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
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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 MUjGeY5kfGmxbjDBd5NigQ>? NH\XXIMxNjFxMT:1NFAwOTByMDDuUS=> NImxZolqdmirYnn0d{BRSVKSIHHjeIl3cXS7IHH0JJN1[XK2aX7nJINwdmOncn70doF1cW:wIH;mJFUxOCCwTR?= MofWNlUyOjh2NUW=
BT474 MW\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NFrENIE2ODBibl2= M1H6UlEx6oDVMUZCpIQ> MXXy[YR2[2W|IHPlcIwh\3Kxd4ToJIlvKHSqZTDmc5VzKGyrbnXzJIFv\CC|aXfubYZq[2GwdHz5 NH2xXoMzPTF{OES1OS=>
SKBR3 M{i0fmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NEPtZ242ODBibl2= Mln5NVDjiJNzNdMg[C=> MXTy[YR2[2W|IHPlcIwh\3Kxd4ToJIlvKHSqZTDmc5VzKGyrbnXzJIFv\CC|aXfubYZq[2GwdHz5 NY\yWmVvOjVzMki0OVU>
AU565 NXnkOXkyT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NGrVbY82ODBibl2= Mle3NVDjiJNzNdMg[C=> NVPLNpNVemWmdXPld{Bk\WyuIHfyc5d1cCCrbjD0bIUh\m:3cjDsbY5meyCjbnSgd4lodmmoaXPhcpRtgQ>? MWiyOVEzQDR3NR?=
EFM192A MmrSS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MYC1NFAhdk1? M1zF[lEx6oDVMUZCpIQ> NUnoUIVxemWmdXPld{Bk\WyuIHfyc5d1cCCrbjD0bIUh\m:3cjDsbY5meyCjbnSgd4lodmmoaXPhcpRtgQ>? M{DkW|I2OTJ6NEW1
MDA-MB-231 M3qxWmZ2dmO2aX;uJGF{e2G7 MVuxNE8zOC92MDFOwG0> NXS5eW1sOjRiaB?= NHrwVmpqdmO{ZXHz[ZMheC2DS2SgcIV3\Wy|IHnuJIEh\G:|ZT3k[ZBmdmSnboSgcYFvdmW{ M1XlcVI1PDJyMUWy
MDA-MB-231 M{TRe2Fxd3C2b4Ppd{BCe3OjeR?= NGD5PGgyOC9{MD:0NEDPxE1? NEnsfIEzPCCq M3PJVolv\HWlZYOgZZBweHSxc3nzJIRwe2ViZHXw[Y5l\W62bIm= NWnOcYtwOjR2MkCxOVI>
MDA-MB-231 NYLHS29OT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MorTNVAwOjBxNECg{txO NGX0NFUzPCCq NUG4fIZW[myxY3vzJINmdGxiY4njcIUheHKxZ4Lld5Nqd25iaX6gS|IwVSCyaHHz[S=> NH7sVXIzPDR{MEG1Ni=>
H460 NW\W[mFrT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NV72OmJOPDByIH7N Mn\hNlTDqGh? MV3pcoNz\WG|ZYOgZ4VtdHWuYYKgdoFlcW:|ZX7zbZRqfmm2eR?= MVqyOFQyOTZzMR?=
A549  NWLsR5dyT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NVn2NItlPDByIH7N MWGyOOKhcA>? MU\pcoNz\WG|ZYOgZ4VtdHWuYYKgdoFlcW:|ZX7zbZRqfmm2eR?= M2LyUVI1PDFzNkGx
DT40 M1rxOmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MmLTTWM2OD1{MTDuUS=> MYeyOFM2PjhzMx?=
DU145 NYXvcG5PT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NYDSPG1xUUN3ME2xPEBvVQ>? MVSyOFM2PjhzMx?=
COLO704 NGrYdIFIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NXHvbFhpUUN3ME2yMlUzKMLzIECuOlch|ryP MmTENlM4Ojl2MEK=
OVMANAb MU\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M13ncGlEPTB;Mj61PEDDuSByLkO4JO69VQ>? NILGUGgzOzd{OUSwNi=>
OV177 NEm4PIVIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M3XWRmlEPTB;Mj63PEDDuSByLkexJO69VQ>? M3zQeFI{PzJ7NECy
OAW28 MVXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M{O4TWlEPTB;Mz62NUDDuSByLkK4JO69VQ>? MoX0NlM4Ojl2MEK=
OVSAHO MULHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M2nzdWlEPTB;Mz62OEDDuSByLkOzJO69VQ>? MXqyN|czQTRyMh?=
OVKATE NGn3NG5Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= Moe0TWM2OD1|Lk[0JOKyKDFwN{mg{txO MnXWNlM4Ojl2MEK=
OVCAR3 NFHmUpRIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M2n3UWlEPTB;Mz63OEDDuSByLkSwJO69VQ>? MX2yN|czQTRyMh?=
PEO14 M1Hjcmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MkPUTWM2OD1|Lki0JOKyKDBwN{[g{txO NX\HRpVHOjN5Mkm0NFI>
A2780 M2\pOGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NHTOZ|hKSzVyPUOuPVQhyrFiMD6yOUDPxE1? Mn7WNlM4Ojl2MEK=
KURAMOCHIb M4LLSWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MYXJR|UxRTRwM{SgxtEhOC5{OTFOwG0> Ml[5NlM4Ojl2MEK=
TOV21G MkS0S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NWHpeY5oUUN3ME21MlA4KMLzIEGuN|Ah|ryP M3fXRlI{PzJ7NECy
OVISE NVrwVHpJT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MmjnTWM2OD13Lk[4JOKyKDBwMkOg{txO NVLBbYl1OjN5Mkm0NFI>
KK MWnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? Mkj4TWM2OD14LkG1JOKyKDFwNEKg{txO NFLGUowzOzd{OUSwNi=>
RMUGS M2HwUGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NF;mOYJKSzVyPUeuNFMhyrFiMT64N{DPxE1? M{HjTlI{PzJ7NECy
PEO6 M2fJWWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MW\JR|UxRTdwME[gxtEhOC55NDFOwG0> MnPHNlM4Ojl2MEK=
OVCA429 M1PXO2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NFuxZlhKSzVyPUiuNlkhyrFiMT62OEDPxE1? MoqyNlM4Ojl2MEK=
OV167 NUe2SldmT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MXPJR|UxRThwM{OgxtEhOS5zODFOwG0> MmnuNlM4Ojl2MEK=
RMG1 NI\ESXRIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M1fremlEPTB;OT6zNkDDuSB{LkO2JO69VQ>? NUXjd45VOjN5Mkm0NFI>
OVCAR5 MV3Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MVfJR|UxRTlwNUCgxtEhOi53OTFOwG0> MXuyN|czQTRyMh?=
EFO21 MXzHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MkPSTWM2OD17LkmyJOKyKDFwOEeg{txO MnfoNlM4Ojl2MEK=
ES2 NIna[YtIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MYTJR|UxRTFyLkGyJOKyKDFwMkOg{txO MnmzNlM4Ojl2MEK=
Tyk-nu M4DvVGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NHTBNYhKSzVyPUGwMlIxKMLzIEGuNVIh|ryP MVWyN|czQTRyMh?=
CAOV3 MnG1S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NWnBWoRXUUN3ME2xNE4{PyEEsTCwMlg4KM7:TR?= MWCyN|czQTRyMh?=
OV207 NFztfIlIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MWPJR|UxRTF{LkK3JOKyKDBwM{Kg{txO MoO5NlM4Ojl2MEK=
HEY MXLHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NYjFSZE5UUN3ME2xN{4xOSEEsTCwMlc2KM7:TR?= NHP6OI4zOzd{OUSwNi=>
EFO27 NW\ZfWlOT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NILo[4JKSzVyPkG1JO69VQ>? M{f3OFI{PzJ7NECy
HEY C2 M3vodmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NX62[YFCUUN3ME6xOUDPxE1? MXeyN|czQTRyMh?=
KOC-7cc M1r4fWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NYP3O2VOUUN3ME6xOUDPxE1? MXqyN|czQTRyMh?=
MCASb NEnY[I1Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NYHJbGtnUUN3ME6xOUDPxE1? M3S4RlI{PzJ7NECy
OV2008 NH3CPWRIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NV;6cJJlUUN3ME6xOUDPxE1? MWOyN|czQTRyMh?=
OV90 Mn7jS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MnT4TWM2OD5zNTFOwG0> NVXweIhqOjN5Mkm0NFI>
OVCA420b MUTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NFPze5lKSzVyPkG1JO69VQ>? NY\ue3RqOjN5Mkm0NFI>
OVCA432 M3zpTWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M{LqdGlEPTB-MUWg{txO NF:2OYIzOzd{OUSwNi=>
PEA2 MY\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MoPJTWM2OD5zNTFOwG0> MmHmNlM4Ojl2MEK=
SKOV3 M3TBOGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MYnJR|UxRjF3IN88US=> MX:yN|czQTRyMh?=
TOV112D MofkS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M{KwXVAuOyEQvF2= MXLJR|UxRjF3IN88US=> Ml\uNlM4Ojl2MEK=
C4-2 MlPXS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M2f1PFAuOyEQvF2= NF6xbnEyPCCm M3;pSmROW09? NWHGdolJ\GWlcnXhd4V{KGOxbH;ufUBvfW2kZYKg[I9{\SCmZYDlcoRmdnSueR?= NUTTVWRmOjN3NkWyOFQ>
PC3 NEDTRmZIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M{jhWVAuOyEQvF2= MUmxOEBl NUPDdlRDTE2VTx?= NVH0bndk\GWlcnXhd4V{KGOxbH;ufUBvfW2kZYKg[I9{\SCmZYDlcoRmdnSueR?= MYiyN|U3PTJ2NB?=
DU145 MVfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M3LyZVAuOyEQvF2= NWK4cWFqOTRiZB?= NF;OTWJFVVOR NFLZTGZl\WO{ZXHz[ZMh[2:ub375JI52dWKncjDkc5NmKGSncHXu[IVvfGy7 NGnvZmQzOzV4NUK0OC=>
VCaP  M1v6cWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MnTkNE0{KM7:TR?= NIWwTFQyPCCm M2Sxb2ROW09? M3z6W4Rm[3KnYYPld{Bkd2yxbomgcpVu[mW{IHTvd4Uh\GWyZX7k[Y51dHl? MWqyN|U3PTJ2NB?=
LNCaP  MWTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MoHINE0{KM7:TR?= NYD5XZdNOTRiZB?= M1fmS2ROW09? NFP2Z3dl\WO{ZXHz[ZMh[2:ub375JI52dWKncjDkc5NmKGSncHXu[IVvfGy7 M4j0U|I{PTZ3MkS0
Cal-51 M3vVSWNmdGxiVnnhZoltcXS7IFHzd4F6 M{WwXWlEPTB;OD62JO69VQ>? MlvDNlI3PzhzNkG=

... 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
+ 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
+ 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
+ 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
NCT02740712 Recruiting Neoplasms Clovis Oncology, Inc. March 2016 Phase 1
NCT02505048 Not yet recruiting Metastatic Breast Cancer UNICANCER|Clovis Oncology, Inc.|Fondation ARC March 2016 Phase 2
NCT02042378 Completed Pancreatic Cancer|Pancreatic Ductal Adenocarcinoma Clovis Oncology, Inc. April 2014 Phase 2
NCT01968213 Active, not recruiting Ovarian Cancer|Fallopian Tube Cancer|Peritoneal Cancer Clovis Oncology, Inc. January 2014 Phase 3
NCT01891344 Active, not recruiting Ovarian Cancer|Epithelial Ovarian Cancer|Fallopian Tube Cancer|Peritoneal Cancer Clovis Oncology, Inc.|Foundation Medicine September 2013 Phase 2
NCT01482715 Active, not recruiting Ovarian Cancer|Fallopian Tube Cancer|Peritoneal Cancer|Advanced Solid Tumor With Evidence of Germline or Somatic BRCA Clovis Oncology, Inc. November 2011 Phase 1|Phase 2

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID