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 M1myTmZ2dmO2aX;uJGF{e2G7 NILEVWUxNjFxMT:1NFAwOTByMDDuUS=> NW\HO3dPcW6qaXLpeJMhWEGUUDDhZ5Rqfmm2eTDheEB{fGG{dHnu[{Bkd26lZYLueJJifGmxbjDv[kA2ODBibl2= NIHMO4ozPTF{OES1OS=>
BT474 MlzuS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M1zSV|UxOCCwTR?= MYSxNQKBmzF3wrDk MXzy[YR2[2W|IHPlcIwh\3Kxd4ToJIlvKHSqZTDmc5VzKGyrbnXzJIFv\CC|aXfubYZq[2GwdHz5 MkjjNlUyOjh2NUW=
SKBR3 M3P3Omdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MXq1NFAhdk1? Mm\hNVDjiJNzNdMg[C=> MVfy[YR2[2W|IHPlcIwh\3Kxd4ToJIlvKHSqZTDmc5VzKGyrbnXzJIFv\CC|aXfubYZq[2GwdHz5 M2H0blI2OTJ6NEW1
AU565 MY\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NUHI[45lPTByIH7N NVGxbZJ3OTEkgKOxOeKh\A>? MoXBdoVlfWOnczDj[YxtKGe{b4f0bEBqdiC2aHWg[o92eiCuaX7ld{BidmRic3nncolncWOjboTsfS=> M3y5VFI2OTJ6NEW1
EFM192A NIXMd3lIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= Mn3jOVAxKG6P NWrs[lE2OTEkgKOxOeKh\A>? NWnK[mI{emWmdXPld{Bk\WyuIHfyc5d1cCCrbjD0bIUh\m:3cjDsbY5meyCjbnSgd4lodmmoaXPhcpRtgQ>? Mme1NlUyOjh2NUW=
MDA-MB-231 NITvemxHfW6ldHnvckBCe3OjeR?= M1LEUVExNzJyL{SwJO69VQ>? NX7sSpRSOjRiaB?= NXG5foJbcW6lcnXhd4V{KHBvQVvUJIxmfmWuczDpckBiKGSxc3Wt[IVx\W6mZX70JI1idm6nch?= M3fje|I1PDJyMUWy
MDA-MB-231 MmOzR4VtdCCYaXHibYxqfHliQYPzZZk> NU\x[VVDOC5zLUSwJO69VQ>? Mn\1NlQhcA>? M3z6NGlEPTEkgJm95qCKOTdwN{hCpO69VQ>? NUPYNlJDOjR2MkCxOVI>
MDA-MB-231 Mnq2RZBweHSxc3nzJGF{e2G7 NGD0TGQyOC9{MD:0NEDPxE1? MXKyOEBp NW[4fWE3cW6mdXPld{BieG:ydH;zbZMh\G:|ZTDk[ZBmdmSnboTsfS=> NFr0eWkzPDR{MEG1Ni=>
MDA-MB-231 M3K4TWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NVrVUJlnOTBxMkCvOFAh|ryP MoHMNlQhcA>? MofxZoxw[2u|IHPlcIwh[3mlbHWgdJJw\3Knc4Ppc44hcW5iR{KvUUBxcGG|ZR?= M3rjd|I1PDJyMUWy
H460 NV\hXY42T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MojSOFAxKG6P NV22UWdjOjUEoHi= M{TXZ4lv[3KnYYPld{Bk\WyudXzhdkBz[WSrb4PlcpNqfGm4aYT5 MVuyOFQyOTZzMR?=
A549  M{j6c2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MXe0NFAhdk1? M3jL[|I1yqCq MX\pcoNz\WG|ZYOgZ4VtdHWuYYKgdoFlcW:|ZX7zbZRqfmm2eR?= NIfrW3MzPDRzMU[xNS=>
DT40 NHjmVVBIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MmLCTWM2OD1{MTDuUS=> MnLQNlQ{PTZ6MUO=
DU145 NY\tNYlKT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NEDzTpNKSzVyPUG4JI5O NUPJc2p3OjR|NU[4NVM>
COLO704 MXPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M1XON2lEPTB;Mj61NkDDuSByLk[3JO69VQ>? MoPyNlM4Ojl2MEK=
OVMANAb NGfrZY5Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NYn3PW5HUUN3ME2yMlU5KMLzIECuN|gh|ryP M1HSUVI{PzJ7NECy
OV177 Ml7HS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MnX4TWM2OD1{Lke4JOKyKDBwN{Gg{txO NXm5RVlJOjN5Mkm0NFI>
OAW28 NVjXRWJDT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MVvJR|UxRTNwNkGgxtEhOC5{ODFOwG0> MUGyN|czQTRyMh?=
OVSAHO MVrHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NFjMWnRKSzVyPUOuOlQhyrFiMD6zN{DPxE1? NFnKUWMzOzd{OUSwNi=>
OVKATE NF7aOHBIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M1\zd2lEPTB;Mz62OEDDuSBzLke5JO69VQ>? M3npeVI{PzJ7NECy
OVCAR3 M{\LN2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NXi5ZVk4UUN3ME2zMlc1KMLzIECuOFAh|ryP Mlj5NlM4Ojl2MEK=
PEO14 M4DUV2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M3;uWmlEPTB;Mz64OEDDuSByLke2JO69VQ>? MXiyN|czQTRyMh?=
A2780 M1e5XGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M4\NbGlEPTB;Mz65OEDDuSByLkK1JO69VQ>? NGPYTYczOzd{OUSwNi=>
OVTOKO NInlNnJIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M4DZWGlEPTB;ND6xOEDDuSBzLkWzJO69VQ>? MVqyN|czQTRyMh?=
KURAMOCHIb NX7ueYVqT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MnXtTWM2OD12LkO0JOKyKDBwMkmg{txO MYWyN|czQTRyMh?=
TOV21G MmHQS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NVraOFFzUUN3ME21MlA4KMLzIEGuN|Ah|ryP M3;YNVI{PzJ7NECy
OVISE NHLmRWhIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MXPJR|UxRTVwNkigxtEhOC5{MzFOwG0> M2nyeFI{PzJ7NECy
KK M3foTGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NYrxTXV4UUN3ME22MlE2KMLzIEGuOFIh|ryP MXuyN|czQTRyMh?=
RMUGS MUXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NYDF[ZpWUUN3ME23MlA{KMLzIEGuPFMh|ryP Mn7MNlM4Ojl2MEK=
PEO6 M3rTc2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MU\JR|UxRTdwME[gxtEhOC55NDFOwG0> MWOyN|czQTRyMh?=
OVCA429 Ml7hS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NIfOWVZKSzVyPUiuNlkhyrFiMT62OEDPxE1? MVqyN|czQTRyMh?=
OV167 NWjs[2pYT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MYHJR|UxRThwM{OgxtEhOS5zODFOwG0> M1vKWVI{PzJ7NECy
RMG1 M1zxXGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NVjMRXpnUUN3ME25MlMzKMLzIEKuN|Yh|ryP NH74eHkzOzd{OUSwNi=>
OVCAR5 MnLFS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NVu0VYVEUUN3ME25MlUxKMLzIEKuOVkh|ryP MWOyN|czQTRyMh?=
EFO21 MYXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NGT0d41KSzVyPUmuPVIhyrFiMT64O{DPxE1? NEf6cnYzOzd{OUSwNi=>
ES2 NWPmR4dMT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= Ml\zTWM2OD1zMD6xNkDDuSBzLkKzJO69VQ>? M3vGSlI{PzJ7NECy
Tyk-nu M{\xSmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M3nMd2lEPTB;MUCuNlAhyrFiMT6xNkDPxE1? NYjDTXJLOjN5Mkm0NFI>
CAOV3 NV3LeFhbT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MWjJR|UxRTFyLkO3JOKyKDBwOEeg{txO NIjCUI4zOzd{OUSwNi=>
OV207 M2j1RWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MknpTWM2OD1zMj6yO{DDuSByLkOyJO69VQ>? Ml;kNlM4Ojl2MEK=
HEY M4[wd2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MmfTTWM2OD1zMz6wNUDDuSByLke1JO69VQ>? M1HROVI{PzJ7NECy
DOV13 MmLuS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NIKybmJKSzVyPkG1JO69VQ>? NVPTTVg2OjN5Mkm0NFI>
EFO27 NH7SfppIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MmHKTWM2OD5zNTFOwG0> NVjWXpdCOjN5Mkm0NFI>
HEY C2 NG\hO|dIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NVLDSWJ4UUN3ME6xOUDPxE1? M4nLe|I{PzJ7NECy
KOC-7cc MUHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MWnJR|UxRjF3IN88US=> MYCyN|czQTRyMh?=
MCASb M4nhdGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MkfxTWM2OD5zNTFOwG0> NVKwdXJoOjN5Mkm0NFI>
OAW42 M2G1V2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MUXJR|UxRjF3IN88US=> NHfHS5gzOzd{OUSwNi=>
OV2008 MnrtS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MUPJR|UxRjF3IN88US=> M4L1elI{PzJ7NECy
OV90 M2HsNWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NWjUU2J2UUN3ME6xOUDPxE1? NIXr[nEzOzd{OUSwNi=>
OVCA420b NYTBS21xT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M3Tpb2lEPTB-MUWg{txO M4q3Z|I{PzJ7NECy
OVCA432 NY\vdoxJT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MkjvTWM2OD5zNTFOwG0> MnzoNlM4Ojl2MEK=
PEA2 Mn:xS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MYfJR|UxRjF3IN88US=> M{XMTFI{PzJ7NECy
SKOV3 MVTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MofWTWM2OD5zNTFOwG0> NIPCO3kzOzd{OUSwNi=>
TOV112D MWLHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NY\QNnhPOC1|IN88US=> Mki0TWM2OD5zNTFOwG0> NF;BTXEzOzd{OUSwNi=>
C4-2 Mlm1S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MlX1NE0{KM7:TR?= NVXrVYdYOTRiZB?= NWXJTII5TE2VTx?= NUPmWXM{\GWlcnXhd4V{KGOxbH;ufUBvfW2kZYKg[I9{\SCmZYDlcoRmdnSueR?= MnX0NlM2PjV{NES=
PC3 MmTjS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NVz3W2dYOC1|IN88US=> NWf4Z403OTRiZB?= NGLyUYJFVVOR MV\k[YNz\WG|ZYOgZ49td267IH71cYJmeiCmb4PlJIRmeGWwZHXueIx6 NVjGblA2OjN3NkWyOFQ>
DU145 NWHjSYhOT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MnTPNE0{KM7:TR?= MXexOEBl M2j2VGROW09? M1OzV4Rm[3KnYYPld{Bkd2yxbomgcpVu[mW{IHTvd4Uh\GWyZX7k[Y51dHl? MmLRNlM2PjV{NES=
VCaP  Mn\QS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MnjtNE0{KM7:TR?= M33mbFE1KGR? NWi1fndUTE2VTx?= MWrk[YNz\WG|ZYOgZ49td267IH71cYJmeiCmb4PlJIRmeGWwZHXueIx6 M1O5blI{PTZ3MkS0
LNCaP  MkezS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NVmxOWs4OC1|IN88US=> NYe0T483OTRiZB?= M1fwOGROW09? NIfSUnVl\WO{ZXHz[ZMh[2:ub375JI52dWKncjDkc5NmKGSncHXu[IVvfGy7 MkLFNlM2PjV{NES=
MDA-MB-468 NYjlTYlYS2WubDDWbYFjcWyrdImgRZN{[Xl? NYq4UVdGUUN3ME25Mlch|ryP MUmyNlY4QDF4MR?=
MDA-MB-231 M3vwbGNmdGxiVnnhZoltcXS7IFHzd4F6 M4jBcGlEPTB;MUOg{txO MnvsNlI3PzhzNkG=
Cal-51 NFK1bVRE\WyuIG\pZYJqdGm2eTDBd5NigQ>? M1Xi[mlEPTB;OD62JO69VQ>? NWTt[3hHOjJ4N{ixOlE>

他の多くの細胞株試験データをご覧になる場合はこちらをクリックして下さい

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(NMPから)右の順に溶剤を製品に加えます(文献ではなく、Selleckの実験によるデータ):
2% DMSO+30% PEG 300+2% Tween 80+ddH2O
混合させたのち直ちに使用することを推奨します。
10mg/mL

* 溶解度測定はSelleck技術部門によって行われており、その他文献に示されている溶解度と差異がある可能性がありますが、同一ロットの生産工程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
in solvent
別名 N/A

便利ツール

モル濃度計算器

モル濃度計算器

求めたい質量、体積または濃度を計算してください。

質量 (g) = 濃度 (mol/L) x 体積 (L) x 分子量 (g/mol)

モル濃度計算器方程式

  • 質量
    濃度
    体積
    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

貯蔵液を準備するために必要な希釈率を計算してください。Selleck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 ( 入力 出力 )

  • 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

質量 濃度 体積 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

他に質問がある場合は、お気軽にお問い合わせください。

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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