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.

Size Price Stock Quantity  
In DMSO USD 134 In stock
USD 120 In stock
USD 210 In stock
USD 670 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 Mn3YSpVv[3Srb36gRZN{[Xl? MnvSNE4yNzFxNUCwM|ExODBibl2= NX73[IlGcW6qaXLpeJMhWEGUUDDhZ5Rqfmm2eTDheEB{fGG{dHnu[{Bkd26lZYLueJJifGmxbjDv[kA2ODBibl2= Mn;JNlUyOjh2NUW=
BT474 MXrHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M1Pa[VUxOCCwTR?= MWqxNQKBmzF3wrDk MlrZdoVlfWOnczDj[YxtKGe{b4f0bEBqdiC2aHWg[o92eiCuaX7ld{BidmRic3nncolncWOjboTsfS=> NIG0c4kzPTF{OES1OS=>
SKBR3 M1PqcGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NU[xZm1{PTByIH7N MYixNQKBmzF3wrDk NWOxNo05emWmdXPld{Bk\WyuIHfyc5d1cCCrbjD0bIUh\m:3cjDsbY5meyCjbnSgd4lodmmoaXPhcpRtgQ>? MVWyOVEzQDR3NR?=
AU565 MYfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MmPDOVAxKG6P MkLTNVDjiJNzNdMg[C=> NVjjdlNSemWmdXPld{Bk\WyuIHfyc5d1cCCrbjD0bIUh\m:3cjDsbY5meyCjbnSgd4lodmmoaXPhcpRtgQ>? M{f4R|I2OTJ6NEW1
EFM192A MXzHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NY\V[nhxPTByIH7N NEPPbWEyOOLCk{G1xsBl NFP3PWpz\WS3Y3XzJINmdGxiZ4Lve5RpKGmwIITo[UBnd3W{IHzpcoV{KGGwZDDzbYdvcW[rY3HueIx6 MXSyOVEzQDR3NR?=
MDA-MB-231 Mn;BSpVv[3Srb36gRZN{[Xl? NVrTeHZGOTBxMkCvOFAh|ryP NV7lcolYOjRiaB?= M{PJXYlv[3KnYYPld{BxNUGNVDDs[ZZmdHNiaX6gZUBld3OnLXTldIVv\GWwdDDtZY5v\XJ? M3rjW|I1PDJyMUWy
MDA-MB-231 MUPD[YxtKF[rYXLpcIl1gSCDc4PhfS=> NYrqZ2g1OC5zLUSwJO69VQ>? MVmyOEBp NV\FdIlxUUN3MPMAjV3jiIlzNz63O:Kh|ryP MWmyOFQzODF3Mh?=
MDA-MB-231 M1TNXmFxd3C2b4Ppd{BCe3OjeR?= MXqxNE8zOC92MDFOwG0> MX2yOEBp M1v0cIlv\HWlZYOgZZBweHSxc3nzJIRwe2ViZHXw[Y5l\W62bIm= MlXTNlQ1OjBzNUK=
MDA-MB-231 MXnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MWOxNE8zOC92MDFOwG0> M2XkblI1KGh? NIrlUXBjdG:la4OgZ4VtdCCleXPs[UBxem:pcnXzd4lwdiCrbjDHNk9OKHCqYYPl MXqyOFQzODF3Mh?=
H460 NY\xZWx[T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MVK0NFAhdk1? MYSyOOKhcA>? M3TuXolv[3KnYYPld{Bk\WyudXzhdkBz[WSrb4PlcpNqfGm4aYT5 MnPWNlQ1OTF4MUG=
A549  NGizTFNIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MmDTOFAxKG6P Mm[2NlTDqGh? NYTmeFBHcW6lcnXhd4V{KGOnbHz1cIFzKHKjZHnvd4Vve2m2aY\peJk> MljqNlQ1OTF4MUG=
DT40 MlLxS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MlzUTWM2OD1{MTDuUS=> MWSyOFM2PjhzMx?=
COLO704 MonsS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? Ml7vTWM2OD1{LkWyJOKyKDBwNkeg{txO MXeyN|czQTRyMh?=
OVMANAb MmDMS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MlTJTWM2OD1{LkW4JOKyKDBwM{ig{txO MVmyN|czQTRyMh?=
OV177 NYnndIo5T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MmDzTWM2OD1{Lke4JOKyKDBwN{Gg{txO NUT4VIkzOjN5Mkm0NFI>
OAW28 M4fUc2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NVztXXFLUUN3ME2zMlYyKMLzIECuNlgh|ryP NV;HT45vOjN5Mkm0NFI>
OVKATE M4rRXmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 Mom0TWM2OD1|Lk[0JOKyKDFwN{mg{txO NUTZTYFqOjN5Mkm0NFI>
PEO14 MkTmS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NH;CSmlKSzVyPUOuPFQhyrFiMD63OkDPxE1? MlnYNlM4Ojl2MEK=
A2780 NVXPeY4zT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M17SdmlEPTB;Mz65OEDDuSByLkK1JO69VQ>? MmrFNlM4Ojl2MEK=
KURAMOCHIb Mlv0S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NH[5NGdKSzVyPUSuN|QhyrFiMD6yPUDPxE1? Mn\vNlM4Ojl2MEK=
TOV21G MnXTS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MnLiTWM2OD13LkC3JOKyKDFwM{Cg{txO NIHK[oMzOzd{OUSwNi=>
OVISE MkPsS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M3TlT2lEPTB;NT62PEDDuSByLkKzJO69VQ>? NGHK[20zOzd{OUSwNi=>
PEO6 MoPrS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NVvoTVlVUUN3ME23MlA3KMLzIECuO|Qh|ryP MXeyN|czQTRyMh?=
OVCA429 NYXYbJFuT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NVXvdm9XUUN3ME24MlI6KMLzIEGuOlQh|ryP M1ficlI{PzJ7NECy
OV167 NHj1VWRIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MVXJR|UxRThwM{OgxtEhOS5zODFOwG0> M4jzdVI{PzJ7NECy
RMG1 NEn2SZdIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MoPWTWM2OD17LkOyJOKyKDJwM{[g{txO M{TYR|I{PzJ7NECy
EFO21 NEfwVpFIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NXvkXphOUUN3ME25MlkzKMLzIEGuPFch|ryP M3vVOlI{PzJ7NECy
Tyk-nu MnnES5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MV;JR|UxRTFyLkKwJOKyKDFwMUKg{txO MVSyN|czQTRyMh?=
OV207 NF3LVW9Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MWnJR|UxRTF{LkK3JOKyKDBwM{Kg{txO NX7vSHZZOjN5Mkm0NFI>
HEY MWfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NX\ZVoQ2UUN3ME2xN{4xOSEEsTCwMlc2KM7:TR?= NFLoOpgzOzd{OUSwNi=>
DOV13 MVTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NE\PWHpKSzVyPkG1JO69VQ>? NGrMN48zOzd{OUSwNi=>
HEY C2 NIi0TW9Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NIjacFZKSzVyPkG1JO69VQ>? NEDNS24zOzd{OUSwNi=>
KOC-7cc MV\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M{HB[mlEPTB-MUWg{txO NGXpW|IzOzd{OUSwNi=>
MCASb MmTFS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NU\XTWdOUUN3ME6xOUDPxE1? MX6yN|czQTRyMh?=
OAW42 MULHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MonaTWM2OD5zNTFOwG0> M1OwR|I{PzJ7NECy
OV2008 MoXlS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MXjJR|UxRjF3IN88US=> M2jadVI{PzJ7NECy
OV90 M2jYRWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NUjTdZo6UUN3ME6xOUDPxE1? M4XMfFI{PzJ7NECy
OVCA420b NF3vN2xIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NIHqNXdKSzVyPkG1JO69VQ>? MV2yN|czQTRyMh?=
OVCA432 MWHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M3vB[mlEPTB-MUWg{txO NWDUOIV6OjN5Mkm0NFI>
PEA2 MkPLS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MVjJR|UxRjF3IN88US=> MWmyN|czQTRyMh?=
SKOV3 MUnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NELB[JBKSzVyPkG1JO69VQ>? Ml\xNlM4Ojl2MEK=
TOV112D MXnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? Mn\2NE0{KM7:TR?= NHT5c3VKSzVyPkG1JO69VQ>? NEP0dm8zOzd{OUSwNi=>
C4-2 NIHXVppIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MkPrNE0{KM7:TR?= NGfKUZcyPCCm NI\ON3pFVVOR M1nKOYRm[3KnYYPld{Bkd2yxbomgcpVu[mW{IHTvd4Uh\GWyZX7k[Y51dHl? M4DZVFI{PTZ3MkS0
PC3 NVW1[YduT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MYCwMVMh|ryP NF;DdGkyPCCm NEHWZYtFVVOR NWH4eWxi\GWlcnXhd4V{KGOxbH;ufUBvfW2kZYKg[I9{\SCmZYDlcoRmdnSueR?= MoHONlM2PjV{NES=
DU145 MUPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NIXWXJkxNTNizszN MnjFNVQh\A>? M1\2PGROW09? Mori[IVkemWjc3XzJINwdG:weTDueY1j\XJiZH;z[UBl\XCnbnTlcpRtgQ>? M2\2TFI{PTZ3MkS0
VCaP  MknWS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? Ml7HNE0{KM7:TR?= NIe3fo0yPCCm NX[zR45ZTE2VTx?= M{HhW4Rm[3KnYYPld{Bkd2yxbomgcpVu[mW{IHTvd4Uh\GWyZX7k[Y51dHl? M2TpZ|I{PTZ3MkS0
LNCaP  MorFS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NFzYbWsxNTNizszN NHOze48yPCCm NU\kXmdyTE2VTx?= M3zCR4Rm[3KnYYPld{Bkd2yxbomgcpVu[mW{IHTvd4Uh\GWyZX7k[Y51dHl? NYS3PHpjOjN3NkWyOFQ>
MDA-MB-468 MUTD[YxtKF[rYXLpcIl1gSCDc4PhfS=> NVrWUXI2UUN3ME25Mlch|ryP NH7kenMzOjZ5OEG2NS=>
Cal-51 NILtTXRE\WyuIG\pZYJqdGm2eTDBd5NigQ>? NYXh[ZgxUUN3ME24MlYh|ryP NXrlOJdbOjJ4N{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