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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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) 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.

Purity & Quality Control

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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.
Targets
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 NUnoR2h5TnWwY4Tpc44hSXO|YYm= Mo\ZNE4yNzFxNUCwM|ExODBibl2= MoPXbY5pcWKrdIOgVGFTWCCjY4Tpeol1gSCjdDDzeIFzfGmwZzDjc45k\XKwdILheIlwdiCxZjC1NFAhdk1? MUmyOVEzQDR3NR?=
BT474 NUfuS5JzT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NIK0Woo2ODBibl2= MmHhNVDjiJNzNdMg[C=> NHLWXpRz\WS3Y3XzJINmdGxiZ4Lve5RpKGmwIITo[UBnd3W{IHzpcoV{KGGwZDDzbYdvcW[rY3HueIx6 NVP1VlNNOjVzMki0OVU>
SKBR3 MmLhS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M2XwSlUxOCCwTR?= Mm\vNVDjiJNzNdMg[C=> NEPvU49z\WS3Y3XzJINmdGxiZ4Lve5RpKGmwIITo[UBnd3W{IHzpcoV{KGGwZDDzbYdvcW[rY3HueIx6 NIXWSnEzPTF{OES1OS=>
AU565 MkHiS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MkK0OVAxKG6P MXWxNQKBmzF3wrDk MYHy[YR2[2W|IHPlcIwh\3Kxd4ToJIlvKHSqZTDmc5VzKGyrbnXzJIFv\CC|aXfubYZq[2GwdHz5 NVrzS|F5OjVzMki0OVU>
EFM192A NXXnOY95T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NXHRWlBiPTByIH7N MmP0NVDjiJNzNdMg[C=> MmXRdoVlfWOnczDj[YxtKGe{b4f0bEBqdiC2aHWg[o92eiCuaX7ld{BidmRic3nncolncWOjboTsfS=> MVSyOVEzQDR3NR?=
MDA-MB-231 Mln2SpVv[3Srb36gRZN{[Xl? MnGxNVAwOjBxNECg{txO NWHBcoRIOjRiaB?= M2m5Rolv[3KnYYPld{BxNUGNVDDs[ZZmdHNiaX6gZUBld3OnLXTldIVv\GWwdDDtZY5v\XJ? M3vyVVI1PDJyMUWy
MDA-MB-231 M2Xyd2NmdGxiVnnhZoltcXS7IFHzd4F6 MUGwMlEuPDBizszN M1vLelI1KGh? MorYTWM2OOLCiU5ihKkyPy55N9Mg{txO MoH3NlQ1OjBzNUK=
MDA-MB-231 MYXBdI9xfG:|aYOgRZN{[Xl? NHjQ[ooyOC9{MD:0NEDPxE1? MUeyOEBp NFvtWoJqdmS3Y3XzJIFxd3C2b4Ppd{Bld3OnIHTldIVv\GWwdHz5 M4XFOlI1PDJyMUWy
MDA-MB-231 Mki1S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NULZV5N7OTBxMkCvOFAh|ryP MXeyOEBp MmPSZoxw[2u|IHPlcIwh[3mlbHWgdJJw\3Knc4Ppc44hcW5iR{KvUUBxcGG|ZR?= NFLHUFIzPDR{MEG1Ni=>
H460 MV3Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NF;Ydmo1ODBibl2= M3:3e|I1yqCq NG\lNmFqdmO{ZXHz[ZMh[2WubIXsZZIhemGmaX;z[Y5{cXSrdnn0fS=> MnLvNlQ1OTF4MUG=
A549  MW\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M37oclQxOCCwTR?= NX;TVIpTOjUEoHi= MX7pcoNz\WG|ZYOgZ4VtdHWuYYKgdoFlcW:|ZX7zbZRqfmm2eR?= NELL[4QzPDRzMU[xNS=>
DT40 NGPKSm1Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NYPrPIpkUUN3ME2yNUBvVQ>? NFOwdIszPDN3NkixNy=>
DU145 MVvHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NEi5fFBKSzVyPUG4JI5O NXjsd2FUOjR|NU[4NVM>
COLO704 MVLHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M3q4PGlEPTB;Mj61NkDDuSByLk[3JO69VQ>? NFTZ[mQzOzd{OUSwNi=>
OVMANAb NVniXIc1T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MUnJR|UxRTJwNUigxtEhOC5|ODFOwG0> NICyRlYzOzd{OUSwNi=>
OV177 NHzC[ZJIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MmPRTWM2OD1{Lke4JOKyKDBwN{Gg{txO MVyyN|czQTRyMh?=
OAW28 M2HIcWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MVzJR|UxRTNwNkGgxtEhOC5{ODFOwG0> M1yzfVI{PzJ7NECy
