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.

サイズ 価格(税別)  
JPY 22244.00
JPY 19920.00
JPY 34860.00
JPY 111220.00


  • Representative images for RAD51 and γH2AX foci formation, surrogate DSB markers, in stable shK-H or shSCR 231 cells after rucaparib or vehicle (0.01% DMSO) treatment for 24 hours. DAPI-stained cell nuclei. Scale bars, 10 μm.

    Clin Cancer Res, 2018, doi:10.1158/1078-0432.CCR-17-1118. Rucaparib (AG-014699,PF-01367338) phosphate purchased from Selleck.

    MDA-MB-231 cells were inoculated into mammary fad pad of nude mice, and the mice with established tumors were treated with olaparib or rucaparib. Tumors were then isolated to evaluate PD-L1 expression by IHC staining (C). Black arrowheads indicate the detected PD-L1 signals. Scale bar, 50 μm.

    Clin Cancer Res, 2017, 23(14):3711-3720. Rucaparib (AG-014699,PF-01367338) phosphate purchased from Selleck.

  • 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 M2G2VmZ2dmO2aX;uJGF{e2G7 Mk\wNE4yNzFxNUCwM|ExODBibl2= MYrpcohq[mm2czDQRXJRKGGldHn2bZR6KGG2IIP0ZZJ1cW6pIHPvcoNmem62cnH0bY9vKG:oIEWwNEBvVQ>? NY\Wfo9{OjVzMki0OVU>
BT474 NGO5T5ZIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NHfh[JE2ODBibl2= NX7udpdxOTEkgKOxOeKh\A>? MVHy[YR2[2W|IHPlcIwh\3Kxd4ToJIlvKHSqZTDmc5VzKGyrbnXzJIFv\CC|aXfubYZq[2GwdHz5 Mn;WNlUyOjh2NUW=
SKBR3 MXPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NEHGeIs2ODBibl2= NFHt[lEyOOLCk{G1xsBl M4[4RZJm\HWlZYOgZ4VtdCCpcn;3eIghcW5idHjlJIZwfXJibHnu[ZMh[W6mIIPp[45q\mmlYX70cJk> NWC0Wlk5OjVzMki0OVU>
AU565 MWTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NGe4foc2ODBibl2= NFfad4QyOOLCk{G1xsBl M3LLSJJm\HWlZYOgZ4VtdCCpcn;3eIghcW5idHjlJIZwfXJibHnu[ZMh[W6mIIPp[45q\mmlYX70cJk> M{TMblI2OTJ6NEW1
EFM192A MWjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NI[1fpM2ODBibl2= M4OwXVEx6oDVMUZCpIQ> MmTvdoVlfWOnczDj[YxtKGe{b4f0bEBqdiC2aHWg[o92eiCuaX7ld{BidmRic3nncolncWOjboTsfS=> M4T0fFI2OTJ6NEW1
MDA-MB-231 NX3OSmlVTnWwY4Tpc44hSXO|YYm= MWqxNE8zOC92MDFOwG0> MY[yOEBp MYPpcoNz\WG|ZYOgdE1CU1RibHX2[Yx{KGmwIHGg[I9{\S2mZYDlcoRmdnRibXHucoVz NV3a[Wd5OjR2MkCxOVI>
MDA-MB-231 M3HhdWNmdGxiVnnhZoltcXS7IFHzd4F6 M4L1NFAvOS12MDFOwG0> M2\5R|I1KGh? NXO3VWtsUUN3MPMAjV3jiIlzNz63O:Kh|ryP MUKyOFQzODF3Mh?=
MDA-MB-231 NXK1d3ZiSXCxcITvd4l{KEG|c3H5 NGPERnIyOC9{MD:0NEDPxE1? MlT2NlQhcA>? M{XyeIlv\HWlZYOgZZBweHSxc3nzJIRwe2ViZHXw[Y5l\W62bIm= NWPaRo1pOjR2MkCxOVI>
MDA-MB-231 NWfZbWNYT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MlXENVAwOjBxNECg{txO M3PEcFI1KGh? MkHjZoxw[2u|IHPlcIwh[3mlbHWgdJJw\3Knc4Ppc44hcW5iR{KvUUBxcGG|ZR?= M1W2RVI1PDJyMUWy
H460 NFLvd2ZIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NY\wb|JDPDByIH7N M13tXFI1yqCq NHW4UZNqdmO{ZXHz[ZMh[2WubIXsZZIhemGmaX;z[Y5{cXSrdnn0fS=> NF7HcZczPDRzMU[xNS=>
A549  NEDMWZhIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NXvWeFZXPDByIH7N NXfLWnN4OjUEoHi= Ml;2bY5kemWjc3XzJINmdGy3bHHyJJJi\Gmxc3Xud4l1cX[rdIm= MnPhNlQ1OTF4MUG=
DU145 MUnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M4K3W2lEPTB;MUigcm0> NIC2UFYzPDN3NkixNy=>
COLO704 MnrUS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MkfMTWM2OD1{LkWyJOKyKDBwNkeg{txO MYCyN|czQTRyMh?=
OVMANAb NUe4WoxFT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M1z0e2lEPTB;Mj61PEDDuSByLkO4JO69VQ>? M2\NPFI{PzJ7NECy
OV177 NGLjVGtIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MXTJR|UxRTJwN{igxtEhOC55MTFOwG0> MX:yN|czQTRyMh?=
OAW28 NUWwe2M4T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NYPMUoJYUUN3ME2zMlYyKMLzIECuNlgh|ryP MkXmNlM4Ojl2MEK=
OVSAHO NEWzfIpIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MmfVTWM2OD1|Lk[0JOKyKDBwM{Og{txO MUKyN|czQTRyMh?=
OVKATE MWXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MYPJR|UxRTNwNkSgxtEhOS55OTFOwG0> NWnB[o5zOjN5Mkm0NFI>
PEO14 MXPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MnzuTWM2OD1|Lki0JOKyKDBwN{[g{txO M4TTSFI{PzJ7NECy
A2780 MWfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NYTCN2Z7UUN3ME2zMlk1KMLzIECuNlUh|ryP Ml7XNlM4Ojl2MEK=
TOV21G MkizS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M3j3TWlEPTB;NT6wO{DDuSBzLkOwJO69VQ>? NVL6eWtKOjN5Mkm0NFI>
OVISE NIPQ[oRIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NX\2[5dWUUN3ME21MlY5KMLzIECuNlMh|ryP M1vwSVI{PzJ7NECy
KK MUjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M2mz[WlEPTB;Nj6xOUDDuSBzLkSyJO69VQ>? MlvkNlM4Ojl2MEK=
RMUGS MnroS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NEX1ZZdKSzVyPUeuNFMhyrFiMT64N{DPxE1? M4T4elI{PzJ7NECy
PEO6 MYLHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MYHJR|UxRTdwME[gxtEhOC55NDFOwG0> NWjPbJFuOjN5Mkm0NFI>
OVCA429 M1zRXWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NV3DWXdzUUN3ME24MlI6KMLzIEGuOlQh|ryP M1S3clI{PzJ7NECy
OV167 MoHBS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MVTJR|UxRThwM{OgxtEhOS5zODFOwG0> NFvOd4czOzd{OUSwNi=>
RMG1 MX3Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NFi3b3dKSzVyPUmuN|IhyrFiMj6zOkDPxE1? NY\KXlIxOjN5Mkm0NFI>
OVCAR5 MYDHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NE\LZZFKSzVyPUmuOVAhyrFiMj61PUDPxE1? NInJeoQzOzd{OUSwNi=>
EFO21 NWLIT2lZT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NED3O3lKSzVyPUmuPVIhyrFiMT64O{DPxE1? MmHMNlM4Ojl2MEK=
Tyk-nu MYPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NESzZ4RKSzVyPUGwMlIxKMLzIEGuNVIh|ryP Mlm4NlM4Ojl2MEK=
CAOV3 MX\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MnXiTWM2OD1zMD6zO{DDuSByLki3JO69VQ>? NXztW2ZiOjN5Mkm0NFI>
OV207 MUTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MV3JR|UxRTF{LkK3JOKyKDBwM{Kg{txO NXnC[|c2OjN5Mkm0NFI>
HEY MXPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NYTsd45FUUN3ME2xN{4xOSEEsTCwMlc2KM7:TR?= NH3Yb5MzOzd{OUSwNi=>
DOV13 MX\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M3fkSmlEPTB-MUWg{txO MX[yN|czQTRyMh?=
EFO27 NHTlUXdIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NIjKdW9KSzVyPkG1JO69VQ>? MX2yN|czQTRyMh?=
KOC-7cc MmewS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NX;SdodGUUN3ME6xOUDPxE1? MnrJNlM4Ojl2MEK=
MCASb NF;jTXRIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M1W4WmlEPTB-MUWg{txO Ml\SNlM4Ojl2MEK=
OAW42 MnrrS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M1jT[WlEPTB-MUWg{txO NVrEW4V4OjN5Mkm0NFI>
OV2008 MXjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NVLNToIxUUN3ME6xOUDPxE1? NEW2VZQzOzd{OUSwNi=>
OV90 MkfOS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MkHpTWM2OD5zNTFOwG0> NULmfppPOjN5Mkm0NFI>
OVCA420b MlK1S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MkjRTWM2OD5zNTFOwG0> NVTablAxOjN5Mkm0NFI>
OVCA432 MkS2S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M2DteWlEPTB-MUWg{txO NIHVVXAzOzd{OUSwNi=>
PEA2 MXrHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MXTJR|UxRjF3IN88US=> NW\MRnJKOjN5Mkm0NFI>
SKOV3 MWPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M3;sd2lEPTB-MUWg{txO M4Xr[|I{PzJ7NECy
TOV112D M17xVGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MYGwMVMh|ryP Mnj1TWM2OD5zNTFOwG0> MoTpNlM4Ojl2MEK=
C4-2 M1\H[2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MXqwMVMh|ryP M3vmXlE1KGR? MVnEUXNQ MYLk[YNz\WG|ZYOgZ49td267IH71cYJmeiCmb4PlJIRmeGWwZHXueIx6 NVfKO2Q1OjN3NkWyOFQ>
PC3 MmPzS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NUXMS4xJOC1|IN88US=> NWrLflh2OTRiZB?= MUHEUXNQ Mm\l[IVkemWjc3XzJINwdG:weTDueY1j\XJiZH;z[UBl\XCnbnTlcpRtgQ>? NFfEZokzOzV4NUK0OC=>
DU145 NYfzWFFwT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MV[wMVMh|ryP NXLqRXFjOTRiZB?= NXv4e3RCTE2VTx?= MnWx[IVkemWjc3XzJINwdG:weTDueY1j\XJiZH;z[UBl\XCnbnTlcpRtgQ>? NETwPXAzOzV4NUK0OC=>
VCaP  MY\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MVmwMVMh|ryP NGnPO2YyPCCm M2\JeGROW09? MnLw[IVkemWjc3XzJINwdG:weTDueY1j\XJiZH;z[UBl\XCnbnTlcpRtgQ>? NEeyVVMzOzV4NUK0OC=>
LNCaP  Mnv0S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NVnXcnd7OC1|IN88US=> MorWNVQh\A>? NELUWZpFVVOR NVnycGdv\GWlcnXhd4V{KGOxbH;ufUBvfW2kZYKg[I9{\SCmZYDlcoRmdnSueR?= MVuyN|U3PTJ2NB?=
Cal-51 M1naS2NmdGxiVnnhZoltcXS7IFHzd4F6 MonWTWM2OD16Lk[g{txO M1rxfVIzPjd6MU[x


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
NCT03694262 Not yet recruiting Endometrial Cancer Medical College of Wisconsin February 1 2019 Phase 2
NCT03559049 Not yet recruiting Stage IV Non-small Cell Lung Cancer University of Michigan Cancer Center|Merck Sharp & Dohme Corp.|Clovis Oncology Inc. January 2019 Phase 1|Phase 2
NCT03617679 Not yet recruiting Metastatic Endometrial Cancer University of Colorado Denver|Clovis Oncology Inc. December 2018 Phase 2
NCT03639935 Not yet recruiting Biliary Tract Cancer University of Michigan Cancer Center|Dana-Farber Cancer Institute|Vanderbilt University Medical Center November 2018 Phase 2
NCT03654833 Not yet recruiting Mesothelioma Malignant University of Leicester|British Lung Foundation|Clovis Oncology Inc.|Eli Lilly and Company|Merck Sharp & Dohme Corp.|BerGenBio ASA|Roche Pharma AG|University Hospitals Leicester|The Christie NHS Foundation Trust October 1 2018 Phase 2
NCT03413995 Recruiting Prostate Cancer Metastatic Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins September 10 2018 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