Rucaparib (AG-014699,PF-01367338)

Catalog No.S1098

Rucaparib (AG-014699,PF-01367338) 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
USD 120 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) 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) 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) 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) 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) 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) purchased from Selleck.

Purity & Quality Control

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2. For more details, such as half maximal inhibitory concentrations (IC50s) and working concentrations of each inhibitor, please click on the link of the inhibitor of interest.
3. "+" indicates inhibitory effect. Increased inhibition is marked by a higher "+" designation.
4. Orange "√" refers to compounds which do inhibitory effects on the related isoform, but without specific value.

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.
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 NHrpR4pHfW6ldHnvckBCe3OjeR?= MofFNE4yNzFxNUCwM|ExODBibl2= M{juVYlvcGmkaYTzJHBCWlBiYXP0bZZqfHliYYSgd5RienSrbnegZ49v[2W{boTyZZRqd25ib3[gOVAxKG6P MnPRNlUyOjh2NUW=
BT474 NYq2XJI1T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MmjsOVAxKG6P MkDYNVDjiJNzNdMg[C=> MVHy[YR2[2W|IHPlcIwh\3Kxd4ToJIlvKHSqZTDmc5VzKGyrbnXzJIFv\CC|aXfubYZq[2GwdHz5 NX3BNFR3OjVzMki0OVU>
SKBR3 M1TiT2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MWe1NFAhdk1? M2L2O|Ex6oDVMUZCpIQ> NHfxV4xz\WS3Y3XzJINmdGxiZ4Lve5RpKGmwIITo[UBnd3W{IHzpcoV{KGGwZDDzbYdvcW[rY3HueIx6 MkLVNlUyOjh2NUW=
AU565 NHL6WJpIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M17DTlUxOCCwTR?= NVTMOGU5OTEkgKOxOeKh\A>? MmG0doVlfWOnczDj[YxtKGe{b4f0bEBqdiC2aHWg[o92eiCuaX7ld{BidmRic3nncolncWOjboTsfS=> NEHV[nczPTF{OES1OS=>
EFM192A NG\1XJZIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M4DC[VUxOCCwTR?= MUixNQKBmzF3wrDk NWLuTJRMemWmdXPld{Bk\WyuIHfyc5d1cCCrbjD0bIUh\m:3cjDsbY5meyCjbnSgd4lodmmoaXPhcpRtgQ>? NHP3fXQzPTF{OES1OS=>
MDA-MB-231 NUi3WJdITnWwY4Tpc44hSXO|YYm= M3v6RlExNzJyL{SwJO69VQ>? NX\nXW5COjRiaB?= M2CwXYlv[3KnYYPld{BxNUGNVDDs[ZZmdHNiaX6gZUBld3OnLXTldIVv\GWwdDDtZY5v\XJ? MWqyOFQzODF3Mh?=
MDA-MB-231 NHq5U3BIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NHyzdWkyOC9{MD:0NEDPxE1? MUOyOEBp M4XWUoJtd2OtczDj[YxtKGO7Y3zlJJBzd2e{ZYPzbY9vKGmwIFeyM20heGijc3W= MXSyOFQzODF3Mh?=
H460 NGfoPWRIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M1rpdlQxOCCwTR?= MUmyOOKhcA>? M{njVYlv[3KnYYPld{Bk\WyudXzhdkBz[WSrb4PlcpNqfGm4aYT5 MknzNlQ1OTF4MUG=
A549  M3HuRmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NH3HeGo1ODBibl2= MUOyOOKhcA>? M{HHW4lv[3KnYYPld{Bk\WyudXzhdkBz[WSrb4PlcpNqfGm4aYT5 M3fjRlI1PDFzNkGx
DT40 MorvS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MXPJR|UxRTJzIH7N M4ja[FI1OzV4OEGz
COLO704 MYjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MVzJR|UxRTJwNUKgxtEhOC54NzFOwG0> NFLjbmUzOzd{OUSwNi=>
OV177 M3vtVmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M4PRWGlEPTB;Mj63PEDDuSByLkexJO69VQ>? M1[3cVI{PzJ7NECy
OVSAHO NGfn[2ZIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NI[z[2xKSzVyPUOuOlQhyrFiMD6zN{DPxE1? MWGyN|czQTRyMh?=
OVCAR3 M2\xV2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MUPJR|UxRTNwN{SgxtEhOC52MDFOwG0> MXqyN|czQTRyMh?=
PEO14 NUfSOopVT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M4DsSGlEPTB;Mz64OEDDuSByLke2JO69VQ>? M{DPd|I{PzJ7NECy
A2780 NHzQ[41Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M1O3R2lEPTB;Mz65OEDDuSByLkK1JO69VQ>? NGfNdGQzOzd{OUSwNi=>
OVTOKO MmDpS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NGq5eHFKSzVyPUSuNVQhyrFiMT61N{DPxE1? Mn3ZNlM4Ojl2MEK=
TOV21G M{\vSmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NUDyT4VVUUN3ME21MlA4KMLzIEGuN|Ah|ryP NH[5UIwzOzd{OUSwNi=>
OVISE M3jTcGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 Mn;zTWM2OD13Lk[4JOKyKDBwMkOg{txO NInlTYIzOzd{OUSwNi=>
KK MXzHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M4TC[mlEPTB;Nj6xOUDDuSBzLkSyJO69VQ>? M1LYOlI{PzJ7NECy
RMUGS MnL5S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MYHJR|UxRTdwMEOgxtEhOS56MzFOwG0> MXuyN|czQTRyMh?=
PEO6 M4jNXGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 Mk\qTWM2OD15LkC2JOKyKDBwN{Sg{txO Mo\SNlM4Ojl2MEK=
OVCA429 MXLHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MlHXTWM2OD16LkK5JOKyKDFwNkSg{txO M1q4SVI{PzJ7NECy
OV167 MWjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MYfJR|UxRThwM{OgxtEhOS5zODFOwG0> M1XESVI{PzJ7NECy
RMG1 NVjaVYUxT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MmmyTWM2OD17LkOyJOKyKDJwM{[g{txO MlP3NlM4Ojl2MEK=
OVCAR5 Mnv4S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NYrOfoppUUN3ME25MlUxKMLzIEKuOVkh|ryP NX7XPFN1OjN5Mkm0NFI>
EFO21 M1T5SGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M{TFd2lEPTB;OT65NkDDuSBzLki3JO69VQ>? MkXjNlM4Ojl2MEK=
ES2 NFTzWnBIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NYjSO5hWUUN3ME2xNE4yOiEEsTCxMlI{KM7:TR?= NILGco8zOzd{OUSwNi=>
Tyk-nu M1jjeGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M2P2fGlEPTB;MUCuNlAhyrFiMT6xNkDPxE1? NUH6VVE4OjN5Mkm0NFI>
CAOV3 MkjuS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NFTEcm9KSzVyPUGwMlM4KMLzIECuPFch|ryP MWmyN|czQTRyMh?=
OV207 NXXtXpRoT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NVPafoNnUUN3ME2xNk4zPyEEsTCwMlMzKM7:TR?= MljDNlM4Ojl2MEK=
HEY MWfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NXLiWZoyUUN3ME2xN{4xOSEEsTCwMlc2KM7:TR?= NXm4SnoyOjN5Mkm0NFI>
DOV13 NEjsRW1Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MWPJR|UxRjF3IN88US=> NEf1[mczOzd{OUSwNi=>
HEY C2 MnzFS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M{fYfmlEPTB-MUWg{txO MV6yN|czQTRyMh?=
KOC-7cc M{D6emdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MkHFTWM2OD5zNTFOwG0> NEfB[mEzOzd{OUSwNi=>
MCASb NF\5dXBIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NFTlV49KSzVyPkG1JO69VQ>? NILRfJkzOzd{OUSwNi=>
OAW42 MVLHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MnvhTWM2OD5zNTFOwG0> M33iR|I{PzJ7NECy
OV2008 MmTES5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MlXOTWM2OD5zNTFOwG0> MnHnNlM4Ojl2MEK=
OV90 NYK2S4R6T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NH[xZpNKSzVyPkG1JO69VQ>? M37Pc|I{PzJ7NECy
OVCA420b NXvQdVk2T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= Ml\DTWM2OD5zNTFOwG0> NGLBWIUzOzd{OUSwNi=>
OVCA432 MkDSS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NWXFdlJDUUN3ME6xOUDPxE1? MXqyN|czQTRyMh?=
PEA2 MkDkS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M3LN[GlEPTB-MUWg{txO M4Tvb|I{PzJ7NECy
SKOV3 NHjUc4xIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NIPIfm5KSzVyPkG1JO69VQ>? MnH3NlM4Ojl2MEK=
TOV112D MYfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MWGwMVMh|ryP NIDWOmlKSzVyPkG1JO69VQ>? Mo\FNlM4Ojl2MEK=
C4-2 MXHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NXfobFBIOC1|IN88US=> NF\jVGwyPCCm M3\SdGROW09? NH7IR4Vl\WO{ZXHz[ZMh[2:ub375JI52dWKncjDkc5NmKGSncHXu[IVvfGy7 M2m5b|I{PTZ3MkS0
PC3 NFu3eHVIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NH\oXFIxNTNizszN NXOy[VJ4OTRiZB?= NEDQ[5VFVVOR NGq2d4hl\WO{ZXHz[ZMh[2:ub375JI52dWKncjDkc5NmKGSncHXu[IVvfGy7 Mn;iNlM2PjV{NES=
DU145 MVrHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M2LZRVAuOyEQvF2= MUWxOEBl M1XqNGROW09? MXjk[YNz\WG|ZYOgZ49td267IH71cYJmeiCmb4PlJIRmeGWwZHXueIx6 Mkj6NlM2PjV{NES=
VCaP  M16zeGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M4DjVlAuOyEQvF2= M2XyWFE1KGR? MXrEUXNQ NIW1[o5l\WO{ZXHz[ZMh[2:ub375JI52dWKncjDkc5NmKGSncHXu[IVvfGy7 NHqydW8zOzV4NUK0OC=>
LNCaP  M3fDS2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MmjJNE0{KM7:TR?= MXGxOEBl NXqwVoVGTE2VTx?= M4jHeoRm[3KnYYPld{Bkd2yxbomgcpVu[mW{IHTvd4Uh\GWyZX7k[Y51dHl? M2jWV|I{PTZ3MkS0
MDA-MB-468 MX;D[YxtKF[rYXLpcIl1gSCDc4PhfS=> M3vjdWlEPTB;OT63JO69VQ>? NH7oVlMzOjZ5OEG2NS=>
MDA-MB-231 NX3Dd2VkS2WubDDWbYFjcWyrdImgRZN{[Xl? MlPUTWM2OD1zMzFOwG0> MmfjNlI3PzhzNkG=
Cal-51 MXrD[YxtKF[rYXLpcIl1gSCDc4PhfS=> MkG0TWM2OD16Lk[g{txO NWr5[I9rOjJ4N{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]


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 <1 mg/mL
Ethanol <1 mg/mL
In vivo 30% propylene glycol, 5% Tween 80, 65% D5W 30 mg/mL

* 1 mg/ml means slightly soluble or insoluble.
* 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


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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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID