Rucaparib (AG-014699,PF-01367338) phosphate

製品コードS1098

Rucaparib (AG-014699,PF-01367338) phosphate化学構造

分子量(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.

サイズ 価格(税別)  
JPY 22244.00
JPY 19920.00
JPY 34860.00
JPY 111220.00

カスタマーフィードバック(6)

  • 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.

製品安全説明書

PARP阻害剤の選択性比較

生物活性

製品説明 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.
特性 The first PARP inhibitor used in clinical trials combined with temozolomide.
ターゲット
PARP [1]
(Cell-free assay)
1.4 nM(Ki)
体外試験

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]

細胞データ
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
BT-474 Mn\NSpVv[3Srb36gRZN{[Xl? NULLeXlEOC5zL{GvOVAxNzFyMECgcm0> MXjpcohq[mm2czDQRXJRKGGldHn2bZR6KGG2IIP0ZZJ1cW6pIHPvcoNmem62cnH0bY9vKG:oIEWwNEBvVQ>? NITrZm0zPTF{OES1OS=>
BT474 M1njT2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MlLROVAxKG6P NHTBVoYyOOLCk{G1xsBl MV\y[YR2[2W|IHPlcIwh\3Kxd4ToJIlvKHSqZTDmc5VzKGyrbnXzJIFv\CC|aXfubYZq[2GwdHz5 MY[yOVEzQDR3NR?=
SKBR3 MULHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? Mn3ROVAxKG6P MWGxNQKBmzF3wrDk NEX3dFdz\WS3Y3XzJINmdGxiZ4Lve5RpKGmwIITo[UBnd3W{IHzpcoV{KGGwZDDzbYdvcW[rY3HueIx6 M2LZfFI2OTJ6NEW1
AU565 MXLHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MVu1NFAhdk1? NFzSbJgyOOLCk{G1xsBl M3LsWZJm\HWlZYOgZ4VtdCCpcn;3eIghcW5idHjlJIZwfXJibHnu[ZMh[W6mIIPp[45q\mmlYX70cJk> MXWyOVEzQDR3NR?=
EFM192A M2DxbWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NWLkfVJtPTByIH7N M1rIVlEx6oDVMUZCpIQ> MX\y[YR2[2W|IHPlcIwh\3Kxd4ToJIlvKHSqZTDmc5VzKGyrbnXzJIFv\CC|aXfubYZq[2GwdHz5 NWfZOGZrOjVzMki0OVU>
MDA-MB-231 NYXPboZQTnWwY4Tpc44hSXO|YYm= NIjZbZAyOC9{MD:0NEDPxE1? NXLEVFZIOjRiaB?= MYXpcoNz\WG|ZYOgdE1CU1RibHX2[Yx{KGmwIHGg[I9{\S2mZYDlcoRmdnRibXHucoVz NHi1VJQzPDR{MEG1Ni=>
MDA-MB-231 NUjTVIx[S2WubDDWbYFjcWyrdImgRZN{[Xl? NI\Ic3cxNjFvNECg{txO MlXmNlQhcA>? M{nremlEPTEkgJm95qCKOTdwN{hCpO69VQ>? NFXyVGMzPDR{MEG1Ni=>
MDA-MB-231 MYDBdI9xfG:|aYOgRZN{[Xl? NIPtN2kyOC9{MD:0NEDPxE1? MoLFNlQhcA>? MmLwbY5lfWOnczDhdI9xfG:|aYOg[I9{\SCmZYDlcoRmdnSueR?= MXOyOFQzODF3Mh?=
MDA-MB-231 NH;CT5VIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NVHSfFBJOTBxMkCvOFAh|ryP MXKyOEBp NEXUXVFjdG:la4OgZ4VtdCCleXPs[UBxem:pcnXzd4lwdiCrbjDHNk9OKHCqYYPl M1\XXVI1PDJyMUWy
H460 MWPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NXHNO5VGPDByIH7N M{HWfFI1yqCq MUPpcoNz\WG|ZYOgZ4VtdHWuYYKgdoFlcW:|ZX7zbZRqfmm2eR?= MkLpNlQ1OTF4MUG=
A549  M3n2O2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MYG0NFAhdk1? NYrNfnZrOjUEoHi= NXfpSGV4cW6lcnXhd4V{KGOnbHz1cIFzKHKjZHnvd4Vve2m2aY\peJk> NHHCTWYzPDRzMU[xNS=>
DT40 NXzXPYFDT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NWqxboI2UUN3ME2yNUBvVQ>? M2rDUVI1OzV4OEGz
DU145 MlLDS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MWfJR|UxRTF6IH7N M4S1PFI1OzV4OEGz
COLO704 MXvHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NUjZUWZbUUN3ME2yMlUzKMLzIECuOlch|ryP MmKyNlM4Ojl2MEK=
OVMANAb MXTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NWDpN4k6UUN3ME2yMlU5KMLzIECuN|gh|ryP NY\rdG9POjN5Mkm0NFI>
OV177 NEnWXXFIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MUjJR|UxRTJwN{igxtEhOC55MTFOwG0> NWjOWGhPOjN5Mkm0NFI>
OAW28 MnjyS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MVLJR|UxRTNwNkGgxtEhOC5{ODFOwG0> NH35VJYzOzd{OUSwNi=>
OVSAHO NEnROHZIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M2jEeGlEPTB;Mz62OEDDuSByLkOzJO69VQ>? NIfoU2gzOzd{OUSwNi=>
OVKATE MVvHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NGD3VGVKSzVyPUOuOlQhyrFiMT63PUDPxE1? MXqyN|czQTRyMh?=
OVCAR3 NV7YNIdyT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M3nNSGlEPTB;Mz63OEDDuSByLkSwJO69VQ>? MmDhNlM4Ojl2MEK=
PEO14 MmjES5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MmP2TWM2OD1|Lki0JOKyKDBwN{[g{txO MXuyN|czQTRyMh?=
A2780 NHOxdFVIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MX7JR|UxRTNwOUSgxtEhOC5{NTFOwG0> MVmyN|czQTRyMh?=
OVTOKO NFj6ZXpIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NETmUldKSzVyPUSuNVQhyrFiMT61N{DPxE1? NYPOS5Z6OjN5Mkm0NFI>
KURAMOCHIb MonLS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NYrZbHUxUUN3ME20MlM1KMLzIECuNlkh|ryP Ml7xNlM4Ojl2MEK=
TOV21G M4njbGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NFTycJZKSzVyPUWuNFchyrFiMT6zNEDPxE1? NVvxbHUzOjN5Mkm0NFI>
OVISE NGm5UFZIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= Mn25TWM2OD13Lk[4JOKyKDBwMkOg{txO MW[yN|czQTRyMh?=
KK MXLHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MoHtTWM2OD14LkG1JOKyKDFwNEKg{txO NHPV[28zOzd{OUSwNi=>
RMUGS NYPoV|ZDT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MWnJR|UxRTdwMEOgxtEhOS56MzFOwG0> NIPnVHMzOzd{OUSwNi=>
PEO6 Mmn3S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? Ml:5TWM2OD15LkC2JOKyKDBwN{Sg{txO MXOyN|czQTRyMh?=
OVCA429 M2TXTmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 Mo\3TWM2OD16LkK5JOKyKDFwNkSg{txO M{PT[FI{PzJ7NECy
OV167 NHjobYRIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NYjrcmk{UUN3ME24MlM{KMLzIEGuNVgh|ryP MmjMNlM4Ojl2MEK=
RMG1 NUXFZZd1T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NVTETmhGUUN3ME25MlMzKMLzIEKuN|Yh|ryP MlL1NlM4Ojl2MEK=
OVCAR5 M4L5cWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M2f0V2lEPTB;OT61NEDDuSB{LkW5JO69VQ>? NWHXcVdiOjN5Mkm0NFI>
EFO21 NHS5NZNIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M4TyTWlEPTB;OT65NkDDuSBzLki3JO69VQ>? M{TNZVI{PzJ7NECy
ES2 M4HPfGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M{focWlEPTB;MUCuNVIhyrFiMT6yN{DPxE1? NHrsNWQzOzd{OUSwNi=>
Tyk-nu MXHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M{O0XWlEPTB;MUCuNlAhyrFiMT6xNkDPxE1? MUeyN|czQTRyMh?=
CAOV3 NGnvU2hIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MnfSTWM2OD1zMD6zO{DDuSByLki3JO69VQ>? NUDK[HlDOjN5Mkm0NFI>
OV207 M335dmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 Mm\tTWM2OD1zMj6yO{DDuSByLkOyJO69VQ>? MVGyN|czQTRyMh?=
HEY M1;MTmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MkDmTWM2OD1zMz6wNUDDuSByLke1JO69VQ>? NXTpNlVHOjN5Mkm0NFI>
DOV13 NVfq[GZoT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MV;JR|UxRjF3IN88US=> Mom1NlM4Ojl2MEK=
EFO27 MVjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MnLGTWM2OD5zNTFOwG0> NYDWWmZXOjN5Mkm0NFI>
HEY C2 NInpdlBIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MUDJR|UxRjF3IN88US=> NELMOIczOzd{OUSwNi=>
KOC-7cc M4mxVGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MVjJR|UxRjF3IN88US=> NVvYNZFJOjN5Mkm0NFI>
MCASb NH:wOZdIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MmHLTWM2OD5zNTFOwG0> MnXQNlM4Ojl2MEK=
OAW42 M1jvSGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NIHFO2lKSzVyPkG1JO69VQ>? MnvWNlM4Ojl2MEK=
OV2008 MmLYS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MlW1TWM2OD5zNTFOwG0> NVniUng5OjN5Mkm0NFI>
OV90 NVXNSW42T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NWe3bFBNUUN3ME6xOUDPxE1? MYmyN|czQTRyMh?=
OVCA420b NUTJ[3l6T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MWDJR|UxRjF3IN88US=> NITjcI4zOzd{OUSwNi=>
OVCA432 M1\XPGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MW\JR|UxRjF3IN88US=> M3vBdFI{PzJ7NECy
PEA2 NFThO4NIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NXLmR|RjUUN3ME6xOUDPxE1? M{PVSlI{PzJ7NECy
SKOV3 NVrITZZnT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NFvQcXJKSzVyPkG1JO69VQ>? M3XOTVI{PzJ7NECy
TOV112D MnXuS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MUiwMVMh|ryP MXLJR|UxRjF3IN88US=> Mn;JNlM4Ojl2MEK=
C4-2 NF\FXopIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NFrJS2kxNTNizszN NYfJZ2tMOTRiZB?= MlnTSG1UVw>? M1PycIRm[3KnYYPld{Bkd2yxbomgcpVu[mW{IHTvd4Uh\GWyZX7k[Y51dHl? M3njelI{PTZ3MkS0
PC3 M4XDVWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MV6wMVMh|ryP MV2xOEBl M{HJS2ROW09? MULk[YNz\WG|ZYOgZ49td267IH71cYJmeiCmb4PlJIRmeGWwZHXueIx6 MVOyN|U3PTJ2NB?=
DU145 M1HPfGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NH\4fmsxNTNizszN NUm3Z3JwOTRiZB?= MY\EUXNQ NGPiU3Fl\WO{ZXHz[ZMh[2:ub375JI52dWKncjDkc5NmKGSncHXu[IVvfGy7 M4fu[FI{PTZ3MkS0
VCaP  Ml3MS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NIP5V|MxNTNizszN M123[lE1KGR? Mn3ySG1UVw>? MULk[YNz\WG|ZYOgZ49td267IH71cYJmeiCmb4PlJIRmeGWwZHXueIx6 M1vmUFI{PTZ3MkS0
LNCaP  NVPFXVd6T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NGLKcXIxNTNizszN MWSxOEBl NU\ododDTE2VTx?= NVTIVZI2\GWlcnXhd4V{KGOxbH;ufUBvfW2kZYKg[I9{\SCmZYDlcoRmdnSueR?= MUmyN|U3PTJ2NB?=
MDA-MB-468 M2[yWGNmdGxiVnnhZoltcXS7IFHzd4F6 MUTJR|UxRTlwNzFOwG0> MYSyNlY4QDF4MR?=
MDA-MB-231 M3;JeGNmdGxiVnnhZoltcXS7IFHzd4F6 M17ocmlEPTB;MUOg{txO M4TTcFIzPjd6MU[x
Cal-51 NWfZOWNzS2WubDDWbYFjcWyrdImgRZN{[Xl? M4iydGlEPTB;OD62JO69VQ>? MmPENlI3PzhzNkG=

多くの細胞株試験データを見る場合、クリックしてください

体内試験 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]

お薦めの試験操作(参考用のみ)

キナーゼ試験:[1]
+ 展開

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.
細胞試験: [4]
+ 展開
  • 細胞株: D425Med, D283Med and D384Med cells
  • 濃度: 0.4 μM
  • 反応時間: 3 or 5 days
  • 実験の流れ: 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.
    (参考用のみ)
動物試験:[4]
+ 展開
  • 動物モデル: CD-1 nude mice bearing established D283Med xenografts
  • 製剤: Normal saline
  • 投薬量: 1 mg/kg
  • 投与方法: One or four daily by i.p.
    (参考用のみ)

溶解度 (25°C)

体外 DMSO 84 mg/mL (199.35 mM)
Water Insoluble
Ethanol Insoluble
体内 左から右までの手順で、溶剤を製品に加えることです:
2% DMSO+30% PEG 300+2% Tween 80+ddH2O
いい結果が出るために、混じった後、直ちに使うと推めます。
10mg/mL

* 溶解度検測はSelleck技術部門によって行いますので、文献より提供された溶解度と差異がある可能性がありますが、生産工芸と不同ロット(lot)で起きる正常な現象ですから、ご安心ください。

化学情報

分子量 421.36
化学式

C19H18FN3O.H3PO4

CAS No. 459868-92-9
保管
別名 N/A

便利ツール

モル濃度計算器

モル濃度計算器

解決のために必要とされるマス、ボリュームまたは濃度を計算してください。

マス (g) = 濃度 (mol/L) x ボリューム (L) x 分子量 (g/mol)

モル濃度計算器方程式

  • マス
    濃度
    ボリューム
    分子量

*貯蔵液を準備するとき、常に、オンであるとわかる製品のバッチに特有の分子量を使って、を通してラベルとMSDS/COA(製品ページで利用可能な)。

希釈計算器

希釈計算器

貯蔵液を準備することを要求される希釈剤を計算してください. セレック希釈計算器は、以下の方程式に基づきます:

開始濃度 x 開始体積 = 最終濃度 x 最終体積

希釈の計算式

この方程式は、一般に略語を使われます:C1V1 = C2V2 ( 輸入 輸出 )

  • C1
    V1
    C2
    V2

常に貯蔵液を準備するとき、小びんラベルとMSDS/COA(オンラインで利用できる)で見つかる製品のバッチに特有の分子量を使ってください。

連続希釈計算器方程式

  • 連続希釈剤

  • 計算結果

  • C1=C0/X C1: LOG(C1):
    C2=C1/X C2: LOG(C2):
    C3=C2/X C3: LOG(C3):
    C4=C3/X C4: LOG(C4):
    C5=C4/X C5: LOG(C5):
    C6=C5/X C6: LOG(C6):
    C7=C6/X C7: LOG(C7):
    C8=C7/X C8: LOG(C8):
分子量計算器

分子量计算器

そのモル質量と元素組成を計算するために、合成物の化学式を入力してください:

総分子量:g/mol

チップス: 化学式は大文字と小文字の区別ができます。C10H16N2O2 c10h16n2o2

モル濃度計算器

マス 濃度 ボリューム 分子量

臨床試験

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

技術サポート

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Handling Instructions

他の質問がある場合は、お気軽くお問合せください。

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PARPシグナル伝達経路

PARP Inhibitors with Unique Features

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細胞株 試験類型 濃度 培養時間 溶剤類型 活性叙述 PMID