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.

Purity & Quality Control

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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.
Targets
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 MlqwSpVv[3Srb36gRZN{[Xl? MVGwMlEwOS93MECvNVAxOCCwTR?= MWHpcohq[mm2czDQRXJRKGGldHn2bZR6KGG2IIP0ZZJ1cW6pIHPvcoNmem62cnH0bY9vKG:oIEWwNEBvVQ>? NXnjfXhDOjVzMki0OVU>
BT474 M3LYUGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NFr3SFU2ODBibl2= M1jYOFEx6oDVMUZCpIQ> Ml6zdoVlfWOnczDj[YxtKGe{b4f0bEBqdiC2aHWg[o92eiCuaX7ld{BidmRic3nncolncWOjboTsfS=> M4PYeVI2OTJ6NEW1
SKBR3 MoHMS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NWLVd5BTPTByIH7N NG\tb4IyOOLCk{G1xsBl MXzy[YR2[2W|IHPlcIwh\3Kxd4ToJIlvKHSqZTDmc5VzKGyrbnXzJIFv\CC|aXfubYZq[2GwdHz5 MlKyNlUyOjh2NUW=
AU565 NV;Hb|B7T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MX61NFAhdk1? NH\1OFcyOOLCk{G1xsBl MULy[YR2[2W|IHPlcIwh\3Kxd4ToJIlvKHSqZTDmc5VzKGyrbnXzJIFv\CC|aXfubYZq[2GwdHz5 M{LlOVI2OTJ6NEW1
EFM192A NVvoXJRrT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MYm1NFAhdk1? NWXBd3dQOTEkgKOxOeKh\A>? MWfy[YR2[2W|IHPlcIwh\3Kxd4ToJIlvKHSqZTDmc5VzKGyrbnXzJIFv\CC|aXfubYZq[2GwdHz5 MWOyOVEzQDR3NR?=
MDA-MB-231 NI\yXVNHfW6ldHnvckBCe3OjeR?= NIT5V2cyOC9{MD:0NEDPxE1? NWSxdFlzOjRiaB?= NImzW4JqdmO{ZXHz[ZMheC2DS2SgcIV3\Wy|IHnuJIEh\G:|ZT3k[ZBmdmSnboSgcYFvdmW{ MYSyOFQzODF3Mh?=
MDA-MB-231 NFjUbFJE\WyuIG\pZYJqdGm2eTDBd5NigQ>? M1j4UVAvOS12MDFOwG0> NH;FNmczPCCq MnO1TWM2OOLCiU5ihKkyPy55N9Mg{txO NIjZXoEzPDR{MEG1Ni=>
MDA-MB-231 MUfBdI9xfG:|aYOgRZN{[Xl? MXexNE8zOC92MDFOwG0> MorFNlQhcA>? MUjpcoR2[2W|IHHwc5B1d3OrczDkc5NmKGSncHXu[IVvfGy7 NU\id|dbOjR2MkCxOVI>
MDA-MB-231 NGHxfW9Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MWOxNE8zOC92MDFOwG0> MWSyOEBp NFS4T2tjdG:la4OgZ4VtdCCleXPs[UBxem:pcnXzd4lwdiCrbjDHNk9OKHCqYYPl NYroPZJkOjR2MkCxOVI>
H460 MVzHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MlHZOFAxKG6P M37rN|I1yqCq NUPOd5BDcW6lcnXhd4V{KGOnbHz1cIFzKHKjZHnvd4Vve2m2aY\peJk> NWizS3RMOjR2MUG2NVE>
A549  MnrHS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MnnhOFAxKG6P NV\sdpJ7OjUEoHi= MonHbY5kemWjc3XzJINmdGy3bHHyJJJi\Gmxc3Xud4l1cX[rdIm= NX\KWXRFOjR2MUG2NVE>
DT40 MUfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NITTZo1KSzVyPUKxJI5O MnLSNlQ{PTZ6MUO=
DU145 NUjxb4V4T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MV;JR|UxRTF6IH7N NV;yO3Z1OjR|NU[4NVM>
COLO704 Mom2S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NW\nSlNUUUN3ME2yMlUzKMLzIECuOlch|ryP MnLTNlM4Ojl2MEK=
OVMANAb MWDHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MUfJR|UxRTJwNUigxtEhOC5|ODFOwG0> MWOyN|czQTRyMh?=
OV177 M{XUdGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NFTNOVRKSzVyPUKuO|ghyrFiMD63NUDPxE1? NEnYXGUzOzd{OUSwNi=>
OAW28 M{[yeWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MVHJR|UxRTNwNkGgxtEhOC5{ODFOwG0> M1zJRVI{PzJ7NECy
OVSAHO NVy1dWhsT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MlOwTWM2OD1|Lk[0JOKyKDBwM{Og{txO M{W0[VI{PzJ7NECy
OVKATE MXPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M1zO[GlEPTB;Mz62OEDDuSBzLke5JO69VQ>? M{ex[VI{PzJ7NECy
OVCAR3 NX;oXlBPT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NFHrXIVKSzVyPUOuO|QhyrFiMD60NEDPxE1? NInYZ5ozOzd{OUSwNi=>
PEO14 MYXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M4\ZRWlEPTB;Mz64OEDDuSByLke2JO69VQ>? NIXvfIszOzd{OUSwNi=>
A2780 MorJS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M4PVXWlEPTB;Mz65OEDDuSByLkK1JO69VQ>? Ml\FNlM4Ojl2MEK=
OVTOKO MoCwS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MV\JR|UxRTRwMUSgxtEhOS53MzFOwG0> M2e0RlI{PzJ7NECy
KURAMOCHIb NVnIWZZGT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M17YVmlEPTB;ND6zOEDDuSByLkK5JO69VQ>? MnLsNlM4Ojl2MEK=
TOV21G MoPWS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NYrJNIl7UUN3ME21MlA4KMLzIEGuN|Ah|ryP M4TOWVI{PzJ7NECy
OVISE NUDXcYhrT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M4X3WWlEPTB;NT62PEDDuSByLkKzJO69VQ>? NGflcG0zOzd{OUSwNi=>
KK NEXBSIJIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MXHJR|UxRTZwMUWgxtEhOS52MjFOwG0> MYOyN|czQTRyMh?=
RMUGS MYrHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M2TsVGlEPTB;Nz6wN{DDuSBzLkizJO69VQ>? NInNc2ozOzd{OUSwNi=>
PEO6 NGfWWJBIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M1rnWWlEPTB;Nz6wOkDDuSByLke0JO69VQ>? NHHxSWYzOzd{OUSwNi=>
OVCA429 MWTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NEHZR41KSzVyPUiuNlkhyrFiMT62OEDPxE1? NF3t[5MzOzd{OUSwNi=>
OV167 MmnOS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MlHUTWM2OD16LkOzJOKyKDFwMUig{txO NGPQbWMzOzd{OUSwNi=>
RMG1 M1vubWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 Mne1TWM2OD17LkOyJOKyKDJwM{[g{txO MX:yN|czQTRyMh?=
OVCAR5 NYHqPXBDT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M4DE[GlEPTB;OT61NEDDuSB{LkW5JO69VQ>? M1T3elI{PzJ7NECy
EFO21 MlfOS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MUPJR|UxRTlwOUKgxtEhOS56NzFOwG0> NVfEOVNjOjN5Mkm0NFI>
ES2 MnO3S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M1yxXGlEPTB;MUCuNVIhyrFiMT6yN{DPxE1? Mn\6NlM4Ojl2MEK=
Tyk-nu M36zOGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NW\abHVGUUN3ME2xNE4zOCEEsTCxMlEzKM7:TR?= M2jnRlI{PzJ7NECy
CAOV3 NELpTI9Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= Mme2TWM2OD1zMD6zO{DDuSByLki3JO69VQ>? MoOyNlM4Ojl2MEK=
OV207 MXrHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NXPZRpZlUUN3ME2xNk4zPyEEsTCwMlMzKM7:TR?= NFzBXI8zOzd{OUSwNi=>
HEY MXnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MX\JR|UxRTF|LkCxJOKyKDBwN{Wg{txO NV7aTlMxOjN5Mkm0NFI>
DOV13 MlTBS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MVTJR|UxRjF3IN88US=> MoPxNlM4Ojl2MEK=
EFO27 NHr4NpRIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= Mn;VTWM2OD5zNTFOwG0> NGOxNWozOzd{OUSwNi=>
HEY C2 NH;xbHRIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NV\QXVF3UUN3ME6xOUDPxE1? Mo\GNlM4Ojl2MEK=
KOC-7cc MVXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M1LnNWlEPTB-MUWg{txO M3yxbFI{PzJ7NECy
MCASb M1mxd2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MV\JR|UxRjF3IN88US=> NHjYbWszOzd{OUSwNi=>
OAW42 MWrHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NWPmd3UzUUN3ME6xOUDPxE1? NYmyfJdTOjN5Mkm0NFI>
OV2008 NF\0RYhIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MVjJR|UxRjF3IN88US=> NHXnXnYzOzd{OUSwNi=>
OV90 NV3td2FpT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NWnEb5RKUUN3ME6xOUDPxE1? NWSzUZppOjN5Mkm0NFI>
OVCA420b MVjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NEjzUpZKSzVyPkG1JO69VQ>? MnPBNlM4Ojl2MEK=
OVCA432 NYPXOnZKT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MVPJR|UxRjF3IN88US=> M1Pqb|I{PzJ7NECy
PEA2 MVnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NYLpWXBrUUN3ME6xOUDPxE1? MkDRNlM4Ojl2MEK=
SKOV3 M{LIXmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MWHJR|UxRjF3IN88US=> NYG5UJlvOjN5Mkm0NFI>
TOV112D MkTRS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M3jVNFAuOyEQvF2= NIm0SXVKSzVyPkG1JO69VQ>? NWeyUllGOjN5Mkm0NFI>
C4-2 MVzHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MojpNE0{KM7:TR?= MV[xOEBl NGPNTopFVVOR NVSyTWN3\GWlcnXhd4V{KGOxbH;ufUBvfW2kZYKg[I9{\SCmZYDlcoRmdnSueR?= NXjjWFVwOjN3NkWyOFQ>
PC3 M4fFdWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NW\nT3NEOC1|IN88US=> MnLONVQh\A>? NXP5VmFNTE2VTx?= MXPk[YNz\WG|ZYOgZ49td267IH71cYJmeiCmb4PlJIRmeGWwZHXueIx6 NFvZeoQzOzV4NUK0OC=>
DU145 NHfNfo5Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MXSwMVMh|ryP NUDNXYgzOTRiZB?= NHzrdmZFVVOR NITqbI5l\WO{ZXHz[ZMh[2:ub375JI52dWKncjDkc5NmKGSncHXu[IVvfGy7 NUjwb2Y{OjN3NkWyOFQ>
VCaP  MkL6S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NXPrbWx3OC1|IN88US=> M2XPNlE1KGR? NXjUd4lFTE2VTx?= MYHk[YNz\WG|ZYOgZ49td267IH71cYJmeiCmb4PlJIRmeGWwZHXueIx6 NVHpUXhKOjN3NkWyOFQ>
LNCaP  MUTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NXLFT492OC1|IN88US=> NHrBWIoyPCCm M1jvUmROW09? NWXubGRD\GWlcnXhd4V{KGOxbH;ufUBvfW2kZYKg[I9{\SCmZYDlcoRmdnSueR?= NWLMXZJtOjN3NkWyOFQ>
MDA-MB-468 Mn\ER4VtdCCYaXHibYxqfHliQYPzZZk> M1WwbmlEPTB;OT63JO69VQ>? M1yzeVIzPjd6MU[x
MDA-MB-231 NHfCZVdE\WyuIG\pZYJqdGm2eTDBd5NigQ>? M{PKcWlEPTB;MUOg{txO NVnlXo9XOjJ4N{ixOlE>
Cal-51 M1flZmNmdGxiVnnhZoltcXS7IFHzd4F6 NEHOXZhKSzVyPUiuOkDPxE1? Ml3zNlI3PzhzNkG=

... 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]

Protocol

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 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
Formula

C19H18FN3O.H3PO4

CAS No. 459868-92-9
Storage powder
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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Answers to questions you may have can be found in the inhibitor handling instructions. Topics include how to prepare stock solutions, how to store inhibitors, and issues that need special attention for cell-based assays and animal experiments.

Handling Instructions

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID