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 M17UcmZ2dmO2aX;uJGF{e2G7 MYewMlEwOS93MECvNVAxOCCwTR?= NVnoZlFocW6qaXLpeJMhWEGUUDDhZ5Rqfmm2eTDheEB{fGG{dHnu[{Bkd26lZYLueJJifGmxbjDv[kA2ODBibl2= NFjr[|EzPTF{OES1OS=>
BT474 NY\UcIZMT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NIKwV4Y2ODBibl2= M{TtcVEx6oDVMUZCpIQ> Ml76doVlfWOnczDj[YxtKGe{b4f0bEBqdiC2aHWg[o92eiCuaX7ld{BidmRic3nncolncWOjboTsfS=> MWGyOVEzQDR3NR?=
SKBR3 MojxS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MVO1NFAhdk1? MUixNQKBmzF3wrDk NF30TWdz\WS3Y3XzJINmdGxiZ4Lve5RpKGmwIITo[UBnd3W{IHzpcoV{KGGwZDDzbYdvcW[rY3HueIx6 NW\pWJQxOjVzMki0OVU>
AU565 MYnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MUW1NFAhdk1? M2rDbFEx6oDVMUZCpIQ> NWHLbnBpemWmdXPld{Bk\WyuIHfyc5d1cCCrbjD0bIUh\m:3cjDsbY5meyCjbnSgd4lodmmoaXPhcpRtgQ>? MoH6NlUyOjh2NUW=
EFM192A MVHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? Mlz4OVAxKG6P M{THXlEx6oDVMUZCpIQ> NXHSdXVremWmdXPld{Bk\WyuIHfyc5d1cCCrbjD0bIUh\m:3cjDsbY5meyCjbnSgd4lodmmoaXPhcpRtgQ>? MknmNlUyOjh2NUW=
MDA-MB-231 NFzUbHVHfW6ldHnvckBCe3OjeR?= MlLYNVAwOjBxNECg{txO MUSyOEBp MVfpcoNz\WG|ZYOgdE1CU1RibHX2[Yx{KGmwIHGg[I9{\S2mZYDlcoRmdnRibXHucoVz M{TvdVI1PDJyMUWy
MDA-MB-231 NYnPXYZPSXCxcITvd4l{KEG|c3H5 MYixNE8zOC92MDFOwG0> NH\UOJAzPCCq Moq5bY5lfWOnczDhdI9xfG:|aYOg[I9{\SCmZYDlcoRmdnSueR?= M4\2U|I1PDJyMUWy
MDA-MB-231 NFHrVGxIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M3;tUlExNzJyL{SwJO69VQ>? NWn2bXc4OjRiaB?= MkHqZoxw[2u|IHPlcIwh[3mlbHWgdJJw\3Knc4Ppc44hcW5iR{KvUUBxcGG|ZR?= MXeyOFQzODF3Mh?=
H460 NFXkb5pIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M1LzeFQxOCCwTR?= NInWSJkzPMLiaB?= MVrpcoNz\WG|ZYOgZ4VtdHWuYYKgdoFlcW:|ZX7zbZRqfmm2eR?= NX70fW9pOjR2MUG2NVE>
A549  MXTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NVrq[JhJPDByIH7N NVniXXYzOjUEoHi= NXXRd3JOcW6lcnXhd4V{KGOnbHz1cIFzKHKjZHnvd4Vve2m2aY\peJk> NEnYZ2UzPDRzMU[xNS=>
DT40 MoX0S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M4DZOWlEPTB;MkGgcm0> NHu5PFkzPDN3NkixNy=>
DU145 NXXHeJRlT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= Mn2zTWM2OD1zODDuUS=> MWGyOFM2PjhzMx?=
COLO704 MknOS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NESyO5ZKSzVyPUKuOVIhyrFiMD62O{DPxE1? MkXyNlM4Ojl2MEK=
OVMANAb M1TYOGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NXTOZlVxUUN3ME2yMlU5KMLzIECuN|gh|ryP NXLacIdoOjN5Mkm0NFI>
OV177 M4nYWmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NUDTVnZVUUN3ME2yMlc5KMLzIECuO|Eh|ryP NGTTS2QzOzd{OUSwNi=>
OAW28 MnXhS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M1v4TmlEPTB;Mz62NUDDuSByLkK4JO69VQ>? NUjOUFhnOjN5Mkm0NFI>
OVSAHO NGP0d|RIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NX74d3JHUUN3ME2zMlY1KMLzIECuN|Mh|ryP NF;YSHozOzd{OUSwNi=>
OVKATE NVThe2dnT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NYDveFhyUUN3ME2zMlY1KMLzIEGuO|kh|ryP MVOyN|czQTRyMh?=
OVCAR3 MkjsS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MWfJR|UxRTNwN{SgxtEhOC52MDFOwG0> M{Wyc|I{PzJ7NECy
PEO14 MV7Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MnSyTWM2OD1|Lki0JOKyKDBwN{[g{txO M2TsWFI{PzJ7NECy
A2780 NFfjdIlIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MnHLTWM2OD1|Lkm0JOKyKDBwMkWg{txO MWSyN|czQTRyMh?=
KURAMOCHIb MV7Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NX\DN3d2UUN3ME20MlM1KMLzIECuNlkh|ryP NIXmeYQzOzd{OUSwNi=>
TOV21G M1;5WGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NVPQTHo2UUN3ME21MlA4KMLzIEGuN|Ah|ryP MnfiNlM4Ojl2MEK=
OVISE NUfkRmdtT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NVvhT3I{UUN3ME21MlY5KMLzIECuNlMh|ryP NIO3[4czOzd{OUSwNi=>
KK NIrZNGNIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NGPEOZpKSzVyPU[uNVUhyrFiMT60NkDPxE1? NVyzbIlTOjN5Mkm0NFI>
RMUGS NEjzc2xIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M1TkSGlEPTB;Nz6wN{DDuSBzLkizJO69VQ>? MXiyN|czQTRyMh?=
PEO6 NUKz[XFmT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NIDyeXNKSzVyPUeuNFYhyrFiMD63OEDPxE1? MYiyN|czQTRyMh?=
OVCA429 NITCflNIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= Mn\yTWM2OD16LkK5JOKyKDFwNkSg{txO Mnv5NlM4Ojl2MEK=
OV167 M2HWdGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MWXJR|UxRThwM{OgxtEhOS5zODFOwG0> NX7rbWtSOjN5Mkm0NFI>
RMG1 MVHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MVfJR|UxRTlwM{KgxtEhOi5|NjFOwG0> MW[yN|czQTRyMh?=
OVCAR5 NHjj[lhIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MYnJR|UxRTlwNUCgxtEhOi53OTFOwG0> MlTzNlM4Ojl2MEK=
EFO21 NXrBWXU1T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MV\JR|UxRTlwOUKgxtEhOS56NzFOwG0> MV2yN|czQTRyMh?=
ES2 MYPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MY\JR|UxRTFyLkGyJOKyKDFwMkOg{txO Ml\kNlM4Ojl2MEK=
Tyk-nu MlXmS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M2TNbGlEPTB;MUCuNlAhyrFiMT6xNkDPxE1? NWH3ToxYOjN5Mkm0NFI>
CAOV3 NXrVSGVlT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MlLlTWM2OD1zMD6zO{DDuSByLki3JO69VQ>? NH;YZ|kzOzd{OUSwNi=>
OV207 MVnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MYDJR|UxRTF{LkK3JOKyKDBwM{Kg{txO NGPYZnYzOzd{OUSwNi=>
HEY MmLTS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NXrkWWFbUUN3ME2xN{4xOSEEsTCwMlc2KM7:TR?= NFfBVIwzOzd{OUSwNi=>
DOV13 Mon1S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NXXiZ4JVUUN3ME6xOUDPxE1? NVPNOmV[OjN5Mkm0NFI>
EFO27 MYTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MnLBTWM2OD5zNTFOwG0> NU\4fVllOjN5Mkm0NFI>
HEY C2 MnvqS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M1zLRmlEPTB-MUWg{txO MUSyN|czQTRyMh?=
KOC-7cc NH:5bnlIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M1:xZmlEPTB-MUWg{txO NX7oSo9ZOjN5Mkm0NFI>
MCASb NW\ueWh{T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MVvJR|UxRjF3IN88US=> NX;QOmxsOjN5Mkm0NFI>
OAW42 NVj4OHdwT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MX\JR|UxRjF3IN88US=> MUiyN|czQTRyMh?=
OV2008 NV\uR5ZwT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MkK5TWM2OD5zNTFOwG0> NYT5UYsyOjN5Mkm0NFI>
OV90 Ml\FS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NGLJcY5KSzVyPkG1JO69VQ>? NXjUUoxGOjN5Mkm0NFI>
OVCA420b NIDnOFdIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MXrJR|UxRjF3IN88US=> NHHYWZQzOzd{OUSwNi=>
OVCA432 Ml;wS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NXPORlVuUUN3ME6xOUDPxE1? NFPaRpkzOzd{OUSwNi=>
PEA2 M3\tR2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MVHJR|UxRjF3IN88US=> NIDsOowzOzd{OUSwNi=>
TOV112D MVvHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NEKzbVExNTNizszN Mn;oTWM2OD5zNTFOwG0> MVOyN|czQTRyMh?=
C4-2 MX3Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NV\O[ndlOC1|IN88US=> M1T3XlE1KGR? M2j0XWROW09? NV3KOmMy\GWlcnXhd4V{KGOxbH;ufUBvfW2kZYKg[I9{\SCmZYDlcoRmdnSueR?= Mme2NlM2PjV{NES=
PC3 Mkm4S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? Mnz5NE0{KM7:TR?= MWWxOEBl M{DhO2ROW09? MWPk[YNz\WG|ZYOgZ49td267IH71cYJmeiCmb4PlJIRmeGWwZHXueIx6 NGLXXYUzOzV4NUK0OC=>
DU145 NH3GSo1Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NVjBPWFSOC1|IN88US=> NV;ndHBlOTRiZB?= MnjFSG1UVw>? NHvmVWtl\WO{ZXHz[ZMh[2:ub375JI52dWKncjDkc5NmKGSncHXu[IVvfGy7 MnrRNlM2PjV{NES=
VCaP  MXfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? Mlz0NE0{KM7:TR?= Mm[2NVQh\A>? NGKyT|FFVVOR NV;OVYFn\GWlcnXhd4V{KGOxbH;ufUBvfW2kZYKg[I9{\SCmZYDlcoRmdnSueR?= M3y3dlI{PTZ3MkS0
LNCaP  NGLTco1Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MnHnNE0{KM7:TR?= NH3sPFcyPCCm NX;Ge3l5TE2VTx?= M3\iWoRm[3KnYYPld{Bkd2yxbomgcpVu[mW{IHTvd4Uh\GWyZX7k[Y51dHl? M1z5N|I{PTZ3MkS0
MDA-MB-468 NWT6N2NtS2WubDDWbYFjcWyrdImgRZN{[Xl? NIjVeGpKSzVyPUmuO{DPxE1? MkHxNlI3PzhzNkG=
Cal-51 M{fjWmNmdGxiVnnhZoltcXS7IFHzd4F6 NUD3ToJ5UUN3ME24MlYh|ryP NXjx[nFqOjJ4N{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 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