Rucaparib (AG-014699,PF-01367338) phosphate


Rucaparib (AG-014699,PF-01367338) phosphate化学構造


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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  • 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.




製品説明 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.
特性 The first PARP inhibitor used in clinical trials combined with temozolomide.
PARP [1]
(Cell-free assay)
1.4 nM(Ki)

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 Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
BT-474 NW[xVmhkTnWwY4Tpc44hSXO|YYm= NXP3eYZZOC5zL{GvOVAxNzFyMECgcm0> NGLISnVqdmirYnn0d{BRSVKSIHHjeIl3cXS7IHH0JJN1[XK2aX7nJINwdmOncn70doF1cW:wIH;mJFUxOCCwTR?= MUSyOVEzQDR3NR?=
BT474 MVTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M2Xr[lUxOCCwTR?= Mo\GNVDjiJNzNdMg[C=> MVLy[YR2[2W|IHPlcIwh\3Kxd4ToJIlvKHSqZTDmc5VzKGyrbnXzJIFv\CC|aXfubYZq[2GwdHz5 M4rPR|I2OTJ6NEW1
SKBR3 MXfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NITN[nc2ODBibl2= Moj4NVDjiJNzNdMg[C=> M2DHfZJm\HWlZYOgZ4VtdCCpcn;3eIghcW5idHjlJIZwfXJibHnu[ZMh[W6mIIPp[45q\mmlYX70cJk> MoDLNlUyOjh2NUW=
AU565 NI\ld29Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NGDBO282ODBibl2= Mnf1NVDjiJNzNdMg[C=> NF;KVWxz\WS3Y3XzJINmdGxiZ4Lve5RpKGmwIITo[UBnd3W{IHzpcoV{KGGwZDDzbYdvcW[rY3HueIx6 NVjxVmRNOjVzMki0OVU>
EFM192A NXrKUHQ4T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M1jVclUxOCCwTR?= NUnU[GNYOTEkgKOxOeKh\A>? NHTSTmRz\WS3Y3XzJINmdGxiZ4Lve5RpKGmwIITo[UBnd3W{IHzpcoV{KGGwZDDzbYdvcW[rY3HueIx6 MoC5NlUyOjh2NUW=
MDA-MB-231 NULvSJZMTnWwY4Tpc44hSXO|YYm= M{\wOlExNzJyL{SwJO69VQ>? NXrJSFhrOjRiaB?= NGnlbpRqdmO{ZXHz[ZMheC2DS2SgcIV3\Wy|IHnuJIEh\G:|ZT3k[ZBmdmSnboSgcYFvdmW{ NXPae2piOjR2MkCxOVI>
MDA-MB-231 NVfKO45zS2WubDDWbYFjcWyrdImgRZN{[Xl? MYiwMlEuPDBizszN MlvuNlQhcA>? NGLMUlBKSzVy4pEJQgKBkTF5Lke3xsDPxE1? MX2yOFQzODF3Mh?=
MDA-MB-231 M{jodmFxd3C2b4Ppd{BCe3OjeR?= NHfR[pYyOC9{MD:0NEDPxE1? M{nrelI1KGh? MWDpcoR2[2W|IHHwc5B1d3OrczDkc5NmKGSncHXu[IVvfGy7 MWqyOFQzODF3Mh?=
MDA-MB-231 MmXPS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NWPjdolnOTBxMkCvOFAh|ryP M1rsZVI1KGh? NGPq[FhjdG:la4OgZ4VtdCCleXPs[UBxem:pcnXzd4lwdiCrbjDHNk9OKHCqYYPl NWHEW5lSOjR2MkCxOVI>
H460 Mn;4S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M2r2[VQxOCCwTR?= NGriSW4zPMLiaB?= M33N[Ylv[3KnYYPld{Bk\WyudXzhdkBz[WSrb4PlcpNqfGm4aYT5 Mlv0NlQ1OTF4MUG=
A549  NHPOb5ZIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NVe1Ump2PDByIH7N NWKzXZRFOjUEoHi= Mlq5bY5kemWjc3XzJINmdGy3bHHyJJJi\Gmxc3Xud4l1cX[rdIm= NHj3UmszPDRzMU[xNS=>
DT40 NXO1ZlZLT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NF33eotKSzVyPUKxJI5O MX6yOFM2PjhzMx?=
DU145 NF21O3VIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MXPJR|UxRTF6IH7N NUn4dHRqOjR|NU[4NVM>
COLO704 NFywVmRIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NUfHR2ZmUUN3ME2yMlUzKMLzIECuOlch|ryP NIPPboIzOzd{OUSwNi=>
OVMANAb NVy4VY1oT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NYLsco1MUUN3ME2yMlU5KMLzIECuN|gh|ryP MlHQNlM4Ojl2MEK=
OV177 M2LPT2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M3zDSWlEPTB;Mj63PEDDuSByLkexJO69VQ>? MmTmNlM4Ojl2MEK=
OAW28 NH7oOGNIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NWjjOY4zUUN3ME2zMlYyKMLzIECuNlgh|ryP M2TpNlI{PzJ7NECy
OVSAHO M2fSTWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NVnVXZdnUUN3ME2zMlY1KMLzIECuN|Mh|ryP MUeyN|czQTRyMh?=
OVKATE M3L5TWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 Mmj1TWM2OD1|Lk[0JOKyKDFwN{mg{txO MV6yN|czQTRyMh?=
PEO14 MWHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NUf0VoVzUUN3ME2zMlg1KMLzIECuO|Yh|ryP MV:yN|czQTRyMh?=
A2780 NEOxOWhIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NHuwbo9KSzVyPUOuPVQhyrFiMD6yOUDPxE1? MoPRNlM4Ojl2MEK=
OVTOKO MV\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NFjOdmtKSzVyPUSuNVQhyrFiMT61N{DPxE1? MVWyN|czQTRyMh?=
KURAMOCHIb NFryeZZIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MX\JR|UxRTRwM{SgxtEhOC5{OTFOwG0> NX\HW41nOjN5Mkm0NFI>
TOV21G Mn7qS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MorLTWM2OD13LkC3JOKyKDFwM{Cg{txO M4HpOFI{PzJ7NECy
OVISE MoC3S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NUO5[4RpUUN3ME21MlY5KMLzIECuNlMh|ryP NUS5fpRoOjN5Mkm0NFI>
RMUGS MkjxS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NHnkephKSzVyPUeuNFMhyrFiMT64N{DPxE1? MmL5NlM4Ojl2MEK=
PEO6 M3u0bGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NHXVbIVKSzVyPUeuNFYhyrFiMD63OEDPxE1? MkSxNlM4Ojl2MEK=
OVCA429 NG\BUGFIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MXvJR|UxRThwMkmgxtEhOS54NDFOwG0> NFK4T2gzOzd{OUSwNi=>
OV167 NWLLTopuT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M3XLWWlEPTB;OD6zN{DDuSBzLkG4JO69VQ>? M{\kdFI{PzJ7NECy
RMG1 MX;Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? Mn;LTWM2OD17LkOyJOKyKDJwM{[g{txO MV6yN|czQTRyMh?=
OVCAR5 NHSzN3hIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NUjEd2dsUUN3ME25MlUxKMLzIEKuOVkh|ryP M4jyZ|I{PzJ7NECy
EFO21 NEnrZ2pIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MXHJR|UxRTlwOUKgxtEhOS56NzFOwG0> MniyNlM4Ojl2MEK=
ES2 MYjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NETTeZJKSzVyPUGwMlEzKMLzIEGuNlMh|ryP NFPGR3YzOzd{OUSwNi=>
Tyk-nu NHPZSI1Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MnvxTWM2OD1zMD6yNEDDuSBzLkGyJO69VQ>? M2fVc|I{PzJ7NECy
CAOV3 MUnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NWjoUVFDUUN3ME2xNE4{PyEEsTCwMlg4KM7:TR?= MnXiNlM4Ojl2MEK=
OV207 NYW5cZhTT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NIL2XoNKSzVyPUGyMlI4KMLzIECuN|Ih|ryP NWmwdog{OjN5Mkm0NFI>
HEY MYHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NGHQSpdKSzVyPUGzMlAyKMLzIECuO|Uh|ryP NEf5VHMzOzd{OUSwNi=>
EFO27 NFnV[HpIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M3voUGlEPTB-MUWg{txO M3:5dVI{PzJ7NECy
HEY C2 MVHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MoDxTWM2OD5zNTFOwG0> MVyyN|czQTRyMh?=
KOC-7cc NIr1dHhIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MX\JR|UxRjF3IN88US=> MUiyN|czQTRyMh?=
OAW42 MYTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? Ml75TWM2OD5zNTFOwG0> MVWyN|czQTRyMh?=
OV2008 Mn\RS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NVHPdVZmUUN3ME6xOUDPxE1? MYKyN|czQTRyMh?=
OV90 MUDHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NIT3OWVKSzVyPkG1JO69VQ>? M17XfFI{PzJ7NECy
OVCA432 M4flZ2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NYjicm81UUN3ME6xOUDPxE1? M4G3R|I{PzJ7NECy
PEA2 MoHtS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MV7JR|UxRjF3IN88US=> MmHXNlM4Ojl2MEK=
SKOV3 MXjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M3PyWWlEPTB-MUWg{txO M1rmeVI{PzJ7NECy
TOV112D M1P5R2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NV;CeZNOOC1|IN88US=> NX7qS4xmUUN3ME6xOUDPxE1? M1XvflI{PzJ7NECy
C4-2 MWTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NFHLVm4xNTNizszN NXGxTZQyOTRiZB?= NGPaV2pFVVOR NFfRZpNl\WO{ZXHz[ZMh[2:ub375JI52dWKncjDkc5NmKGSncHXu[IVvfGy7 MmTiNlM2PjV{NES=
PC3 NXHuZXJnT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MYmwMVMh|ryP NF7nWmUyPCCm MYDEUXNQ NVLae4VK\GWlcnXhd4V{KGOxbH;ufUBvfW2kZYKg[I9{\SCmZYDlcoRmdnSueR?= NI\nW|QzOzV4NUK0OC=>
DU145 NXjudotWT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NIH5PGcxNTNizszN M{LQblE1KGR? MUHEUXNQ MoPw[IVkemWjc3XzJINwdG:weTDueY1j\XJiZH;z[UBl\XCnbnTlcpRtgQ>? NVvPOldqOjN3NkWyOFQ>
VCaP  MkLxS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NVTTeIZJOC1|IN88US=> NGrLW3cyPCCm NV3yZ5ZGTE2VTx?= NIHuWYxl\WO{ZXHz[ZMh[2:ub375JI52dWKncjDkc5NmKGSncHXu[IVvfGy7 M4i1UVI{PTZ3MkS0
LNCaP  M3j1V2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NFTiNm4xNTNizszN M2nGWlE1KGR? M2HxRWROW09? M{[yWoRm[3KnYYPld{Bkd2yxbomgcpVu[mW{IHTvd4Uh\GWyZX7k[Y51dHl? NIX5SHozOzV4NUK0OC=>
MDA-MB-231 M2fVOWNmdGxiVnnhZoltcXS7IFHzd4F6 M{HBdmlEPTB;MUOg{txO MkPLNlI3PzhzNkG=
Cal-51 MYnD[YxtKF[rYXLpcIl1gSCDc4PhfS=> M{PvNmlEPTB;OD62JO69VQ>? NGnMelkzOjZ5OEG2NS=>


体内試験 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]


+ 展開

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.
細胞試験: [4]
+ 展開
  • 細胞株: D425Med, D283Med and D384Med cells
  • 濃度: 0.4 μM
  • 反応時間: 3 or 5 days
  • 実験の流れ: 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.
+ 展開
  • 動物モデル: CD-1 nude mice bearing established D283Med xenografts
  • 製剤: Normal saline
  • 投薬量: 1 mg/kg
  • 投与方法: One or four daily by i.p.

溶解度 (25°C)

体外 DMSO 84 mg/mL (199.35 mM)
Water Insoluble
Ethanol Insoluble
体内 左から(NMPから)右の順に溶剤を製品に加えます(文献ではなく、Selleckの実験によるデータ):
2% DMSO+30% PEG 300+2% Tween 80+ddH2O

* 溶解度測定はSelleck技術部門によって行われており、その他文献に示されている溶解度と差異がある可能性がありますが、同一ロットの生産工程で起きる正常な現象ですからご安心ください。


分子量 421.36


CAS No. 459868-92-9
in solvent
別名 N/A





質量 (g) = 濃度 (mol/L) x 体積 (L) x 分子量 (g/mol)


  • 質量





開始濃度 x 開始体積 = 最終濃度 x 最終体積


この方程式は、一般に略語を使われます:C1V1 = C2V2 ( 入力 出力 )

  • C1



  • 連続希釈剤

  • 計算結果

  • C1=C0/X C1: LOG(C1):
    C2=C1/X C2: LOG(C2):
    C3=C2/X C3: LOG(C3):
    C4=C3/X C4: LOG(C4):
    C5=C4/X C5: LOG(C5):
    C6=C5/X C6: LOG(C6):
    C7=C6/X C7: LOG(C7):
    C8=C7/X C8: LOG(C8):




チップス: 化学式は大文字と小文字の区別ができます。C10H16N2O2 c10h16n2o2


質量 濃度 体積 分子量


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



Handling Instructions


  • * 必須


PARP Inhibitors with Unique Features


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細胞株 試験類型 濃度 培養時間 溶剤類型 活性叙述 PMID