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.

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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 NEm2TJdHfW6ldHnvckBCe3OjeR?= M4n3VlAvOS9zL{WwNE8yODByIH7N NW\WUIxGcW6qaXLpeJMhWEGUUDDhZ5Rqfmm2eTDheEB{fGG{dHnu[{Bkd26lZYLueJJifGmxbjDv[kA2ODBibl2= M3K1dVI2OTJ6NEW1
BT474 Ml76S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NIjpdI82ODBibl2= MnrINVDjiJNzNdMg[C=> NH6xTJdz\WS3Y3XzJINmdGxiZ4Lve5RpKGmwIITo[UBnd3W{IHzpcoV{KGGwZDDzbYdvcW[rY3HueIx6 NVizbpNkOjVzMki0OVU>
SKBR3 NVe3XIxFT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MoD5OVAxKG6P NFHx[pcyOOLCk{G1xsBl NEHwcWVz\WS3Y3XzJINmdGxiZ4Lve5RpKGmwIITo[UBnd3W{IHzpcoV{KGGwZDDzbYdvcW[rY3HueIx6 NFnzV4wzPTF{OES1OS=>
AU565 NWTGfms2T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NV3QeJJmPTByIH7N MmXVNVDjiJNzNdMg[C=> MUfy[YR2[2W|IHPlcIwh\3Kxd4ToJIlvKHSqZTDmc5VzKGyrbnXzJIFv\CC|aXfubYZq[2GwdHz5 MVOyOVEzQDR3NR?=
EFM192A M3j5XWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M3jUfVUxOCCwTR?= NVjLfHJYOTEkgKOxOeKh\A>? MkHGdoVlfWOnczDj[YxtKGe{b4f0bEBqdiC2aHWg[o92eiCuaX7ld{BidmRic3nncolncWOjboTsfS=> NEO0b2UzPTF{OES1OS=>
MDA-MB-231 NHPBTYlHfW6ldHnvckBCe3OjeR?= MXWxNE8zOC92MDFOwG0> MYeyOEBp MmmzbY5kemWjc3XzJJAuSUuWIHzleoVteyCrbjDhJIRwe2VvZHXw[Y5l\W62IH3hco5meg>? NVnsXWtxOjR2MkCxOVI>
MDA-MB-231 M1P5dmNmdGxiVnnhZoltcXS7IFHzd4F6 NYLSSVFTOC5zLUSwJO69VQ>? NIfUU3YzPCCq NV\ZSZg5UUN3MPMAjV3jiIlzNz63O:Kh|ryP MV[yOFQzODF3Mh?=
MDA-MB-231 MXXBdI9xfG:|aYOgRZN{[Xl? MoC4NVAwOjBxNECg{txO Ml7iNlQhcA>? MXXpcoR2[2W|IHHwc5B1d3OrczDkc5NmKGSncHXu[IVvfGy7 NHTKPXozPDR{MEG1Ni=>
MDA-MB-231 M1\nb2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MWqxNE8zOC92MDFOwG0> NYLFU2t6OjRiaB?= NHS5RppjdG:la4OgZ4VtdCCleXPs[UBxem:pcnXzd4lwdiCrbjDHNk9OKHCqYYPl MWOyOFQzODF3Mh?=
H460 NWDtOYlKT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MYW0NFAhdk1? NVHCfZdwOjUEoHi= NWHMVFg6cW6lcnXhd4V{KGOnbHz1cIFzKHKjZHnvd4Vve2m2aY\peJk> NWHGc3pqOjR2MUG2NVE>
A549  NXPBXI5uT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NVHuZ3Z5PDByIH7N Mnv3NlTDqGh? MWTpcoNz\WG|ZYOgZ4VtdHWuYYKgdoFlcW:|ZX7zbZRqfmm2eR?= NGPHTmIzPDRzMU[xNS=>
DT40 NHXReJRIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NX35dlR5UUN3ME2yNUBvVQ>? NYjQcW81OjR|NU[4NVM>
DU145 Mnz3S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NH3UN49KSzVyPUG4JI5O MVGyOFM2PjhzMx?=
COLO704 NGXjWZlIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MnTJTWM2OD1{LkWyJOKyKDBwNkeg{txO M2D0O|I{PzJ7NECy
OVMANAb MkjLS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NYP6cGZ6UUN3ME2yMlU5KMLzIECuN|gh|ryP M1\VcFI{PzJ7NECy
OV177 MkPMS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NV61b4JzUUN3ME2yMlc5KMLzIECuO|Eh|ryP MmXmNlM4Ojl2MEK=
OAW28 NFm3Z3lIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NI[1VYNKSzVyPUOuOlEhyrFiMD6yPEDPxE1? MoPpNlM4Ojl2MEK=
OVSAHO MV;Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NG\oVYJKSzVyPUOuOlQhyrFiMD6zN{DPxE1? NVPvTVVJOjN5Mkm0NFI>
OVKATE MXXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M{fndGlEPTB;Mz62OEDDuSBzLke5JO69VQ>? M4XDTVI{PzJ7NECy
OVCAR3 NWfNRlA6T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M{XmNGlEPTB;Mz63OEDDuSByLkSwJO69VQ>? MUmyN|czQTRyMh?=
PEO14 M4T0dmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NXKzRpZTUUN3ME2zMlg1KMLzIECuO|Yh|ryP Mlf3NlM4Ojl2MEK=
A2780 MmTmS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? Mk[3TWM2OD1|Lkm0JOKyKDBwMkWg{txO M2\UV|I{PzJ7NECy
OVTOKO MVvHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MX3JR|UxRTRwMUSgxtEhOS53MzFOwG0> M1:zcFI{PzJ7NECy
KURAMOCHIb NVfpN2ZkT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NYq0UGFUUUN3ME20MlM1KMLzIECuNlkh|ryP NYf2XWptOjN5Mkm0NFI>
TOV21G NEXYXGxIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MVLJR|UxRTVwMEegxtEhOS5|MDFOwG0> M1fWRlI{PzJ7NECy
OVISE Ml3MS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NIfC[G9KSzVyPUWuOlghyrFiMD6yN{DPxE1? MVqyN|czQTRyMh?=
KK NWf0ZYQ1T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NICwVG1KSzVyPU[uNVUhyrFiMT60NkDPxE1? NWnr[GhmOjN5Mkm0NFI>
RMUGS MljPS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MVrJR|UxRTdwMEOgxtEhOS56MzFOwG0> MX6yN|czQTRyMh?=
PEO6 MUXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M4PTc2lEPTB;Nz6wOkDDuSByLke0JO69VQ>? NWSyU2s4OjN5Mkm0NFI>
OVCA429 MX;Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NWr3NpVyUUN3ME24MlI6KMLzIEGuOlQh|ryP NH\lUI8zOzd{OUSwNi=>
OV167 M1;GZ2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NWfuRo5TUUN3ME24MlM{KMLzIEGuNVgh|ryP MkPZNlM4Ojl2MEK=
RMG1 MkXZS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M3qweWlEPTB;OT6zNkDDuSB{LkO2JO69VQ>? NFnURmIzOzd{OUSwNi=>
OVCAR5 NU\SNZNZT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M4DwemlEPTB;OT61NEDDuSB{LkW5JO69VQ>? NV[3fY5MOjN5Mkm0NFI>
EFO21 NWPBNJVCT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M4Dlc2lEPTB;OT65NkDDuSBzLki3JO69VQ>? M{j3OVI{PzJ7NECy
ES2 NHfuV4tIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MkPXTWM2OD1zMD6xNkDDuSBzLkKzJO69VQ>? NVm3PYJXOjN5Mkm0NFI>
Tyk-nu MXLHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M1n5UGlEPTB;MUCuNlAhyrFiMT6xNkDPxE1? M{m2U|I{PzJ7NECy
CAOV3 M{Sy[mdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NVjRWWlLUUN3ME2xNE4{PyEEsTCwMlg4KM7:TR?= MYiyN|czQTRyMh?=
OV207 NIe3WWJIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M4HyZWlEPTB;MUKuNlchyrFiMD6zNkDPxE1? MkC4NlM4Ojl2MEK=
HEY MmjHS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NVLk[4hMUUN3ME2xN{4xOSEEsTCwMlc2KM7:TR?= M1O1UVI{PzJ7NECy
DOV13 NIXke2FIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NELiR3BKSzVyPkG1JO69VQ>? NVPDXGRJOjN5Mkm0NFI>
EFO27 M2TT[Gdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MXPJR|UxRjF3IN88US=> NV3odVF7OjN5Mkm0NFI>
HEY C2 NVj0XmhvT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M1;NTWlEPTB-MUWg{txO MYGyN|czQTRyMh?=
KOC-7cc NW\YZ3hET3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M4THV2lEPTB-MUWg{txO NYjv[FN{OjN5Mkm0NFI>
MCASb MkH4S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M3;YXmlEPTB-MUWg{txO Ml\lNlM4Ojl2MEK=
OAW42 M4K5Smdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MkfoTWM2OD5zNTFOwG0> MXWyN|czQTRyMh?=
OV2008 MY\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NUT2V45PUUN3ME6xOUDPxE1? MV2yN|czQTRyMh?=
OV90 MVLHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NF;vSW9KSzVyPkG1JO69VQ>? NIHiOFczOzd{OUSwNi=>
OVCA420b MXHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NYr4NIVnUUN3ME6xOUDPxE1? NE\JPVAzOzd{OUSwNi=>
OVCA432 MmLKS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MX;JR|UxRjF3IN88US=> MorrNlM4Ojl2MEK=
PEA2 NH\Bb3pIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MWHJR|UxRjF3IN88US=> NFz0bGUzOzd{OUSwNi=>
SKOV3 NW\QSY5{T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MkDTTWM2OD5zNTFOwG0> NWWxVmlNOjN5Mkm0NFI>
TOV112D NET6UlFIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MnHtNE0{KM7:TR?= MX;JR|UxRjF3IN88US=> MWiyN|czQTRyMh?=
C4-2 MmnpS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M3nx[VAuOyEQvF2= MYixOEBl NIfZVHVFVVOR NFjYcYJl\WO{ZXHz[ZMh[2:ub375JI52dWKncjDkc5NmKGSncHXu[IVvfGy7 MlzINlM2PjV{NES=
PC3 NUHaTo9LT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NIL2cXIxNTNizszN M2\ZRlE1KGR? NVmzSItFTE2VTx?= NFXMWJpl\WO{ZXHz[ZMh[2:ub375JI52dWKncjDkc5NmKGSncHXu[IVvfGy7 NVq1W4V[OjN3NkWyOFQ>
DU145 M3\1SGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NHy1cHgxNTNizszN NHLzSJMyPCCm MoDjSG1UVw>? MXjk[YNz\WG|ZYOgZ49td267IH71cYJmeiCmb4PlJIRmeGWwZHXueIx6 NXHuVGlzOjN3NkWyOFQ>
VCaP  M1LBXGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MXiwMVMh|ryP NEXkZZkyPCCm Ml\DSG1UVw>? MoHD[IVkemWjc3XzJINwdG:weTDueY1j\XJiZH;z[UBl\XCnbnTlcpRtgQ>? M4\aO|I{PTZ3MkS0
LNCaP  MlS5S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M3njdlAuOyEQvF2= MkTsNVQh\A>? NX3menIxTE2VTx?= NFHndpBl\WO{ZXHz[ZMh[2:ub375JI52dWKncjDkc5NmKGSncHXu[IVvfGy7 MkHTNlM2PjV{NES=
MDA-MB-468 MULD[YxtKF[rYXLpcIl1gSCDc4PhfS=> MVLJR|UxRTlwNzFOwG0> NEXmVJMzOjZ5OEG2NS=>
MDA-MB-231 NVSxcZpuS2WubDDWbYFjcWyrdImgRZN{[Xl? MXvJR|UxRTF|IN88US=> Mlq4NlI3PzhzNkG=
Cal-51 NWe3VZhvS2WubDDWbYFjcWyrdImgRZN{[Xl? MYHJR|UxRThwNjFOwG0> NWLTdlhrOjJ4N{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(Data is from Selleck tests instead of citations):
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
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

Tech Support

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