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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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.

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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 Ml;ISpVv[3Srb36gRZN{[Xl? M1jNZ|AvOS9zL{WwNE8yODByIH7N MoDubY5pcWKrdIOgVGFTWCCjY4Tpeol1gSCjdDDzeIFzfGmwZzDjc45k\XKwdILheIlwdiCxZjC1NFAhdk1? M4\KPVI2OTJ6NEW1
BT474 MUfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NHPuXow2ODBibl2= MnHjNVDjiJNzNdMg[C=> NUnKfVA2emWmdXPld{Bk\WyuIHfyc5d1cCCrbjD0bIUh\m:3cjDsbY5meyCjbnSgd4lodmmoaXPhcpRtgQ>? NVLsWI1zOjVzMki0OVU>
SKBR3 MULHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NEPnd2Y2ODBibl2= MmjZNVDjiJNzNdMg[C=> MXHy[YR2[2W|IHPlcIwh\3Kxd4ToJIlvKHSqZTDmc5VzKGyrbnXzJIFv\CC|aXfubYZq[2GwdHz5 NYnGWIRtOjVzMki0OVU>
AU565 NEDqfHlIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NFGxc4Y2ODBibl2= MUexNQKBmzF3wrDk NHTsRWtz\WS3Y3XzJINmdGxiZ4Lve5RpKGmwIITo[UBnd3W{IHzpcoV{KGGwZDDzbYdvcW[rY3HueIx6 M3fSZVI2OTJ6NEW1
EFM192A NWnmW2dNT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M2TpPFUxOCCwTR?= M1HPO|Ex6oDVMUZCpIQ> NH7MOm5z\WS3Y3XzJINmdGxiZ4Lve5RpKGmwIITo[UBnd3W{IHzpcoV{KGGwZDDzbYdvcW[rY3HueIx6 MWOyOVEzQDR3NR?=
MDA-MB-231 NE\ufIZHfW6ldHnvckBCe3OjeR?= NHfiPHEyOC9{MD:0NEDPxE1? MYCyOEBp NE\aeGdqdmO{ZXHz[ZMheC2DS2SgcIV3\Wy|IHnuJIEh\G:|ZT3k[ZBmdmSnboSgcYFvdmW{ Mn3sNlQ1OjBzNUK=
MDA-MB-231 NYrteJVnS2WubDDWbYFjcWyrdImgRZN{[Xl? NU\Qc|BuOC5zLUSwJO69VQ>? MYmyOEBp MmfxTWM2OOLCiU5ihKkyPy55N9Mg{txO NYW0d5BUOjR2MkCxOVI>
MDA-MB-231 NGT5ZZhCeG:ydH;zbZMhSXO|YYm= MVqxNE8zOC92MDFOwG0> M3e4O|I1KGh? M2ruTYlv\HWlZYOgZZBweHSxc3nzJIRwe2ViZHXw[Y5l\W62bIm= NIrLTowzPDR{MEG1Ni=>
MDA-MB-231 Ml2yS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MmnRNVAwOjBxNECg{txO MnzKNlQhcA>? M{\hN4Jtd2OtczDj[YxtKGO7Y3zlJJBzd2e{ZYPzbY9vKGmwIFeyM20heGijc3W= NUHK[492OjR2MkCxOVI>
H460 NXXyeVQ5T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MV:0NFAhdk1? NXrBWJhtOjUEoHi= MnrLbY5kemWjc3XzJINmdGy3bHHyJJJi\Gmxc3Xud4l1cX[rdIm= NUHLbpBnOjR2MUG2NVE>
A549  NIqzR|NIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MXm0NFAhdk1? M4O1eVI1yqCq M3i2NYlv[3KnYYPld{Bk\WyudXzhdkBz[WSrb4PlcpNqfGm4aYT5 M3XIbFI1PDFzNkGx
DT40 M4HOcWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 Mlr5TWM2OD1{MTDuUS=> M2nxSlI1OzV4OEGz
DU145 NYD0dZlGT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M4nNWWlEPTB;MUigcm0> NGK3fWozPDN3NkixNy=>
COLO704 MYnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MVHJR|UxRTJwNUKgxtEhOC54NzFOwG0> MkXCNlM4Ojl2MEK=
OVMANAb MUHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MmPBTWM2OD1{LkW4JOKyKDBwM{ig{txO MWCyN|czQTRyMh?=
OV177 MmnzS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NFzwPXpKSzVyPUKuO|ghyrFiMD63NUDPxE1? NVHvSlV2OjN5Mkm0NFI>
OAW28 MlnoS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NYnQUmo1UUN3ME2zMlYyKMLzIECuNlgh|ryP NVzLOlQ5OjN5Mkm0NFI>
OVSAHO MWfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NH;qSpZKSzVyPUOuOlQhyrFiMD6zN{DPxE1? MkSxNlM4Ojl2MEK=
OVKATE MXXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NVzOdWlGUUN3ME2zMlY1KMLzIEGuO|kh|ryP M3znZ|I{PzJ7NECy
OVCAR3 M2S0NGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NFzw[YRKSzVyPUOuO|QhyrFiMD60NEDPxE1? Ml\VNlM4Ojl2MEK=
PEO14 NWfYOG1rT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MX7JR|UxRTNwOESgxtEhOC55NjFOwG0> M1z6WVI{PzJ7NECy
A2780 MYDHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NIfi[29KSzVyPUOuPVQhyrFiMD6yOUDPxE1? NGXZdpczOzd{OUSwNi=>
KURAMOCHIb NGj2XmlIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NIGydlBKSzVyPUSuN|QhyrFiMD6yPUDPxE1? MXyyN|czQTRyMh?=
TOV21G M4jvPGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NH;XXplKSzVyPUWuNFchyrFiMT6zNEDPxE1? MYiyN|czQTRyMh?=
OVISE MmXyS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M3\rZWlEPTB;NT62PEDDuSByLkKzJO69VQ>? M3zGc|I{PzJ7NECy
KK MX3Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NFroZXNKSzVyPU[uNVUhyrFiMT60NkDPxE1? NVXHfnZ5OjN5Mkm0NFI>
RMUGS MYnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MmfITWM2OD15LkCzJOKyKDFwOEOg{txO NFm4N4YzOzd{OUSwNi=>
PEO6 M2Ho[mdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NFjmdJdKSzVyPUeuNFYhyrFiMD63OEDPxE1? MVSyN|czQTRyMh?=
OVCA429 NF\LVYdIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NF\obWZKSzVyPUiuNlkhyrFiMT62OEDPxE1? MVqyN|czQTRyMh?=
OV167 NHzHfldIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NX;ZSHU5UUN3ME24MlM{KMLzIEGuNVgh|ryP NX7z[|dROjN5Mkm0NFI>
RMG1 NFn3do5Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NFrwe2hKSzVyPUmuN|IhyrFiMj6zOkDPxE1? NUfuPXU5OjN5Mkm0NFI>
OVCAR5 M4O4fWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MlfVTWM2OD17LkWwJOKyKDJwNUmg{txO MXSyN|czQTRyMh?=
EFO21 MWPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NInzNYFKSzVyPUmuPVIhyrFiMT64O{DPxE1? M{ntXVI{PzJ7NECy
ES2 M4Wzbmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NHnofmNKSzVyPUGwMlEzKMLzIEGuNlMh|ryP M1vOfVI{PzJ7NECy
Tyk-nu M1zVcWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NFrx[pBKSzVyPUGwMlIxKMLzIEGuNVIh|ryP NIfkU2YzOzd{OUSwNi=>
OV207 M1XOU2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NIq1ZXNKSzVyPUGyMlI4KMLzIECuN|Ih|ryP NICzNFczOzd{OUSwNi=>
DOV13 MY\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M1TCfGlEPTB-MUWg{txO NWD0[JY2OjN5Mkm0NFI>
EFO27 MYHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M2q5fGlEPTB-MUWg{txO NFPwWYczOzd{OUSwNi=>
HEY C2 MmLuS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M3nlO2lEPTB-MUWg{txO NFfZdo4zOzd{OUSwNi=>
KOC-7cc MX7Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MlzCTWM2OD5zNTFOwG0> Mnz0NlM4Ojl2MEK=
MCASb M3jYTWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MV3JR|UxRjF3IN88US=> MkjqNlM4Ojl2MEK=
OAW42 MUnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NHf0ZVNKSzVyPkG1JO69VQ>? NVjF[GdHOjN5Mkm0NFI>
OV2008 NGXGZZJIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M1nwSGlEPTB-MUWg{txO NWD2R2dMOjN5Mkm0NFI>
OV90 NHjZZotIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NHjue|ZKSzVyPkG1JO69VQ>? MV2yN|czQTRyMh?=
OVCA420b MmTqS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M2O5fmlEPTB-MUWg{txO M1;pelI{PzJ7NECy
OVCA432 MmjqS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MUfJR|UxRjF3IN88US=> MWmyN|czQTRyMh?=
PEA2 NWi3Z|BlT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NYnHbY91UUN3ME6xOUDPxE1? MXSyN|czQTRyMh?=
SKOV3 M2exSmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NWfRNnlKUUN3ME6xOUDPxE1? MVuyN|czQTRyMh?=
TOV112D M{LaNGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MljaNE0{KM7:TR?= MkfWTWM2OD5zNTFOwG0> NGCzcWEzOzd{OUSwNi=>
C4-2 NFPqeVZIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MX2wMVMh|ryP NHjHNpQyPCCm MWLEUXNQ NVvje2wz\GWlcnXhd4V{KGOxbH;ufUBvfW2kZYKg[I9{\SCmZYDlcoRmdnSueR?= MmeyNlM2PjV{NES=
PC3 NGO3SohIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M4X1WlAuOyEQvF2= NHH0TocyPCCm MoPtSG1UVw>? NG\NOmdl\WO{ZXHz[ZMh[2:ub375JI52dWKncjDkc5NmKGSncHXu[IVvfGy7 NHHLd2wzOzV4NUK0OC=>
DU145 MlLFS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NIOzVIoxNTNizszN MnziNVQh\A>? NWnTUWhKTE2VTx?= NUfEdVI5\GWlcnXhd4V{KGOxbH;ufUBvfW2kZYKg[I9{\SCmZYDlcoRmdnSueR?= MVeyN|U3PTJ2NB?=
VCaP  MVHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MnHwNE0{KM7:TR?= NGG5[IkyPCCm M2\s[mROW09? MVvk[YNz\WG|ZYOgZ49td267IH71cYJmeiCmb4PlJIRmeGWwZHXueIx6 NF3LR4czOzV4NUK0OC=>
LNCaP  NUj6WpdJT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M4nZVFAuOyEQvF2= NEHsZlYyPCCm NFvxd2pFVVOR M4jVNIRm[3KnYYPld{Bkd2yxbomgcpVu[mW{IHTvd4Uh\GWyZX7k[Y51dHl? M2\ybVI{PTZ3MkS0
Cal-51 M{T1eGNmdGxiVnnhZoltcXS7IFHzd4F6 NV3zXJE3UUN3ME24MlYh|ryP MUiyNlY4QDF4MR?=

... 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