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.

  • 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.
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 NFrkOpFHfW6ldHnvckBCe3OjeR?= MVmwMlEwOS93MECvNVAxOCCwTR?= MWXpcohq[mm2czDQRXJRKGGldHn2bZR6KGG2IIP0ZZJ1cW6pIHPvcoNmem62cnH0bY9vKG:oIEWwNEBvVQ>? NVXiZVg4OjVzMki0OVU>
BT474 M3zEcGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NWDrZnpkPTByIH7N NYi3dmxZOTEkgKOxOeKh\A>? MXry[YR2[2W|IHPlcIwh\3Kxd4ToJIlvKHSqZTDmc5VzKGyrbnXzJIFv\CC|aXfubYZq[2GwdHz5 MYmyOVEzQDR3NR?=
SKBR3 M3z6TGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M{D4elUxOCCwTR?= NHHFVosyOOLCk{G1xsBl NVW4b296emWmdXPld{Bk\WyuIHfyc5d1cCCrbjD0bIUh\m:3cjDsbY5meyCjbnSgd4lodmmoaXPhcpRtgQ>? M3vHe|I2OTJ6NEW1
AU565 M1TF[Gdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NUO4Z5I6PTByIH7N NH7xOZEyOOLCk{G1xsBl MX;y[YR2[2W|IHPlcIwh\3Kxd4ToJIlvKHSqZTDmc5VzKGyrbnXzJIFv\CC|aXfubYZq[2GwdHz5 NIHtOIMzPTF{OES1OS=>
EFM192A NIDoUmRIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MYC1NFAhdk1? M13ZdFEx6oDVMUZCpIQ> Mlj0doVlfWOnczDj[YxtKGe{b4f0bEBqdiC2aHWg[o92eiCuaX7ld{BidmRic3nncolncWOjboTsfS=> NGXx[lAzPTF{OES1OS=>
MDA-MB-231 MmPsSpVv[3Srb36gRZN{[Xl? MYKxNE8zOC92MDFOwG0> MVuyOEBp MWrpcoNz\WG|ZYOgdE1CU1RibHX2[Yx{KGmwIHGg[I9{\S2mZYDlcoRmdnRibXHucoVz MUmyOFQzODF3Mh?=
MDA-MB-231 Mm\hR4VtdCCYaXHibYxqfHliQYPzZZk> MU[wMlEuPDBizszN NEXt[IIzPCCq NXjlUIdOUUN3MPMAjV3jiIlzNz63O:Kh|ryP NH30NmUzPDR{MEG1Ni=>
MDA-MB-231 NHnPdIdCeG:ydH;zbZMhSXO|YYm= NYCwenl4OTBxMkCvOFAh|ryP NXr4d4tVOjRiaB?= M2rPNYlv\HWlZYOgZZBweHSxc3nzJIRwe2ViZHXw[Y5l\W62bIm= MWWyOFQzODF3Mh?=
MDA-MB-231 MUjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NGrLV3cyOC9{MD:0NEDPxE1? NWX5fldJOjRiaB?= MnzPZoxw[2u|IHPlcIwh[3mlbHWgdJJw\3Knc4Ppc44hcW5iR{KvUUBxcGG|ZR?= MkHUNlQ1OjBzNUK=
H460 MV7Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MUe0NFAhdk1? NX7iNWh6OjUEoHi= NXq3SVZUcW6lcnXhd4V{KGOnbHz1cIFzKHKjZHnvd4Vve2m2aY\peJk> NVvldVZIOjR2MUG2NVE>
A549  NVjpRolpT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M1vCcVQxOCCwTR?= NEPMW3QzPMLiaB?= NHvFXGJqdmO{ZXHz[ZMh[2WubIXsZZIhemGmaX;z[Y5{cXSrdnn0fS=> M4ryZ|I1PDFzNkGx
DT40 MWjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M3;IOGlEPTB;MkGgcm0> NGO4T5ozPDN3NkixNy=>
DU145 MoPMS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NWOwTHo6UUN3ME2xPEBvVQ>? NIHjV40zPDN3NkixNy=>
COLO704 NYTtUXN4T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NWPMcmRLUUN3ME2yMlUzKMLzIECuOlch|ryP MWCyN|czQTRyMh?=
OVMANAb MWnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NFTMW5RKSzVyPUKuOVghyrFiMD6zPEDPxE1? MlzMNlM4Ojl2MEK=
OV177 NFvCXGJIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MWTJR|UxRTJwN{igxtEhOC55MTFOwG0> M13LbVI{PzJ7NECy
OAW28 NXvldIxpT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MlPsTWM2OD1|Lk[xJOKyKDBwMkig{txO M2n6NVI{PzJ7NECy
OVSAHO M4fTVGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M3jvTGlEPTB;Mz62OEDDuSByLkOzJO69VQ>? NEHyTmgzOzd{OUSwNi=>
OVKATE Ml:3S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MmrMTWM2OD1|Lk[0JOKyKDFwN{mg{txO MUKyN|czQTRyMh?=
OVCAR3 M3\lWWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NHv3e5ZKSzVyPUOuO|QhyrFiMD60NEDPxE1? MkTXNlM4Ojl2MEK=
PEO14 NFux[pRIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NXHvZ5R{UUN3ME2zMlg1KMLzIECuO|Yh|ryP MV[yN|czQTRyMh?=
A2780 MoDCS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MW\JR|UxRTNwOUSgxtEhOC5{NTFOwG0> NWDRRYJkOjN5Mkm0NFI>
OVTOKO NULCbpJCT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NH3MdXpKSzVyPUSuNVQhyrFiMT61N{DPxE1? NHX1TpkzOzd{OUSwNi=>
KURAMOCHIb MXnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MYDJR|UxRTRwM{SgxtEhOC5{OTFOwG0> MoW1NlM4Ojl2MEK=
TOV21G MYXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MXLJR|UxRTVwMEegxtEhOS5|MDFOwG0> Mn7MNlM4Ojl2MEK=
OVISE MYnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MXjJR|UxRTVwNkigxtEhOC5{MzFOwG0> M120S|I{PzJ7NECy
KK NXmx[YdwT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NEPKTmpKSzVyPU[uNVUhyrFiMT60NkDPxE1? MmnpNlM4Ojl2MEK=
RMUGS M1HsUGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NVS5c5BQUUN3ME23MlA{KMLzIEGuPFMh|ryP MkK3NlM4Ojl2MEK=
PEO6 NUXRd|hzT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NYLMOoRPUUN3ME23MlA3KMLzIECuO|Qh|ryP Mki5NlM4Ojl2MEK=
OVCA429 M{DpS2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MnHyTWM2OD16LkK5JOKyKDFwNkSg{txO NVrNS5k6OjN5Mkm0NFI>
OV167 NFfmTYVIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MYfJR|UxRThwM{OgxtEhOS5zODFOwG0> NVy3UZRyOjN5Mkm0NFI>
RMG1 NWrHT3hUT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NGnCT|NKSzVyPUmuN|IhyrFiMj6zOkDPxE1? MVeyN|czQTRyMh?=
OVCAR5 NEfuWY5Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MXHJR|UxRTlwNUCgxtEhOi53OTFOwG0> NIK3UHozOzd{OUSwNi=>
EFO21 MljDS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NV;VUHJ7UUN3ME25MlkzKMLzIEGuPFch|ryP MonENlM4Ojl2MEK=
ES2 M2THXWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MlLBTWM2OD1zMD6xNkDDuSBzLkKzJO69VQ>? MYSyN|czQTRyMh?=
Tyk-nu MUHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MoDGTWM2OD1zMD6yNEDDuSBzLkGyJO69VQ>? M1jvVlI{PzJ7NECy
CAOV3 M4DNbWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MYHJR|UxRTFyLkO3JOKyKDBwOEeg{txO Mkn6NlM4Ojl2MEK=
OV207 MYrHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M2Hae2lEPTB;MUKuNlchyrFiMD6zNkDPxE1? MmfqNlM4Ojl2MEK=
HEY MWjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NH7RZ4pKSzVyPUGzMlAyKMLzIECuO|Uh|ryP MVWyN|czQTRyMh?=
DOV13 NH7w[nRIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NHr3O|ZKSzVyPkG1JO69VQ>? NFjLVIIzOzd{OUSwNi=>
EFO27 NY\yc3lrT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NILLXJNKSzVyPkG1JO69VQ>? MXSyN|czQTRyMh?=
HEY C2 MXXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MlHhTWM2OD5zNTFOwG0> NF7F[WgzOzd{OUSwNi=>
KOC-7cc NF;rcIZIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MYrJR|UxRjF3IN88US=> MYSyN|czQTRyMh?=
MCASb MljUS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MWTJR|UxRjF3IN88US=> NGP6e5MzOzd{OUSwNi=>
OAW42 Mm\VS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? Mm\WTWM2OD5zNTFOwG0> NXPQNIwxOjN5Mkm0NFI>
OV2008 MXfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M3PJ[GlEPTB-MUWg{txO MWOyN|czQTRyMh?=
OV90 MnTUS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NF3SRmFKSzVyPkG1JO69VQ>? NGLGSIozOzd{OUSwNi=>
OVCA420b MkXIS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NHv6XWZKSzVyPkG1JO69VQ>? M2DCeFI{PzJ7NECy
OVCA432 M1:4PGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NU\1SoNTUUN3ME6xOUDPxE1? MXSyN|czQTRyMh?=
PEA2 NYK4NY5DT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M13p[GlEPTB-MUWg{txO MoHUNlM4Ojl2MEK=
SKOV3 MWrHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NF7OPGFKSzVyPkG1JO69VQ>? NYDqZmZzOjN5Mkm0NFI>
TOV112D MlT6S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MUewMVMh|ryP M{nhWWlEPTB-MUWg{txO MVGyN|czQTRyMh?=
C4-2 M2HtZmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NHm2ZY4xNTNizszN NW[2fllqOTRiZB?= MoDxSG1UVw>? NFjhWWFl\WO{ZXHz[ZMh[2:ub375JI52dWKncjDkc5NmKGSncHXu[IVvfGy7 M3[1e|I{PTZ3MkS0
PC3 NHO4WGZIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M2\ieVAuOyEQvF2= MmG3NVQh\A>? MXfEUXNQ NVXWeYJZ\GWlcnXhd4V{KGOxbH;ufUBvfW2kZYKg[I9{\SCmZYDlcoRmdnSueR?= MVWyN|U3PTJ2NB?=
DU145 M{Hy[mdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NV62[5pYOC1|IN88US=> NGj3bXgyPCCm MnLPSG1UVw>? MWPk[YNz\WG|ZYOgZ49td267IH71cYJmeiCmb4PlJIRmeGWwZHXueIx6 MX:yN|U3PTJ2NB?=
VCaP  MnLHS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NG\VN|MxNTNizszN NH;LVWkyPCCm NH7IO5VFVVOR NYjufFcx\GWlcnXhd4V{KGOxbH;ufUBvfW2kZYKg[I9{\SCmZYDlcoRmdnSueR?= NX3IfY0zOjN3NkWyOFQ>
LNCaP  NVLtPJVMT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NX\ZUJlxOC1|IN88US=> MmjxNVQh\A>? MYPEUXNQ M17XXIRm[3KnYYPld{Bkd2yxbomgcpVu[mW{IHTvd4Uh\GWyZX7k[Y51dHl? NFvzcnYzOzV4NUK0OC=>
MDA-MB-468 MnyyR4VtdCCYaXHibYxqfHliQYPzZZk> NXi2S3NzUUN3ME25Mlch|ryP NHLyRpQzOjZ5OEG2NS=>
MDA-MB-231 MmSwR4VtdCCYaXHibYxqfHliQYPzZZk> MnnsTWM2OD1zMzFOwG0> MWSyNlY4QDF4MR?=
Cal-51 NHzJXlRE\WyuIG\pZYJqdGm2eTDBd5NigQ>? M1LyXWlEPTB;OD62JO69VQ>? MV2yNlY4QDF4MR?=

... 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
NCT03533946 Recruiting Prostate Cancer University of Utah|Clovis Oncology Inc. August 8 2018 Phase 2
NCT03499444 Recruiting Advanced Solid Tumor Clovis Oncology Inc. February 6 2018 Phase 1
NCT03101280 Recruiting Gynecologic Neoplasms Hoffmann-La Roche May 4 2017 Phase 1
NCT03337087 Not yet recruiting Biliary System Disorder|BRCA1 Gene Mutation|BRCA2 Gene Mutation|Gastroesophageal Junction Adenocarcinoma|Homologous Recombination Deficiency|Metastatic Pancreatic Adenocarcinoma|PALB2 Gene Mutation|Stage IV Colorectal Cancer AJCC v7|Stage IV Pancreatic Cancer AJCC v6 and v7|Stage IVA Colorectal Cancer AJCC v7|Stage IVB Colorectal Cancer AJCC v7 Academic and Community Cancer Research United|National Cancer Institute (NCI) August 31 2018 Phase 1|Phase 2
NCT03521037 Recruiting Neoplasms Clovis Oncology Inc. March 31 2018 Phase 1
NCT03140670 Recruiting Pancreatic Cancer Abramson Cancer Center of the University of Pennsylvania June 30 2017 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