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)は一種のPARP阻害剤で、無細胞試験でPARP1に作用する時のKi値が1.4 nMになって、残り8つPARPドメインにも結合親和力を表します。臨床3期。

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

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)は一種のPARP阻害剤で、無細胞試験でPARP1に作用する時のKi値が1.4 nMになって、残り8つPARPドメインにも結合親和力を表します。臨床3期。
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 M2fv[GZ2dmO2aX;uJGF{e2G7 MYiwMlEwOS93MECvNVAxOCCwTR?= NYP1RYh3cW6qaXLpeJMhWEGUUDDhZ5Rqfmm2eTDheEB{fGG{dHnu[{Bkd26lZYLueJJifGmxbjDv[kA2ODBibl2= MnW4NlUyOjh2NUW=
BT474 M1LtTGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NHLwVoY2ODBibl2= NGro[nUyOOLCk{G1xsBl NFzFTY5z\WS3Y3XzJINmdGxiZ4Lve5RpKGmwIITo[UBnd3W{IHzpcoV{KGGwZDDzbYdvcW[rY3HueIx6 NGLqO2UzPTF{OES1OS=>
SKBR3 NIXCc3dIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M{fS[FUxOCCwTR?= NEX3UpoyOOLCk{G1xsBl MX7y[YR2[2W|IHPlcIwh\3Kxd4ToJIlvKHSqZTDmc5VzKGyrbnXzJIFv\CC|aXfubYZq[2GwdHz5 NGOwe4UzPTF{OES1OS=>
AU565 NHz5VVhIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NHLSOoY2ODBibl2= NIi0cW4yOOLCk{G1xsBl MWPy[YR2[2W|IHPlcIwh\3Kxd4ToJIlvKHSqZTDmc5VzKGyrbnXzJIFv\CC|aXfubYZq[2GwdHz5 NXrkNXprOjVzMki0OVU>
EFM192A MmrRS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MkfGOVAxKG6P MmTkNVDjiJNzNdMg[C=> MnnMdoVlfWOnczDj[YxtKGe{b4f0bEBqdiC2aHWg[o92eiCuaX7ld{BidmRic3nncolncWOjboTsfS=> MkXmNlUyOjh2NUW=
MDA-MB-231 NGDBNYdHfW6ldHnvckBCe3OjeR?= MUGxNE8zOC92MDFOwG0> M{\ZbFI1KGh? MVvpcoNz\WG|ZYOgdE1CU1RibHX2[Yx{KGmwIHGg[I9{\S2mZYDlcoRmdnRibXHucoVz NIjmbVgzPDR{MEG1Ni=>
MDA-MB-231 MX\D[YxtKF[rYXLpcIl1gSCDc4PhfS=> NHfDUmExNjFvNECg{txO MXmyOEBp M1\WeWlEPTEkgJm95qCKOTdwN{hCpO69VQ>? M170UVI1PDJyMUWy
MDA-MB-231 M1XE[WFxd3C2b4Ppd{BCe3OjeR?= NHnFV|MyOC9{MD:0NEDPxE1? M4HyZ|I1KGh? MVzpcoR2[2W|IHHwc5B1d3OrczDkc5NmKGSncHXu[IVvfGy7 NHL4eYwzPDR{MEG1Ni=>
MDA-MB-231 NVrrSllDT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M4fCO|ExNzJyL{SwJO69VQ>? M2T6OlI1KGh? NYnyelFD[myxY3vzJINmdGxiY4njcIUheHKxZ4Lld5Nqd25iaX6gS|IwVSCyaHHz[S=> MViyOFQzODF3Mh?=
H460 MnrGS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MYO0NFAhdk1? NUTmbINSOjUEoHi= Ml2zbY5kemWjc3XzJINmdGy3bHHyJJJi\Gmxc3Xud4l1cX[rdIm= NYnCTIgxOjR2MUG2NVE>
A549  MV\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NVrBV5F4PDByIH7N MUGyOOKhcA>? MYPpcoNz\WG|ZYOgZ4VtdHWuYYKgdoFlcW:|ZX7zbZRqfmm2eR?= NXf2dJVSOjR2MUG2NVE>
DT40 NYLC[Vh2T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NFz3VGdKSzVyPUKxJI5O NFnrV28zPDN3NkixNy=>
DU145 NWLJNVAxT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NV;LeHFCUUN3ME2xPEBvVQ>? M4DQUlI1OzV4OEGz
COLO704 M3rkb2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MXfJR|UxRTJwNUKgxtEhOC54NzFOwG0> NFXZXYMzOzd{OUSwNi=>
OVMANAb NF7rR3FIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M2TPWWlEPTB;Mj61PEDDuSByLkO4JO69VQ>? MnztNlM4Ojl2MEK=