OVSAHO MXfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MWjJR|UxRTNwNkSgxtEhOC5|MzFOwG0> MYqyN|czQTRyMh?=
OVKATE MlPpS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M1zTO2lEPTB;Mz62OEDDuSBzLke5JO69VQ>? NUHXWm15OjN5Mkm0NFI>
OVCAR3 MYPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MmjJTWM2OD1|Lke0JOKyKDBwNECg{txO M3n0fVI{PzJ7NECy
PEO14 M2TwXWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M4jVc2lEPTB;Mz64OEDDuSByLke2JO69VQ>? M3eweFI{PzJ7NECy
A2780 MYrHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NWKySVc6UUN3ME2zMlk1KMLzIECuNlUh|ryP NU\kWVF2OjN5Mkm0NFI>
OVTOKO MXTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MlHWTWM2OD12LkG0JOKyKDFwNUOg{txO NEG5doozOzd{OUSwNi=>
KURAMOCHIb NFfUUZpIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MYTJR|UxRTRwM{SgxtEhOC5{OTFOwG0> M1XE[FI{PzJ7NECy
TOV21G M2Gyd2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M4jNcGlEPTB;NT6wO{DDuSBzLkOwJO69VQ>? Mk[xNlM4Ojl2MEK=
OVISE NGniN5lIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MUjJR|UxRTVwNkigxtEhOC5{MzFOwG0> NIjPRmMzOzd{OUSwNi=>
KK NYHSb45XT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NEjMPZRKSzVyPU[uNVUhyrFiMT60NkDPxE1? NXPje4RFOjN5Mkm0NFI>
RMUGS NFnLb|JIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NWr2cYN4UUN3ME23MlA{KMLzIEGuPFMh|ryP MYSyN|czQTRyMh?=
PEO6 MYLHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MVPJR|UxRTdwME[gxtEhOC55NDFOwG0> MnfyNlM4Ojl2MEK=
OVCA429 M{LtZWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MUPJR|UxRThwMkmgxtEhOS54NDFOwG0> MUWyN|czQTRyMh?=
OV167 MlXIS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? Mni5TWM2OD16LkOzJOKyKDFwMUig{txO M4TuSFI{PzJ7NECy
RMG1 MlvzS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NELM[HRKSzVyPUmuN|IhyrFiMj6zOkDPxE1? NX3D[lVHOjN5Mkm0NFI>
OVCAR5 M{K4WWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MVvJR|UxRTlwNUCgxtEhOi53OTFOwG0> M4TUbFI{PzJ7NECy
EFO21 M1HMdmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M13GcmlEPTB;OT65NkDDuSBzLki3JO69VQ>? M{nrd|I{PzJ7NECy
ES2 M4DJ[mdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MXTJR|UxRTFyLkGyJOKyKDFwMkOg{txO MnPTNlM4Ojl2MEK=
Tyk-nu NVvKO4U2T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M3niTWlEPTB;MUCuNlAhyrFiMT6xNkDPxE1? MWeyN|czQTRyMh?=
CAOV3 NXrhenpnT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NWjET4tbUUN3ME2xNE4{PyEEsTCwMlg4KM7:TR?= M4LselI{PzJ7NECy
OV207 MVrHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NV71U|JtUUN3ME2xNk4zPyEEsTCwMlMzKM7:TR?= MVeyN|czQTRyMh?=
HEY M17KUmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NGHSTppKSzVyPUGzMlAyKMLzIECuO|Uh|ryP NFf2dZQzOzd{OUSwNi=>
DOV13 NXnRcmJwT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MV7JR|UxRjF3IN88US=> MnnONlM4Ojl2MEK=
EFO27 NWW5V2Y3T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NIfCU3ZKSzVyPkG1JO69VQ>? NFLWOoYzOzd{OUSwNi=>
HEY C2 NYfGXWxxT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NGS3fXRKSzVyPkG1JO69VQ>? MVOyN|czQTRyMh?=
