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.

  • 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.

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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 MYfGeY5kfGmxbjDBd5NigQ>? MXuwMlEwOS93MECvNVAxOCCwTR?= NV7FbXdXcW6qaXLpeJMhWEGUUDDhZ5Rqfmm2eTDheEB{fGG{dHnu[{Bkd26lZYLueJJifGmxbjDv[kA2ODBibl2= NEGwZ5YzPTF{OES1OS=>
BT474 M3:ycmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NVLSZlZGPTByIH7N MnfZNVDjiJNzNdMg[C=> NUL3[XlkemWmdXPld{Bk\WyuIHfyc5d1cCCrbjD0bIUh\m:3cjDsbY5meyCjbnSgd4lodmmoaXPhcpRtgQ>? M2nJUFI2OTJ6NEW1
SKBR3 MlfRS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MYO1NFAhdk1? MUexNQKBmzF3wrDk NHTx[lVz\WS3Y3XzJINmdGxiZ4Lve5RpKGmwIITo[UBnd3W{IHzpcoV{KGGwZDDzbYdvcW[rY3HueIx6 NIHvUpUzPTF{OES1OS=>
AU565 MUfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NX7qfYo4PTByIH7N MYOxNQKBmzF3wrDk MkHLdoVlfWOnczDj[YxtKGe{b4f0bEBqdiC2aHWg[o92eiCuaX7ld{BidmRic3nncolncWOjboTsfS=> M3zaTVI2OTJ6NEW1
EFM192A M{\i[2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MVG1NFAhdk1? NUHxTJJTOTEkgKOxOeKh\A>? M1PxOZJm\HWlZYOgZ4VtdCCpcn;3eIghcW5idHjlJIZwfXJibHnu[ZMh[W6mIIPp[45q\mmlYX70cJk> M3XDSlI2OTJ6NEW1
MDA-MB-231 MkHmSpVv[3Srb36gRZN{[Xl? NXK5bW1XOTBxMkCvOFAh|ryP Mn3zNlQhcA>? NWTSd2hzcW6lcnXhd4V{KHBvQVvUJIxmfmWuczDpckBiKGSxc3Wt[IVx\W6mZX70JI1idm6nch?= NGLTNlIzPDR{MEG1Ni=>
MDA-MB-231 M1faT2NmdGxiVnnhZoltcXS7IFHzd4F6 MYiwMlEuPDBizszN M17DSVI1KGh? MlvxTWM2OOLCiU5ihKkyPy55N9Mg{txO NIOzS4YzPDR{MEG1Ni=>
MDA-MB-231 NVfZW4JnSXCxcITvd4l{KEG|c3H5 M1nMdlExNzJyL{SwJO69VQ>? MmfiNlQhcA>? MXzpcoR2[2W|IHHwc5B1d3OrczDkc5NmKGSncHXu[IVvfGy7 MoXPNlQ1OjBzNUK=
MDA-MB-231 NHjSUFZIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NXXuSZFUOTBxMkCvOFAh|ryP NFTPUlAzPCCq MVjicI9kc3NiY3XscEBkgWOuZTDwdo9oemW|c3nvckBqdiCJMj;NJJBp[XOn NIP5VI4zPDR{MEG1Ni=>
H460 MkfmS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NH3DUos1ODBibl2= M1TENFI1yqCq M2X2T4lv[3KnYYPld{Bk\WyudXzhdkBz[WSrb4PlcpNqfGm4aYT5 NVfiRo43OjR2MUG2NVE>
A549  MnnsS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M1\0[|QxOCCwTR?= NEX6NIUzPMLiaB?= MVjpcoNz\WG|ZYOgZ4VtdHWuYYKgdoFlcW:|ZX7zbZRqfmm2eR?= M{\NeVI1PDFzNkGx
DT40 MWLHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NF[4WYJKSzVyPUKxJI5O M3HWc|I1OzV4OEGz
DU145 NVfIeHJ[T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M3TvNWlEPTB;MUigcm0> MW[yOFM2PjhzMx?=
COLO704 NGXFbJBIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MX;JR|UxRTJwNUKgxtEhOC54NzFOwG0> NFHEc2EzOzd{OUSwNi=>
OVMANAb NW\2eFdPT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NE\zT29KSzVyPUKuOVghyrFiMD6zPEDPxE1? NXLCW4JDOjN5Mkm0NFI>
OV177 NEfofIRIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NUHXb4F5UUN3ME2yMlc5KMLzIECuO|Eh|ryP MnjJNlM4Ojl2MEK=
OAW28 NX\ic5VET3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MWjJR|UxRTNwNkGgxtEhOC5{ODFOwG0> Mlq0NlM4Ojl2MEK=
OVSAHO M1HwO2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MlLmTWM2OD1|Lk[0JOKyKDBwM{Og{txO MV6yN|czQTRyMh?=
OVKATE MW\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MnTBTWM2OD1|Lk[0JOKyKDFwN{mg{txO NHSwfo8zOzd{OUSwNi=>
OVCAR3 MnztS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NUC2WXJyUUN3ME2zMlc1KMLzIECuOFAh|ryP M1\rW|I{PzJ7NECy
PEO14 NVnQbWE3T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MWjJR|UxRTNwOESgxtEhOC55NjFOwG0> MX[yN|czQTRyMh?=
A2780 M{TU[Gdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MlXCTWM2OD1|Lkm0JOKyKDBwMkWg{txO MWOyN|czQTRyMh?=
OVTOKO Mmr1S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NXTSXYRtUUN3ME20MlE1KMLzIEGuOVMh|ryP MUGyN|czQTRyMh?=
KURAMOCHIb NGHjUXlIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MoHvTWM2OD12LkO0JOKyKDBwMkmg{txO NVPkc2FtOjN5Mkm0NFI>
TOV21G NIiwWJFIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M{e1TWlEPTB;NT6wO{DDuSBzLkOwJO69VQ>? MmKzNlM4Ojl2MEK=
OVISE NV7Pb3hqT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MoPUTWM2OD13Lk[4JOKyKDBwMkOg{txO M2SzOlI{PzJ7NECy
KK M4L4Zmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MoLnTWM2OD14LkG1JOKyKDFwNEKg{txO MWGyN|czQTRyMh?=
RMUGS NG\0NGdIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M2TlNGlEPTB;Nz6wN{DDuSBzLkizJO69VQ>? NWTKN4RROjN5Mkm0NFI>
PEO6 NG\jVldIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M{nGVGlEPTB;Nz6wOkDDuSByLke0JO69VQ>? NIn0c4kzOzd{OUSwNi=>
OVCA429 MmizS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NEG3OHNKSzVyPUiuNlkhyrFiMT62OEDPxE1? MkS4NlM4Ojl2MEK=
OV167 MXHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MUfJR|UxRThwM{OgxtEhOS5zODFOwG0> MmHrNlM4Ojl2MEK=
RMG1 NF;5U2hIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NH;UZXZKSzVyPUmuN|IhyrFiMj6zOkDPxE1? MmDxNlM4Ojl2MEK=
OVCAR5 Mk\LS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M3rWdWlEPTB;OT61NEDDuSB{LkW5JO69VQ>? NF;icIUzOzd{OUSwNi=>
EFO21 MUnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NVPlfYtOUUN3ME25MlkzKMLzIEGuPFch|ryP M{HJNFI{PzJ7NECy
ES2 NXvlSoVMT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NEjobGZKSzVyPUGwMlEzKMLzIEGuNlMh|ryP Mn;ENlM4Ojl2MEK=
Tyk-nu NVr3c|E4T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MlLXTWM2OD1zMD6yNEDDuSBzLkGyJO69VQ>? MnvlNlM4Ojl2MEK=
CAOV3 MXrHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NYTrXpV6UUN3ME2xNE4{PyEEsTCwMlg4KM7:TR?= MkGyNlM4Ojl2MEK=
OV207 MkTSS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NFXzN3RKSzVyPUGyMlI4KMLzIECuN|Ih|ryP NYjiOnZGOjN5Mkm0NFI>
HEY NYXBd49WT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MkjvTWM2OD1zMz6wNUDDuSByLke1JO69VQ>? MV:yN|czQTRyMh?=
DOV13 Ml71S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M2LCRWlEPTB-MUWg{txO NIToRm0zOzd{OUSwNi=>
EFO27 NHTNR3hIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NWXHVWtjUUN3ME6xOUDPxE1? MYOyN|czQTRyMh?=
HEY C2 MlnYS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MlT6TWM2OD5zNTFOwG0> MX6yN|czQTRyMh?=
KOC-7cc MVHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MlHFTWM2OD5zNTFOwG0> M1Lsd|I{PzJ7NECy
MCASb NEm1dpJIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NFni[mtKSzVyPkG1JO69VQ>? M2LDZVI{PzJ7NECy
OAW42 NEiyNoFIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M4PBfWlEPTB-MUWg{txO NFOyVJYzOzd{OUSwNi=>
OV2008 MorzS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NFrvUYRKSzVyPkG1JO69VQ>? M2TiTFI{PzJ7NECy
OV90 MX;Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MoLaTWM2OD5zNTFOwG0> NIjkRXQzOzd{OUSwNi=>
OVCA420b MlLyS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MVTJR|UxRjF3IN88US=> M{H1SVI{PzJ7NECy
OVCA432 NYL3[FNtT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NUjTbWlUUUN3ME6xOUDPxE1? NUX2ZnVROjN5Mkm0NFI>
PEA2 M1TxT2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MmG0TWM2OD5zNTFOwG0> NHzPcVAzOzd{OUSwNi=>
SKOV3 MnXSS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NEPqc5VKSzVyPkG1JO69VQ>? MnfBNlM4Ojl2MEK=
TOV112D Mk\6S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M3PCSFAuOyEQvF2= M37RWmlEPTB-MUWg{txO M1HOdVI{PzJ7NECy
C4-2 NWSwdGR2T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NYPRc5h4OC1|IN88US=> NH6xVlAyPCCm M{j1SmROW09? MlvV[IVkemWjc3XzJINwdG:weTDueY1j\XJiZH;z[UBl\XCnbnTlcpRtgQ>? MYGyN|U3PTJ2NB?=
PC3 MUHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MWmwMVMh|ryP MXexOEBl NH\kNJJFVVOR NVnlToFq\GWlcnXhd4V{KGOxbH;ufUBvfW2kZYKg[I9{\SCmZYDlcoRmdnSueR?= Ml7MNlM2PjV{NES=
DU145 NELxe4dIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MUmwMVMh|ryP NE[yfVMyPCCm MnO0SG1UVw>? MVnk[YNz\WG|ZYOgZ49td267IH71cYJmeiCmb4PlJIRmeGWwZHXueIx6 M2DCU|I{PTZ3MkS0
VCaP  MWjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MkjvNE0{KM7:TR?= MojwNVQh\A>? NGez[2VFVVOR NVzIc3VK\GWlcnXhd4V{KGOxbH;ufUBvfW2kZYKg[I9{\SCmZYDlcoRmdnSueR?= NVfSZWpZOjN3NkWyOFQ>
LNCaP  M{D4Nmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MljONE0{KM7:TR?= Moq5NVQh\A>? NIXuZ45FVVOR NEjnUZpl\WO{ZXHz[ZMh[2:ub375JI52dWKncjDkc5NmKGSncHXu[IVvfGy7 MWqyN|U3PTJ2NB?=
MDA-MB-468 NVnqR4N7S2WubDDWbYFjcWyrdImgRZN{[Xl? NX64ZmFNUUN3ME25Mlch|ryP NILYV|MzOjZ5OEG2NS=>
MDA-MB-231 M3LvbmNmdGxiVnnhZoltcXS7IFHzd4F6 MWfJR|UxRTF|IN88US=> MVqyNlY4QDF4MR?=
Cal-51 M2\JO2NmdGxiVnnhZoltcXS7IFHzd4F6 NIrCbppKSzVyPUiuOkDPxE1? NF;zO|QzOjZ5OEG2NS=>

... 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:
2% DMSO+30% PEG 300+2% Tween 80+ddH2O
10mg/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
in solvent
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