OV177 NHzKXohIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NGWxOmpKSzVyPUKuO|ghyrFiMD63NUDPxE1? NVnCbXNOOjN5Mkm0NFI>
OAW28 MWrHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NVr0OlFUUUN3ME2zMlYyKMLzIECuNlgh|ryP MYWyN|czQTRyMh?=
OVSAHO M4Tp[2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NICxR3pKSzVyPUOuOlQhyrFiMD6zN{DPxE1? MWqyN|czQTRyMh?=
OVKATE NEjKbXlIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NH;OXoJKSzVyPUOuOlQhyrFiMT63PUDPxE1? NIjpZ3ozOzd{OUSwNi=>
OVCAR3 MlzWS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NYnOdnVTUUN3ME2zMlc1KMLzIECuOFAh|ryP NXjKfoczOjN5Mkm0NFI>
PEO14 MlHjS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MXPJR|UxRTNwOESgxtEhOC55NjFOwG0> NWT5XJgyOjN5Mkm0NFI>
A2780 NVLJOYpGT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MkWwTWM2OD1|Lkm0JOKyKDBwMkWg{txO M4\vblI{PzJ7NECy
OVTOKO NWfsbnpCT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M4PNZ2lEPTB;ND6xOEDDuSBzLkWzJO69VQ>? MYKyN|czQTRyMh?=
KURAMOCHIb M1G0WGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MmL0TWM2OD12LkO0JOKyKDBwMkmg{txO NHq3c|UzOzd{OUSwNi=>
TOV21G MY\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MmfrTWM2OD13LkC3JOKyKDFwM{Cg{txO MVeyN|czQTRyMh?=
OVISE MW\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MkH4TWM2OD13Lk[4JOKyKDBwMkOg{txO NIXUSFMzOzd{OUSwNi=>
KK NYXPfGNVT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MWDJR|UxRTZwMUWgxtEhOS52MjFOwG0> M4jhOlI{PzJ7NECy
RMUGS NIPobnFIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NFLn[phKSzVyPUeuNFMhyrFiMT64N{DPxE1? M2XjSFI{PzJ7NECy
PEO6 NGHCfpRIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MlvVTWM2OD15LkC2JOKyKDBwN{Sg{txO NEnve|MzOzd{OUSwNi=>
OVCA429 NFjoV2NIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NIDrb4NKSzVyPUiuNlkhyrFiMT62OEDPxE1? NYP0[WxVOjN5Mkm0NFI>
OV167 M1HENWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NGfSS4tKSzVyPUiuN|MhyrFiMT6xPEDPxE1? M2\NdFI{PzJ7NECy
RMG1 MXnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M1\YXWlEPTB;OT6zNkDDuSB{LkO2JO69VQ>? MmP0NlM4Ojl2MEK=
OVCAR5 M{TGc2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MUnJR|UxRTlwNUCgxtEhOi53OTFOwG0> Ml;sNlM4Ojl2MEK=
EFO21 NUXaR5A5T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M1;YSWlEPTB;OT65NkDDuSBzLki3JO69VQ>? MViyN|czQTRyMh?=
ES2 NIjHUHlIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M3vDSGlEPTB;MUCuNVIhyrFiMT6yN{DPxE1? M3TyTlI{PzJ7NECy
Tyk-nu M1foTmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NF;aZVdKSzVyPUGwMlIxKMLzIEGuNVIh|ryP MknUNlM4Ojl2MEK=
CAOV3 MnG3S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MUPJR|UxRTFyLkO3JOKyKDBwOEeg{txO MnL1NlM4Ojl2MEK=
OV207 M2S5fmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MWTJR|UxRTF{LkK3JOKyKDBwM{Kg{txO MYmyN|czQTRyMh?=
HEY MWTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MWDJR|UxRTF|LkCxJOKyKDBwN{Wg{txO NYXy[mxzOjN5Mkm0NFI>
DOV13 NY\O[lNpT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M1X6dWlEPTB-MUWg{txO NWHsbmVUOjN5Mkm0NFI>
EFO27 MWrHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NYKycm5tUUN3ME6xOUDPxE1? NWOyR2Z7OjN5Mkm0NFI>
HEY C2 NIfOUXNIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NWTsfmFbUUN3ME6xOUDPxE1? NYPHNmI4OjN5Mkm0NFI>
KOC-7cc MVzHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M1[1UWlEPTB-MUWg{txO NIfSSZczOzd{OUSwNi=>
MCASb MYnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M3HBNWlEPTB-MUWg{txO MX6yN|czQTRyMh?=
OAW42 NGOzOVhIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NHfScnZKSzVyPkG1JO69VQ>? Mn\TNlM4Ojl2MEK=
OV2008 MX7Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MnH6TWM2OD5zNTFOwG0> MYmyN|czQTRyMh?=
OV90 M2PzR2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M{fncmlEPTB-MUWg{txO M33VXVI{PzJ7NECy
OVCA420b NVrncYFmT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NHvOeXlKSzVyPkG1JO69VQ>? MWeyN|czQTRyMh?=
OVCA432 NVXlfWdyT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MnS3TWM2OD5zNTFOwG0> Mm[yNlM4Ojl2MEK=
PEA2 MkXyS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NVHVVlB6UUN3ME6xOUDPxE1? NXe5R25UOjN5Mkm0NFI>
SKOV3 MYjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M2TobGlEPTB-MUWg{txO NHL1W4MzOzd{OUSwNi=>
TOV112D M2PSeGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NUnZW3g4OC1|IN88US=> M{TBbWlEPTB-MUWg{txO MmjONlM4Ojl2MEK=
C4-2 MlHZS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M2njO|AuOyEQvF2= M4P6dFE1KGR? MmXXSG1UVw>? MWjk[YNz\WG|ZYOgZ49td267IH71cYJmeiCmb4PlJIRmeGWwZHXueIx6 MmTJNlM2PjV{NES=
PC3 NVfTT40{T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NHH0[5ExNTNizszN MXSxOEBl NEi5R49FVVOR MkfC[IVkemWjc3XzJINwdG:weTDueY1j\XJiZH;z[UBl\XCnbnTlcpRtgQ>? NELyOo8zOzV4NUK0OC=>
DU145 MVjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NVHkOHN6OC1|IN88US=> NUnoU5R5OTRiZB?= NF7ZWZJFVVOR MW\k[YNz\WG|ZYOgZ49td267IH71cYJmeiCmb4PlJIRmeGWwZHXueIx6 MmC3NlM2PjV{NES=
VCaP  NV\JcW94T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M1jNelAuOyEQvF2= MnfSNVQh\A>? MXPEUXNQ NGDadVdl\WO{ZXHz[ZMh[2:ub375JI52dWKncjDkc5NmKGSncHXu[IVvfGy7 MmfDNlM2PjV{NES=
LNCaP  MkHqS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M1\UUlAuOyEQvF2= NFjFVlUyPCCm NIfaTJVFVVOR NHn1bIJl\WO{ZXHz[ZMh[2:ub375JI52dWKncjDkc5NmKGSncHXu[IVvfGy7 M3vuOVI{PTZ3MkS0
MDA-MB-468 NIqzT2NE\WyuIG\pZYJqdGm2eTDBd5NigQ>? MmDqTWM2OD17Lkeg{txO M3HUR|IzPjd6MU[x
MDA-MB-231 NVn2Oll6S2WubDDWbYFjcWyrdImgRZN{[Xl? MlPoTWM2OD1zMzFOwG0> MoPqNlI3PzhzNkG=
Cal-51 M3fHR2NmdGxiVnnhZoltcXS7IFHzd4F6 MlLVTWM2OD16Lk[g{txO MljiNlI3PzhzNkG=

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 順序で溶剤を入れること:
2% DMSO+30% PEG 300+2% Tween 80+ddH2O
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信号経路図

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