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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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.

  • 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.

    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.

  • 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.
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 NYf1RphITnWwY4Tpc44hSXO|YYm= MXqwMlEwOS93MECvNVAxOCCwTR?= NFfvVmNqdmirYnn0d{BRSVKSIHHjeIl3cXS7IHH0JJN1[XK2aX7nJINwdmOncn70doF1cW:wIH;mJFUxOCCwTR?= NYDyNYxjOjVzMki0OVU>
BT474 NGXEOJBIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M1nmZlUxOCCwTR?= MXOxNQKBmzF3wrDk MVHy[YR2[2W|IHPlcIwh\3Kxd4ToJIlvKHSqZTDmc5VzKGyrbnXzJIFv\CC|aXfubYZq[2GwdHz5 NEfrbWUzPTF{OES1OS=>
SKBR3 M330Omdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MYC1NFAhdk1? NYP6cpNUOTEkgKOxOeKh\A>? Ml\FdoVlfWOnczDj[YxtKGe{b4f0bEBqdiC2aHWg[o92eiCuaX7ld{BidmRic3nncolncWOjboTsfS=> NEPxVFYzPTF{OES1OS=>
AU565 NILuNGVIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NYfIN2F[PTByIH7N MUGxNQKBmzF3wrDk M{SzOpJm\HWlZYOgZ4VtdCCpcn;3eIghcW5idHjlJIZwfXJibHnu[ZMh[W6mIIPp[45q\mmlYX70cJk> M1HzRVI2OTJ6NEW1
EFM192A Mn7FS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M1\KXFUxOCCwTR?= NUjqXZZzOTEkgKOxOeKh\A>? MlXPdoVlfWOnczDj[YxtKGe{b4f0bEBqdiC2aHWg[o92eiCuaX7ld{BidmRic3nncolncWOjboTsfS=> NFTBSGMzPTF{OES1OS=>
MDA-MB-231 NGC2V5dHfW6ldHnvckBCe3OjeR?= NVWySVlnOTBxMkCvOFAh|ryP MnTlNlQhcA>? MmTqbY5kemWjc3XzJJAuSUuWIHzleoVteyCrbjDhJIRwe2VvZHXw[Y5l\W62IH3hco5meg>? M1XiT|I1PDJyMUWy
MDA-MB-231 Mn;ER4VtdCCYaXHibYxqfHliQYPzZZk> MlTnNE4yNTRyIN88US=> Mn7tNlQhcA>? Ml;oTWM2OOLCiU5ihKkyPy55N9Mg{txO M3zDd|I1PDJyMUWy
MDA-MB-231 NWXSOZVtSXCxcITvd4l{KEG|c3H5 MljHNVAwOjBxNECg{txO NFezdXMzPCCq Ml\LbY5lfWOnczDhdI9xfG:|aYOg[I9{\SCmZYDlcoRmdnSueR?= NUPsSW5SOjR2MkCxOVI>
MDA-MB-231 Mmr5S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M4Oze|ExNzJyL{SwJO69VQ>? MYCyOEBp MYPicI9kc3NiY3XscEBkgWOuZTDwdo9oemW|c3nvckBqdiCJMj;NJJBp[XOn NY\5SlhGOjR2MkCxOVI>
H460 MnfmS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NIDBWW01ODBibl2= MUWyOOKhcA>? MYXpcoNz\WG|ZYOgZ4VtdHWuYYKgdoFlcW:|ZX7zbZRqfmm2eR?= MnfnNlQ1OTF4MUG=
A549  M4\Jfmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MXe0NFAhdk1? MV2yOOKhcA>? MkTNbY5kemWjc3XzJINmdGy3bHHyJJJi\Gmxc3Xud4l1cX[rdIm= MnXsNlQ1OTF4MUG=
DT40 NV;V[ld5T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MXHJR|UxRTJzIH7N MUeyOFM2PjhzMx?=
DU145 NF;EeWRIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MV3JR|UxRTF6IH7N M1TCUlI1OzV4OEGz
COLO704 NV;IbFd{T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= Mnv6TWM2OD1{LkWyJOKyKDBwNkeg{txO M37mc|I{PzJ7NECy
OVMANAb NGXOW4NIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M{\4dGlEPTB;Mj61PEDDuSByLkO4JO69VQ>? NInVOlkzOzd{OUSwNi=>
OV177 MVXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NHXYN4dKSzVyPUKuO|ghyrFiMD63NUDPxE1? NWrpeVZFOjN5Mkm0NFI>
OAW28 NEDifmNIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NVHSTnpvUUN3ME2zMlYyKMLzIECuNlgh|ryP MkWzNlM4Ojl2MEK=
OVKATE NF33N|dIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M3nScmlEPTB;Mz62OEDDuSBzLke5JO69VQ>? M4L1U|I{PzJ7NECy
OVCAR3 MXTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M374fWlEPTB;Mz63OEDDuSByLkSwJO69VQ>? NUDt[Yw1OjN5Mkm0NFI>
PEO14 M2nH[mdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NY\ZWWFvUUN3ME2zMlg1KMLzIECuO|Yh|ryP Ml;HNlM4Ojl2MEK=
A2780 M2DyOGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MlW3TWM2OD1|Lkm0JOKyKDBwMkWg{txO NFT2TpkzOzd{OUSwNi=>
KURAMOCHIb M13YWWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 Mk\kTWM2OD12LkO0JOKyKDBwMkmg{txO M{KyWVI{PzJ7NECy
TOV21G NFzEeFdIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NU\4e25iUUN3ME21MlA4KMLzIEGuN|Ah|ryP NFKzcmQzOzd{OUSwNi=>
OVISE NIHqWodIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MVTJR|UxRTVwNkigxtEhOC5{MzFOwG0> NUDNR4dMOjN5Mkm0NFI>
KK MWHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M2HYNmlEPTB;Nj6xOUDDuSBzLkSyJO69VQ>? MmjQNlM4Ojl2MEK=
RMUGS MmX3S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? Mn;TTWM2OD15LkCzJOKyKDFwOEOg{txO MVmyN|czQTRyMh?=
PEO6 M1Pxfmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M1;SZ2lEPTB;Nz6wOkDDuSByLke0JO69VQ>? MofKNlM4Ojl2MEK=
OV167 MUPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M3fj[2lEPTB;OD6zN{DDuSBzLkG4JO69VQ>? MXWyN|czQTRyMh?=
RMG1 NEfYfJlIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NX3Q[nM4UUN3ME25MlMzKMLzIEKuN|Yh|ryP M1jCflI{PzJ7NECy
OVCAR5 M2fYWmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MUXJR|UxRTlwNUCgxtEhOi53OTFOwG0> M1\xUlI{PzJ7NECy
EFO21 NFXTS4hIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NFPoOplKSzVyPUmuPVIhyrFiMT64O{DPxE1? MmD6NlM4Ojl2MEK=
ES2 MUDHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MVXJR|UxRTFyLkGyJOKyKDFwMkOg{txO M3X0d|I{PzJ7NECy
Tyk-nu MYPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NHXzNWpKSzVyPUGwMlIxKMLzIEGuNVIh|ryP NGXCRlEzOzd{OUSwNi=>
CAOV3 MVfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? Ml\2TWM2OD1zMD6zO{DDuSByLki3JO69VQ>? M3TzZlI{PzJ7NECy
OV207 NXrYcodZT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MVvJR|UxRTF{LkK3JOKyKDBwM{Kg{txO NGfXOFYzOzd{OUSwNi=>
HEY M2eze2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NIjGTG1KSzVyPUGzMlAyKMLzIECuO|Uh|ryP MVqyN|czQTRyMh?=
DOV13 M2rVSWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NYfx[|RtUUN3ME6xOUDPxE1? NFn0bWIzOzd{OUSwNi=>
EFO27 NVyxe|N2T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NH7WSZlKSzVyPkG1JO69VQ>? MkLHNlM4Ojl2MEK=
HEY C2 M3naUWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NGnYOoxKSzVyPkG1JO69VQ>? NYTlPHVEOjN5Mkm0NFI>
KOC-7cc NUPHPZp3T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MWfJR|UxRjF3IN88US=> M1;2N|I{PzJ7NECy
MCASb MknvS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? Mn3lTWM2OD5zNTFOwG0> MVWyN|czQTRyMh?=
OAW42 MVzHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M{H3O2lEPTB-MUWg{txO M3nFTFI{PzJ7NECy
OV2008 MmKxS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MVTJR|UxRjF3IN88US=> MVyyN|czQTRyMh?=
OV90 NWq5boFLT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MXTJR|UxRjF3IN88US=> MW[yN|czQTRyMh?=
OVCA420b MVTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MYPJR|UxRjF3IN88US=> MX6yN|czQTRyMh?=
OVCA432 MWDHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NXrRUpVJUUN3ME6xOUDPxE1? MYCyN|czQTRyMh?=
PEA2 MYLHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NGjVfo1KSzVyPkG1JO69VQ>? Mn[0NlM4Ojl2MEK=
SKOV3 M3vGfWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MlPETWM2OD5zNTFOwG0> M2DBOlI{PzJ7NECy
TOV112D MnzkS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M1jhR|AuOyEQvF2= NVrFVGQ2UUN3ME6xOUDPxE1? M4ThXFI{PzJ7NECy
C4-2 MXLHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NIDzPWQxNTNizszN M1zpUlE1KGR? NHLiNYZFVVOR NELSS45l\WO{ZXHz[ZMh[2:ub375JI52dWKncjDkc5NmKGSncHXu[IVvfGy7 NYTNNIREOjN3NkWyOFQ>
PC3 NI[2NpZIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MUSwMVMh|ryP MWqxOEBl NVf6VooxTE2VTx?= NEDnXnJl\WO{ZXHz[ZMh[2:ub375JI52dWKncjDkc5NmKGSncHXu[IVvfGy7 NW\5cYdtOjN3NkWyOFQ>
DU145 MofLS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NFzU[oIxNTNizszN NVrBPHhwOTRiZB?= NXXBSYZlTE2VTx?= MoHF[IVkemWjc3XzJINwdG:weTDueY1j\XJiZH;z[UBl\XCnbnTlcpRtgQ>? MWmyN|U3PTJ2NB?=
VCaP  NI\abVhIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MVuwMVMh|ryP M1HRUlE1KGR? NHP3eHpFVVOR MYPk[YNz\WG|ZYOgZ49td267IH71cYJmeiCmb4PlJIRmeGWwZHXueIx6 MljUNlM2PjV{NES=
LNCaP  MmnYS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NH3XcJoxNTNizszN NEOwcZgyPCCm MV\EUXNQ NXTDXXh4\GWlcnXhd4V{KGOxbH;ufUBvfW2kZYKg[I9{\SCmZYDlcoRmdnSueR?= M1vrXVI{PTZ3MkS0
MDA-MB-468 NI\jXpRE\WyuIG\pZYJqdGm2eTDBd5NigQ>? NUK1UZV{UUN3ME25Mlch|ryP NFzwbIszOjZ5OEG2NS=>
MDA-MB-231 M3ziRmNmdGxiVnnhZoltcXS7IFHzd4F6 MlHYTWM2OD1zMzFOwG0> M3\qS|IzPjd6MU[x
Cal-51 M2m5SGNmdGxiVnnhZoltcXS7IFHzd4F6 MV3JR|UxRThwNjFOwG0> NFHmSZQzOjZ5OEG2NS=>

... 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 Insoluble
Ethanol Insoluble
In vivo Add solvents to the product individually and in order:
2% DMSO+30% PEG 300+2% Tween 80+ddH2O
For best results, use promptly after mixing.

* 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
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