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 Mnf6SpVv[3Srb36gRZN{[Xl? NWLCfYtCOC5zL{GvOVAxNzFyMECgcm0> MWjpcohq[mm2czDQRXJRKGGldHn2bZR6KGG2IIP0ZZJ1cW6pIHPvcoNmem62cnH0bY9vKG:oIEWwNEBvVQ>? MVWyOVEzQDR3NR?=
BT474 MmfRS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M1TpN|UxOCCwTR?= Ml7RNVDjiJNzNdMg[C=> Ml35doVlfWOnczDj[YxtKGe{b4f0bEBqdiC2aHWg[o92eiCuaX7ld{BidmRic3nncolncWOjboTsfS=> NUPzOVhNOjVzMki0OVU>
SKBR3 NUPXS4tRT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M3XrWlUxOCCwTR?= M1z6c|Ex6oDVMUZCpIQ> NWr5O4ZVemWmdXPld{Bk\WyuIHfyc5d1cCCrbjD0bIUh\m:3cjDsbY5meyCjbnSgd4lodmmoaXPhcpRtgQ>? NXu2XHg5OjVzMki0OVU>
AU565 M1f1d2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MUG1NFAhdk1? NUfVdGRkOTEkgKOxOeKh\A>? MXXy[YR2[2W|IHPlcIwh\3Kxd4ToJIlvKHSqZTDmc5VzKGyrbnXzJIFv\CC|aXfubYZq[2GwdHz5 MnrvNlUyOjh2NUW=
EFM192A M4faeWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M1;IU|UxOCCwTR?= MkPvNVDjiJNzNdMg[C=> M1e4RpJm\HWlZYOgZ4VtdCCpcn;3eIghcW5idHjlJIZwfXJibHnu[ZMh[W6mIIPp[45q\mmlYX70cJk> NEHwPIgzPTF{OES1OS=>
MDA-MB-231 MWHGeY5kfGmxbjDBd5NigQ>? MofQNVAwOjBxNECg{txO NEn0R2kzPCCq M{XUV4lv[3KnYYPld{BxNUGNVDDs[ZZmdHNiaX6gZUBld3OnLXTldIVv\GWwdDDtZY5v\XJ? M{f0OVI1PDJyMUWy
MDA-MB-231 Mn;UR4VtdCCYaXHibYxqfHliQYPzZZk> M3nqSlAvOS12MDFOwG0> MmKyNlQhcA>? MX3JR|Ux6oDLPfMAjVE4Njd5wrFOwG0> M{jmVVI1PDJyMUWy
MDA-MB-231 NGH3Wo1CeG:ydH;zbZMhSXO|YYm= NIr4NVgyOC9{MD:0NEDPxE1? M{L5bVI1KGh? NEjMNWtqdmS3Y3XzJIFxd3C2b4Ppd{Bld3OnIHTldIVv\GWwdHz5 MWmyOFQzODF3Mh?=
MDA-MB-231 MlriS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M1fkOlExNzJyL{SwJO69VQ>? NUL5SGhjOjRiaB?= MlPiZoxw[2u|IHPlcIwh[3mlbHWgdJJw\3Knc4Ppc44hcW5iR{KvUUBxcGG|ZR?= NF7ZcFAzPDR{MEG1Ni=>
H460 NWfJe5hpT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M{n0SVQxOCCwTR?= NUezc|g{OjUEoHi= M4rncYlv[3KnYYPld{Bk\WyudXzhdkBz[WSrb4PlcpNqfGm4aYT5 MWGyOFQyOTZzMR?=
A549  NXHjcHBQT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NGrLeXc1ODBibl2= NWficmY5OjUEoHi= NEXGb2hqdmO{ZXHz[ZMh[2WubIXsZZIhemGmaX;z[Y5{cXSrdnn0fS=> MnixNlQ1OTF4MUG=
DT40 NGHKRXhIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NFXTR3NKSzVyPUKxJI5O MWOyOFM2PjhzMx?=
DU145 MnvwS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MXfJR|UxRTF6IH7N MknTNlQ{PTZ6MUO=
COLO704 NG\xN|JIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NFTNc3dKSzVyPUKuOVIhyrFiMD62O{DPxE1? NULoT4w6OjN5Mkm0NFI>
OVMANAb M{jSXGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M4rNWWlEPTB;Mj61PEDDuSByLkO4JO69VQ>? MnfFNlM4Ojl2MEK=
OV177 NFu4T25Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NWTlW2tKUUN3ME2yMlc5KMLzIECuO|Eh|ryP MlHGNlM4Ojl2MEK=
OAW28 MULHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NGfhNZFKSzVyPUOuOlEhyrFiMD6yPEDPxE1? MoPpNlM4Ojl2MEK=
OVSAHO NGf3V4NIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MWXJR|UxRTNwNkSgxtEhOC5|MzFOwG0> M1;STlI{PzJ7NECy
OVKATE MVXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MUDJR|UxRTNwNkSgxtEhOS55OTFOwG0> MlewNlM4Ojl2MEK=
OVCAR3 NX;oZotPT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NFXJRnBKSzVyPUOuO|QhyrFiMD60NEDPxE1? NGn5eFIzOzd{OUSwNi=>
PEO14 M{LKcGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NV[zdos4UUN3ME2zMlg1KMLzIECuO|Yh|ryP M1:2V|I{PzJ7NECy
A2780 NHLBZWlIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NHPMSHRKSzVyPUOuPVQhyrFiMD6yOUDPxE1? NGrXVGozOzd{OUSwNi=>
OVTOKO M2LWN2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 Mn\JTWM2OD12LkG0JOKyKDFwNUOg{txO MVqyN|czQTRyMh?=
KURAMOCHIb Mn\0S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NXHydJFnUUN3ME20MlM1KMLzIECuNlkh|ryP MorTNlM4Ojl2MEK=
TOV21G M{XwNGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NUTqbXJNUUN3ME21MlA4KMLzIEGuN|Ah|ryP MoH2NlM4Ojl2MEK=
OVISE NGLRfmtIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NF6zeoxKSzVyPUWuOlghyrFiMD6yN{DPxE1? M2jzSVI{PzJ7NECy
KK MnzhS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NHvTOYZKSzVyPU[uNVUhyrFiMT60NkDPxE1? MkDGNlM4Ojl2MEK=
RMUGS NV3HZZZmT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NVf3cmoxUUN3ME23MlA{KMLzIEGuPFMh|ryP NVXWTGFNOjN5Mkm0NFI>
PEO6 MofkS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MmjPTWM2OD15LkC2JOKyKDBwN{Sg{txO Mn7qNlM4Ojl2MEK=
OVCA429 NHvYU29Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MmLBTWM2OD16LkK5JOKyKDFwNkSg{txO Mn\hNlM4Ojl2MEK=
OV167 NHfpfWVIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M4HB[GlEPTB;OD6zN{DDuSBzLkG4JO69VQ>? MlXjNlM4Ojl2MEK=
RMG1 M3\rWWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MW\JR|UxRTlwM{KgxtEhOi5|NjFOwG0> NXLzcHFIOjN5Mkm0NFI>
OVCAR5 M2PE[mdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NF36VGJKSzVyPUmuOVAhyrFiMj61PUDPxE1? M{TWW|I{PzJ7NECy
EFO21 NFjpOZNIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M4PmRmlEPTB;OT65NkDDuSBzLki3JO69VQ>? MmTQNlM4Ojl2MEK=
ES2 NFmxOHdIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M1\zcGlEPTB;MUCuNVIhyrFiMT6yN{DPxE1? MnnyNlM4Ojl2MEK=
Tyk-nu MVTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MU\JR|UxRTFyLkKwJOKyKDFwMUKg{txO NYO3NmF[OjN5Mkm0NFI>
CAOV3 NYPIc2NST3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NXnKTnZDUUN3ME2xNE4{PyEEsTCwMlg4KM7:TR?= NFq3W40zOzd{OUSwNi=>
OV207 NYDxSXBlT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MnuyTWM2OD1zMj6yO{DDuSByLkOyJO69VQ>? MkjBNlM4Ojl2MEK=
HEY MX\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MnLWTWM2OD1zMz6wNUDDuSByLke1JO69VQ>? NIX1RY4zOzd{OUSwNi=>
DOV13 MlPVS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NYrLZYh4UUN3ME6xOUDPxE1? MmDRNlM4Ojl2MEK=
EFO27 M4fTcGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MWDJR|UxRjF3IN88US=> MXOyN|czQTRyMh?=
HEY C2 MVPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NV3aZZdYUUN3ME6xOUDPxE1? M3nDRlI{PzJ7NECy
KOC-7cc NGLLVGpIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NGfzNJlKSzVyPkG1JO69VQ>? NWfNPY14OjN5Mkm0NFI>
MCASb Ml:wS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MY\JR|UxRjF3IN88US=> M4T4[FI{PzJ7NECy
OAW42 NFTxWXpIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MkGyTWM2OD5zNTFOwG0> MXiyN|czQTRyMh?=
OV2008 MV3Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NE\Wb2xKSzVyPkG1JO69VQ>? MWeyN|czQTRyMh?=
OV90 NV7TWFRNT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M3T3R2lEPTB-MUWg{txO MkThNlM4Ojl2MEK=
OVCA420b MXvHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MXjJR|UxRjF3IN88US=> M2PG[lI{PzJ7NECy
OVCA432 NF7zc3JIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MYPJR|UxRjF3IN88US=> MU[yN|czQTRyMh?=
PEA2 MVfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MmjkTWM2OD5zNTFOwG0> MnvZNlM4Ojl2MEK=
SKOV3 NILBbI9Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MmG4TWM2OD5zNTFOwG0> M{fUd|I{PzJ7NECy
TOV112D NE\lZldIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MnzzNE0{KM7:TR?= NFLV[olKSzVyPkG1JO69VQ>? NHXL[nkzOzd{OUSwNi=>
C4-2 MojFS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NVj6PWFzOC1|IN88US=> MUexOEBl MoW3SG1UVw>? M3HlbIRm[3KnYYPld{Bkd2yxbomgcpVu[mW{IHTvd4Uh\GWyZX7k[Y51dHl? MUiyN|U3PTJ2NB?=
PC3 NH\nVZBIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NF7NOlgxNTNizszN NVrMfGZFOTRiZB?= NVe3RnJJTE2VTx?= MkD4[IVkemWjc3XzJINwdG:weTDueY1j\XJiZH;z[UBl\XCnbnTlcpRtgQ>? M1HPWVI{PTZ3MkS0
DU145 MVrHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MVmwMVMh|ryP MWexOEBl MmjHSG1UVw>? M3jRb4Rm[3KnYYPld{Bkd2yxbomgcpVu[mW{IHTvd4Uh\GWyZX7k[Y51dHl? M2PRflI{PTZ3MkS0
VCaP  NUeyTXVHT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NXjLbWRHOC1|IN88US=> NYDXN5FvOTRiZB?= MYXEUXNQ M4CyXIRm[3KnYYPld{Bkd2yxbomgcpVu[mW{IHTvd4Uh\GWyZX7k[Y51dHl? NHf2bWszOzV4NUK0OC=>
LNCaP  MXnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NYLERpRTOC1|IN88US=> NEOzTnMyPCCm M13GbmROW09? NFzZO4Vl\WO{ZXHz[ZMh[2:ub375JI52dWKncjDkc5NmKGSncHXu[IVvfGy7 MXiyN|U3PTJ2NB?=
MDA-MB-468 MlvUR4VtdCCYaXHibYxqfHliQYPzZZk> NXTidpZ2UUN3ME25Mlch|ryP MYGyNlY4QDF4MR?=
MDA-MB-231 MWPD[YxtKF[rYXLpcIl1gSCDc4PhfS=> MWjJR|UxRTF|IN88US=> MYGyNlY4QDF4MR?=
Cal-51 MVnD[YxtKF[rYXLpcIl1gSCDc4PhfS=> M4D0cGlEPTB;OD62JO69VQ>? NYrROYVVOjJ4N{ixOlE>

... 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 to the product individually and in order:
2% DMSO+30% PEG 300+2% Tween 80+ddH2O
For best results, use promptly after mixing.
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
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