KOC-7cc M2f2d2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MkLPTWM2OD5zNTFOwG0> NIm4[HkzOzd{OUSwNi=>
MCASb NIDXXFRIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MWHJR|UxRjF3IN88US=> NFrkTFQzOzd{OUSwNi=>
OAW42 MljiS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NVLMVIdHUUN3ME6xOUDPxE1? NXjXVnNKOjN5Mkm0NFI>
OV2008 M3e4V2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M{HJU2lEPTB-MUWg{txO NW\1WFNUOjN5Mkm0NFI>
OV90 Mnr5S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NHK1OZpKSzVyPkG1JO69VQ>? NUfxcVRCOjN5Mkm0NFI>
OVCA420b MmezS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MmjSTWM2OD5zNTFOwG0> M2\6[lI{PzJ7NECy
OVCA432 NHvQW49Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MlXhTWM2OD5zNTFOwG0> M1PDWFI{PzJ7NECy
PEA2 NV\WRWs5T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NX3WdW1QUUN3ME6xOUDPxE1? MoL2NlM4Ojl2MEK=
SKOV3 MVTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MWTJR|UxRjF3IN88US=> NXO0bHZrOjN5Mkm0NFI>
TOV112D NELOcXFIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M17TZVAuOyEQvF2= NWniN5F1UUN3ME6xOUDPxE1? MlrkNlM4Ojl2MEK=
C4-2 NHHN[|lIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MlLCNE0{KM7:TR?= NHLQfnIyPCCm NIHiUoxFVVOR MYfk[YNz\WG|ZYOgZ49td267IH71cYJmeiCmb4PlJIRmeGWwZHXueIx6 MnHCNlM2PjV{NES=
PC3 NYPvVHJbT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NU\xUZVOOC1|IN88US=> MXixOEBl MU\EUXNQ NUS0XYwy\GWlcnXhd4V{KGOxbH;ufUBvfW2kZYKg[I9{\SCmZYDlcoRmdnSueR?= M17JSlI{PTZ3MkS0
DU145 NX\lPFBPT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NI\xRVYxNTNizszN MnfPNVQh\A>? M3rPRmROW09? MoTN[IVkemWjc3XzJINwdG:weTDueY1j\XJiZH;z[UBl\XCnbnTlcpRtgQ>? MXOyN|U3PTJ2NB?=
VCaP  NUf3UGE1T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MX[wMVMh|ryP M2T3bVE1KGR? MmGySG1UVw>? NW\r[YxE\GWlcnXhd4V{KGOxbH;ufUBvfW2kZYKg[I9{\SCmZYDlcoRmdnSueR?= M4L2TFI{PTZ3MkS0
LNCaP  MWXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MUmwMVMh|ryP MnTVNVQh\A>? NX20bGRGTE2VTx?= NWTyRZRt\GWlcnXhd4V{KGOxbH;ufUBvfW2kZYKg[I9{\SCmZYDlcoRmdnSueR?= NFXGc5czOzV4NUK0OC=>
MDA-MB-468 NGLBc5VE\WyuIG\pZYJqdGm2eTDBd5NigQ>? M3zEcGlEPTB;OT63JO69VQ>? M1rYXFIzPjd6MU[x
MDA-MB-231 MYTD[YxtKF[rYXLpcIl1gSCDc4PhfS=> M4LuV2lEPTB;MUOg{txO MYSyNlY4QDF4MR?=
Cal-51 M36wRWNmdGxiVnnhZoltcXS7IFHzd4F6 M2jVUGlEPTB;OD62JO69VQ>? Mn3HNlI3PzhzNkG=

... 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]

Protocol

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 individually and in order:
2% DMSO+30% PEG 300+2% Tween 80+ddH2O
10mg/mL

* 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
Formula

C19H18FN3O.H3PO4

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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Answers to questions you may have can be found in the inhibitor handling instructions. Topics include how to prepare stock solutions, how to store inhibitors, and issues that need special attention for cell-based assays and animal experiments.

Handling Instructions

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID