzd{OUSwNi=>
OAW42 Mk\tS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MkjNTWM2OD5zNTFOwG0> NX\ZcGRTOjN5Mkm0NFI>
OV2008 NEXPb4NIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MXzJR|UxRjF3IN88US=> NIHSZmgzOzd{OUSwNi=>
OV90 MVjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NUHZV5V3UUN3ME6xOUDPxE1? NYm3emZTOjN5Mkm0NFI>
OVCA420b M4j6bmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M4DlPWlEPTB-MUWg{txO NYHBdopnOjN5Mkm0NFI>
OVCA432 NVf6coVsT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= Mn\4TWM2OD5zNTFOwG0> M3PiOVI{PzJ7NECy
PEA2 NFnkcYFIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NF64dVZKSzVyPkG1JO69VQ>? MlP6NlM4Ojl2MEK=
SKOV3 NUC5ZnFXT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NGnGd|ZKSzVyPkG1JO69VQ>? MViyN|czQTRyMh?=
TOV112D NXPlfVFNT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MW[wMVMh|ryP NHnaUnNKSzVyPkG1JO69VQ>? MoPGNlM4Ojl2MEK=
C4-2 M{HCUGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MXiwMVMh|ryP MkjpNVQh\A>? M4XRNGROW09? Mliy[IVkemWjc3XzJINwdG:weTDueY1j\XJiZH;z[UBl\XCnbnTlcpRtgQ>? M4fOUVI{PTZ3MkS0
PC3 NGfoSmdIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NFP3NpMxNTNizszN NEXXO28yPCCm Mlf3SG1UVw>? MlzC[IVkemWjc3XzJINwdG:weTDueY1j\XJiZH;z[UBl\XCnbnTlcpRtgQ>? M3rz[|I{PTZ3MkS0
DU145 M3nNOmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MmHHNE0{KM7:TR?= MmnwNVQh\A>? Ml3ZSG1UVw>? M1TsZ4Rm[3KnYYPld{Bkd2yxbomgcpVu[mW{IHTvd4Uh\GWyZX7k[Y51dHl? NFrhcWkzOzV4NUK0OC=>
VCaP  NH;1UIxIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NHfWOHoxNTNizszN M1PhblE1KGR? M{fnfGROW09? M2CzOoRm[3KnYYPld{Bkd2yxbomgcpVu[mW{IHTvd4Uh\GWyZX7k[Y51dHl? NFTnc4YzOzV4NUK0OC=>
LNCaP  NI\FdmRIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= Mnj1NE0{KM7:TR?= MVixOEBl MnrZSG1UVw>? NVLTSY01\GWlcnXhd4V{KGOxbH;ufUBvfW2kZYKg[I9{\SCmZYDlcoRmdnSueR?= M1XoSVI{PTZ3MkS0
Cal-51 MVXD[YxtKF[rYXLpcIl1gSCDc4PhfS=> NVzFXYxwUUN3ME24MlYh|ryP M2\GOlIzPjd6MU[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 Insoluble
Ethanol Insoluble
In vivo Add solvents to the product individually and in order(Data is from Selleck tests instead of citations):
2% DMSO+30% PEG 300+2% Tween 80+ddH2O
For best results, use promptly after mixing.

* 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
NCT03533946 Recruiting Prostate Cancer University of Utah|Clovis Oncology Inc. August 8 2018 Phase 2
NCT03499444 Recruiting Advanced Solid Tumor Clovis Oncology Inc. February 6 2018 Phase 1
NCT03101280 Recruiting Gynecologic Neoplasms Hoffmann-La Roche May 4 2017 Phase 1
NCT03337087 Not yet recruiting Biliary System Disorder|BRCA1 Gene Mutation|BRCA2 Gene Mutation|Gastroesophageal Junction Adenocarcinoma|Homologous Recombination Deficiency|Metastatic Pancreatic Adenocarcinoma|PALB2 Gene Mutation|Stage IV Colorectal Cancer AJCC v7|Stage IV Pancreatic Cancer AJCC v6 and v7|Stage IVA Colorectal Cancer AJCC v7|Stage IVB Colorectal Cancer AJCC v7 Academic and Community Cancer Research United|National Cancer Institute (NCI) August 31 2018 Phase 1|Phase 2
NCT03521037 Recruiting Neoplasms Clovis Oncology Inc. March 31 2018 Phase 1
NCT03140670 Recruiting Pancreatic Cancer Abramson Cancer Center of the University of Pennsylvania June 30 2017 Phase 2

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID