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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Cited by 17 Publications

8 Customer Reviews

  • 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.

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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.
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 MWLGeY5kfGmxbjDBd5NigQ>? NHHMV|AxNjFxMT:1NFAwOTByMDDuUS=> NWjlcFhNcW6qaXLpeJMhWEGUUDDhZ5Rqfmm2eTDheEB{fGG{dHnu[{Bkd26lZYLueJJifGmxbjDv[kA2ODBibl2= NE\HPJkzPTF{OES1OS=>
BT474 M4fIcmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NXXTZnJUPTByIH7N M{DM[FEx6oDVMUZCpIQ> NVP2UFBtemWmdXPld{Bk\WyuIHfyc5d1cCCrbjD0bIUh\m:3cjDsbY5meyCjbnSgd4lodmmoaXPhcpRtgQ>? MXqyOVEzQDR3NR?=
SKBR3 NXzEbnFuT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NUSyeJg{PTByIH7N MVqxNQKBmzF3wrDk M4TVSJJm\HWlZYOgZ4VtdCCpcn;3eIghcW5idHjlJIZwfXJibHnu[ZMh[W6mIIPp[45q\mmlYX70cJk> M1TPd|I2OTJ6NEW1
AU565 MmnoS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NV;rNoc4PTByIH7N MX:xNQKBmzF3wrDk MVvy[YR2[2W|IHPlcIwh\3Kxd4ToJIlvKHSqZTDmc5VzKGyrbnXzJIFv\CC|aXfubYZq[2GwdHz5 M1vTN|I2OTJ6NEW1
EFM192A NIfKbVNIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= Mlq5OVAxKG6P MWKxNQKBmzF3wrDk NXe5c3o{emWmdXPld{Bk\WyuIHfyc5d1cCCrbjD0bIUh\m:3cjDsbY5meyCjbnSgd4lodmmoaXPhcpRtgQ>? NY[2PWo2OjVzMki0OVU>
MDA-MB-231 NVXwcVdsTnWwY4Tpc44hSXO|YYm= MX6xNE8zOC92MDFOwG0> NXjnNXRkOjRiaB?= NV3yeVFPcW6lcnXhd4V{KHBvQVvUJIxmfmWuczDpckBiKGSxc3Wt[IVx\W6mZX70JI1idm6nch?= MVWyOFQzODF3Mh?=
MDA-MB-231 MVLD[YxtKF[rYXLpcIl1gSCDc4PhfS=> Ml[1NE4yNTRyIN88US=> Ml\LNlQhcA>? NF;DRlVKSzVy4pEJQgKBkTF5Lke3xsDPxE1? MX:yOFQzODF3Mh?=
MDA-MB-231 NV[wPXVrSXCxcITvd4l{KEG|c3H5 MYKxNE8zOC92MDFOwG0> M1zqXFI1KGh? M3jIdYlv\HWlZYOgZZBweHSxc3nzJIRwe2ViZHXw[Y5l\W62bIm= NFOwSVYzPDR{MEG1Ni=>
MDA-MB-231 MmDTS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MkDWNVAwOjBxNECg{txO MYqyOEBp MmH6Zoxw[2u|IHPlcIwh[3mlbHWgdJJw\3Knc4Ppc44hcW5iR{KvUUBxcGG|ZR?= MmfhNlQ1OjBzNUK=
H460 M3;LXmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 Mli1OFAxKG6P MUCyOOKhcA>? MnPnbY5kemWjc3XzJINmdGy3bHHyJJJi\Gmxc3Xud4l1cX[rdIm= MVGyOFQyOTZzMR?=
A549  NU\McZZJT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M{fIclQxOCCwTR?= NYTHdZFkOjUEoHi= MnTYbY5kemWjc3XzJINmdGy3bHHyJJJi\Gmxc3Xud4l1cX[rdIm= Ml3lNlQ1OTF4MUG=
DT40 MY\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MV3JR|UxRTJzIH7N M37FUlI1OzV4OEGz
DU145 NVTRXWpjT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M3Xyc2lEPTB;MUigcm0> MWCyOFM2PjhzMx?=
COLO704 NYPjdItVT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MYLJR|UxRTJwNUKgxtEhOC54NzFOwG0> Mly0NlM4Ojl2MEK=
OV177 M2jzSmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M1vpcGlEPTB;Mj63PEDDuSByLkexJO69VQ>? MYGyN|czQTRyMh?=
OAW28 MYPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NHO4[JpKSzVyPUOuOlEhyrFiMD6yPEDPxE1? NUPWe44xOjN5Mkm0NFI>
OVSAHO M{LKe2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NGHWTWlKSzVyPUOuOlQhyrFiMD6zN{DPxE1? MnjpNlM4Ojl2MEK=
OVKATE MoXkS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MnWwTWM2OD1|Lk[0JOKyKDFwN{mg{txO M3X2fVI{PzJ7NECy
OVCAR3 MkjFS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M{jNZ2lEPTB;Mz63OEDDuSByLkSwJO69VQ>? MmrDNlM4Ojl2MEK=
PEO14 NUHHc25ZT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NID5U3dKSzVyPUOuPFQhyrFiMD63OkDPxE1? MU[yN|czQTRyMh?=
A2780 MoOwS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MmGyTWM2OD1|Lkm0JOKyKDBwMkWg{txO M2TU[FI{PzJ7NECy
OVTOKO M{[zT2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MojQTWM2OD12LkG0JOKyKDFwNUOg{txO MYSyN|czQTRyMh?=
KURAMOCHIb Mn3yS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MnHUTWM2OD12LkO0JOKyKDBwMkmg{txO M2fke|I{PzJ7NECy
TOV21G M3\sVGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NY\Ze|dpUUN3ME21MlA4KMLzIEGuN|Ah|ryP NX\mUJRjOjN5Mkm0NFI>
OVISE NYWyZ4oxT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M3THe2lEPTB;NT62PEDDuSByLkKzJO69VQ>? NGe4TpEzOzd{OUSwNi=>
KK NHHnO4lIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NXXlc2Y1UUN3ME22MlE2KMLzIEGuOFIh|ryP M3HwSFI{PzJ7NECy
RMUGS NHO3OFlIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MVHJR|UxRTdwMEOgxtEhOS56MzFOwG0> M1mxNVI{PzJ7NECy
PEO6 M1XNbGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NVmwO4FSUUN3ME23MlA3KMLzIECuO|Qh|ryP Mo\KNlM4Ojl2MEK=
OVCA429 MW\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M3\pZWlEPTB;OD6yPUDDuSBzLk[0JO69VQ>? MlrFNlM4Ojl2MEK=
OV167 NWT5TJRtT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MYnJR|UxRThwM{OgxtEhOS5zODFOwG0> MV:yN|czQTRyMh?=
RMG1 MWTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? Ml3STWM2OD17LkOyJOKyKDJwM{[g{txO MmfkNlM4Ojl2MEK=
OVCAR5 Mlv2S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M1nMNGlEPTB;OT61NEDDuSB{LkW5JO69VQ>? MWeyN|czQTRyMh?=
EFO21 Ml\iS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MVPJR|UxRTlwOUKgxtEhOS56NzFOwG0> Ml[4NlM4Ojl2MEK=
ES2 MnXWS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NGqzNllKSzVyPUGwMlEzKMLzIEGuNlMh|ryP Mnr4NlM4Ojl2MEK=
Tyk-nu NF[2SmVIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MofMTWM2OD1zMD6yNEDDuSBzLkGyJO69VQ>? M3;GR|I{PzJ7NECy
OV207 NHvQd|ZIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= Mn;TTWM2OD1zMj6yO{DDuSByLkOyJO69VQ>? MoLkNlM4Ojl2MEK=
EFO27 M{\zcGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 Ml7ITWM2OD5zNTFOwG0> NH\hO20zOzd{OUSwNi=>
HEY C2 NUftdWM5T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NXPsb2lOUUN3ME6xOUDPxE1? NWXRdpcxOjN5Mkm0NFI>
KOC-7cc NVjySHpJT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NF\oPGtKSzVyPkG1JO69VQ>? MWeyN|czQTRyMh?=
MCASb MnnjS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MkXMTWM2OD5zNTFOwG0> M4fJe|I{PzJ7NECy
OAW42 MmHaS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MofLTWM2OD5zNTFOwG0> M4\kVlI{PzJ7NECy
OV2008 NVLBcGV6T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M{LtUWlEPTB-MUWg{txO MVSyN|czQTRyMh?=
OV90 NHf4dFFIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MlvaTWM2OD5zNTFOwG0> M4HTPVI{PzJ7NECy
OVCA420b NF;JN|hIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NV\Jc5NiUUN3ME6xOUDPxE1? MYmyN|czQTRyMh?=
OVCA432 MVrHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NGfMbmFKSzVyPkG1JO69VQ>? MoXUNlM4Ojl2MEK=
PEA2 M1THUmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MlKwTWM2OD5zNTFOwG0> NYK1NoNuOjN5Mkm0NFI>
SKOV3 NHzXZW1Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M17IWGlEPTB-MUWg{txO MmjRNlM4Ojl2MEK=
C4-2 NUTuTlJPT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= Ml3mNE0{KM7:TR?= M1XuVFE1KGR? M3TOSmROW09? M2O1[oRm[3KnYYPld{Bkd2yxbomgcpVu[mW{IHTvd4Uh\GWyZX7k[Y51dHl? Ml3FNlM2PjV{NES=
PC3 NX\Ye3dwT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MUiwMVMh|ryP M{PqRlE1KGR? Mnr0SG1UVw>? NYnBZXBI\GWlcnXhd4V{KGOxbH;ufUBvfW2kZYKg[I9{\SCmZYDlcoRmdnSueR?= M4\ZfVI{PTZ3MkS0
DU145 NInoTZRIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M4jpN|AuOyEQvF2= M4f4d|E1KGR? M2m0dGROW09? NG\tXI5l\WO{ZXHz[ZMh[2:ub375JI52dWKncjDkc5NmKGSncHXu[IVvfGy7 MonTNlM2PjV{NES=
VCaP  NHj4eIRIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MYGwMVMh|ryP NWDlOVB1OTRiZB?= NYHpNW1GTE2VTx?= M4fh[oRm[3KnYYPld{Bkd2yxbomgcpVu[mW{IHTvd4Uh\GWyZX7k[Y51dHl? Mmi5NlM2PjV{NES=
LNCaP  NXz2OWJST3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NUXXeXNHOC1|IN88US=> Ml;0NVQh\A>? MnvlSG1UVw>? NF;FRZFl\WO{ZXHz[ZMh[2:ub375JI52dWKncjDkc5NmKGSncHXu[IVvfGy7 NX7pSXh5OjN3NkWyOFQ>
MDA-MB-468 MY\D[YxtKF[rYXLpcIl1gSCDc4PhfS=> M37pTmlEPTB;OT63JO69VQ>? NF\DcYYzOjZ5OEG2NS=>
MDA-MB-231 MVfD[YxtKF[rYXLpcIl1gSCDc4PhfS=> NIWyXmdKSzVyPUGzJO69VQ>? Mne5NlI3PzhzNkG=
Cal-51 M1HEdmNmdGxiVnnhZoltcXS7IFHzd4F6 M37TcGlEPTB;OD62JO69VQ>? MVOyNlY4QDF4MR?=

... 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
NCT03694262 Not yet recruiting Endometrial Cancer Medical College of Wisconsin April 1 2019 Phase 2
NCT03694262 Not yet recruiting Endometrial Cancer Medical College of Wisconsin April 1 2019 Phase 2
NCT03840200 Not yet recruiting Breast Cancer|Prostate Cancer|Ovarian Cancer Hoffmann-La Roche March 22 2019 Phase 1|Phase 2
NCT03795272 Not yet recruiting Cervical Cancer Nordic Society for Gynaecologic Oncology|Institute of Cancer Research United Kingdom|Central and Eastern European Oncology Group|North Eastern Germany Society of Gynaecologic Oncology|Belgian Gynaecological Oncology Group|Princess Margaret Hospital Canada|PGOG (Polish Gynaecologic Oncology Group)|GSO Global Clinical Research BV|GCP-enhederne March 1 2019 Phase 2
NCT03639935 Recruiting Biliary Tract Cancer University of Michigan Rogel Cancer Center|Dana-Farber Cancer Institute|Vanderbilt University Medical Center March 2019 Phase 2
NCT03617679 Recruiting Metastatic Endometrial Cancer University of Colorado Denver|Clovis Oncology Inc.|National Cancer Institute (NCI) March 6 2019 Phase 2

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID