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 Mlv4SpVv[3Srb36gRZN{[Xl? MmjjNE4yNzFxNUCwM|ExODBibl2= MYLpcohq[mm2czDQRXJRKGGldHn2bZR6KGG2IIP0ZZJ1cW6pIHPvcoNmem62cnH0bY9vKG:oIEWwNEBvVQ>? MmXGNlUyOjh2NUW=
BT474 Mon1S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NYDGV4Y2PTByIH7N M3PaT|Ex6oDVMUZCpIQ> MlT4doVlfWOnczDj[YxtKGe{b4f0bEBqdiC2aHWg[o92eiCuaX7ld{BidmRic3nncolncWOjboTsfS=> NEXLb3UzPTF{OES1OS=>
SKBR3 MX3Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NUjQd4NCPTByIH7N MXyxNQKBmzF3wrDk NX3OZm9zemWmdXPld{Bk\WyuIHfyc5d1cCCrbjD0bIUh\m:3cjDsbY5meyCjbnSgd4lodmmoaXPhcpRtgQ>? M{XENlI2OTJ6NEW1
AU565 MnTtS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NH\DeGg2ODBibl2= NFHIOXcyOOLCk{G1xsBl NVnmeI57emWmdXPld{Bk\WyuIHfyc5d1cCCrbjD0bIUh\m:3cjDsbY5meyCjbnSgd4lodmmoaXPhcpRtgQ>? NXi3V4xEOjVzMki0OVU>
EFM192A MoXrS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NXTYWphIPTByIH7N MWGxNQKBmzF3wrDk M4n3WJJm\HWlZYOgZ4VtdCCpcn;3eIghcW5idHjlJIZwfXJibHnu[ZMh[W6mIIPp[45q\mmlYX70cJk> NXH0U4w4OjVzMki0OVU>
MDA-MB-231 MlTOSpVv[3Srb36gRZN{[Xl? MlW4NVAwOjBxNECg{txO NFvBOXUzPCCq M{n0c4lv[3KnYYPld{BxNUGNVDDs[ZZmdHNiaX6gZUBld3OnLXTldIVv\GWwdDDtZY5v\XJ? Mor1NlQ1OjBzNUK=
MDA-MB-231 MW\D[YxtKF[rYXLpcIl1gSCDc4PhfS=> M1LzOVAvOS12MDFOwG0> MX[yOEBp M1XqS2lEPTEkgJm95qCKOTdwN{hCpO69VQ>? MmPrNlQ1OjBzNUK=
MDA-MB-231 NVvobYJoSXCxcITvd4l{KEG|c3H5 NFrGNnkyOC9{MD:0NEDPxE1? MnP5NlQhcA>? MUXpcoR2[2W|IHHwc5B1d3OrczDkc5NmKGSncHXu[IVvfGy7 NX;xUnN4OjR2MkCxOVI>
MDA-MB-231 M3jwVWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NXP3cZBKOTBxMkCvOFAh|ryP NYHBbIFXOjRiaB?= NIi1NVljdG:la4OgZ4VtdCCleXPs[UBxem:pcnXzd4lwdiCrbjDHNk9OKHCqYYPl MUSyOFQzODF3Mh?=
H460 NYDob|BmT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NH25XG41ODBibl2= Mn3pNlTDqGh? NWe2UplpcW6lcnXhd4V{KGOnbHz1cIFzKHKjZHnvd4Vve2m2aY\peJk> NFWxfGMzPDRzMU[xNS=>
A549  NX3lWVFoT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NXLPeY1CPDByIH7N NGfuV4szPMLiaB?= M{\Pbolv[3KnYYPld{Bk\WyudXzhdkBz[WSrb4PlcpNqfGm4aYT5 NHnhXmozPDRzMU[xNS=>
DT40 M1Prcmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NWjSfVE2UUN3ME2yNUBvVQ>? MWWyOFM2PjhzMx?=
DU145 M3ra[Wdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MnLITWM2OD1zODDuUS=> MkjiNlQ{PTZ6MUO=
COLO704 MnXXS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NWTUO41IUUN3ME2yMlUzKMLzIECuOlch|ryP MY[yN|czQTRyMh?=
OVMANAb NWjBSVZUT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NGfKNVRKSzVyPUKuOVghyrFiMD6zPEDPxE1? M1XvN|I{PzJ7NECy
OV177 M{LBTmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NHXudVBKSzVyPUKuO|ghyrFiMD63NUDPxE1? M37DVVI{PzJ7NECy
OAW28 NYfKUYpkT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= Ml7CTWM2OD1|Lk[xJOKyKDBwMkig{txO NVTXPXlnOjN5Mkm0NFI>
OVSAHO M1rMU2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NIP3folKSzVyPUOuOlQhyrFiMD6zN{DPxE1? M2q2TFI{PzJ7NECy
OVKATE NEf6T|BIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M4O3cmlEPTB;Mz62OEDDuSBzLke5JO69VQ>? NUXlTWNuOjN5Mkm0NFI>
OVCAR3 NWHmOVRiT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NXLlcGNKUUN3ME2zMlc1KMLzIECuOFAh|ryP NHTxWIYzOzd{OUSwNi=>
PEO14 NE\veXlIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NXfqfYh1UUN3ME2zMlg1KMLzIECuO|Yh|ryP M1P6dFI{PzJ7NECy
A2780 M{DXcWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MoPqTWM2OD1|Lkm0JOKyKDBwMkWg{txO MkjDNlM4Ojl2MEK=
OVTOKO MnfkS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MULJR|UxRTRwMUSgxtEhOS53MzFOwG0> MV2yN|czQTRyMh?=
KURAMOCHIb NXfqR4lLT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NH;GbJNKSzVyPUSuN|QhyrFiMD6yPUDPxE1? NXThfpZrOjN5Mkm0NFI>
TOV21G MkLTS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MmjGTWM2OD13LkC3JOKyKDFwM{Cg{txO NEPOXVQzOzd{OUSwNi=>
OVISE M4HoO2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NHntZ|RKSzVyPUWuOlghyrFiMD6yN{DPxE1? NEn5THQzOzd{OUSwNi=>
KK NWLZSFhNT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NUHEdmRIUUN3ME22MlE2KMLzIEGuOFIh|ryP NXzCR5BMOjN5Mkm0NFI>
RMUGS NEPKV3ZIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MmO1TWM2OD15LkCzJOKyKDFwOEOg{txO NEe2NJIzOzd{OUSwNi=>
PEO6 M3fBVGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MUHJR|UxRTdwME[gxtEhOC55NDFOwG0> M3PENVI{PzJ7NECy
OVCA429 MVzHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NFzYS4RKSzVyPUiuNlkhyrFiMT62OEDPxE1? NHyze|kzOzd{OUSwNi=>
OV167 MkfyS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MWLJR|UxRThwM{OgxtEhOS5zODFOwG0> NHzRVW0zOzd{OUSwNi=>
RMG1 Mo[wS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NH[2UpJKSzVyPUmuN|IhyrFiMj6zOkDPxE1? M2izVlI{PzJ7NECy
OVCAR5 MXrHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MUPJR|UxRTlwNUCgxtEhOi53OTFOwG0> M3LvPVI{PzJ7NECy
EFO21 MYDHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NVvDenM6UUN3ME25MlkzKMLzIEGuPFch|ryP MVeyN|czQTRyMh?=
ES2 Mkf0S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NX7OVVFoUUN3ME2xNE4yOiEEsTCxMlI{KM7:TR?= MXiyN|czQTRyMh?=
Tyk-nu MlHZS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NGfGfJFKSzVyPUGwMlIxKMLzIEGuNVIh|ryP MYWyN|czQTRyMh?=
CAOV3 MljFS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MnziTWM2OD1zMD6zO{DDuSByLki3JO69VQ>? Mn\TNlM4Ojl2MEK=
OV207 NI\UVY9Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M2\GZWlEPTB;MUKuNlchyrFiMD6zNkDPxE1? M2fH[FI{PzJ7NECy
HEY NW\PT|djT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NH;HOYRKSzVyPUGzMlAyKMLzIECuO|Uh|ryP NYnFXoxbOjN5Mkm0NFI>
DOV13 MVLHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MlnXTWM2OD5zNTFOwG0> NGDuUJUzOzd{OUSwNi=>
EFO27 MnLQS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NFnsfpZKSzVyPkG1JO69VQ>? M3ThTVI{PzJ7NECy
HEY C2 MX\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MVvJR|UxRjF3IN88US=> MWqyN|czQTRyMh?=
KOC-7cc Mn3kS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MVTJR|UxRjF3IN88US=> NH6wcXczOzd{OUSwNi=>
MCASb Mk\jS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MX;JR|UxRjF3IN88US=> MlLNNlM4Ojl2MEK=
OAW42 M{DUVmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MlLuTWM2OD5zNTFOwG0> NGDxSpAzOzd{OUSwNi=>
OV2008 M{LoPGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MYrJR|UxRjF3IN88US=> NVTtPVhxOjN5Mkm0NFI>
OV90 NX7ZbIFxT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M1HqcGlEPTB-MUWg{txO MU[yN|czQTRyMh?=
OVCA420b M{TES2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NVq4V3kyUUN3ME6xOUDPxE1? MmrFNlM4Ojl2MEK=
OVCA432 NI\JfG9Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MWrJR|UxRjF3IN88US=> NX7NbnRbOjN5Mkm0NFI>
PEA2 MWDHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NY\5fYdGUUN3ME6xOUDPxE1? MnGwNlM4Ojl2MEK=
SKOV3 MmTCS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M1y5W2lEPTB-MUWg{txO MU[yN|czQTRyMh?=
TOV112D NXrMSHBDT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MVGwMVMh|ryP MmThTWM2OD5zNTFOwG0> Mn3HNlM4Ojl2MEK=
C4-2 MnnSS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MmnCNE0{KM7:TR?= NWi1NWNYOTRiZB?= M4P4b2ROW09? MlXX[IVkemWjc3XzJINwdG:weTDueY1j\XJiZH;z[UBl\XCnbnTlcpRtgQ>? NUnpZ3B{OjN3NkWyOFQ>
PC3 MnT4S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M3zHUFAuOyEQvF2= M2LFNlE1KGR? NEnr[llFVVOR NUTBRpEx\GWlcnXhd4V{KGOxbH;ufUBvfW2kZYKg[I9{\SCmZYDlcoRmdnSueR?= MkLrNlM2PjV{NES=
DU145 NVvFdXlyT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MlTmNE0{KM7:TR?= M4r3fVE1KGR? NWnNb3dMTE2VTx?= MUHk[YNz\WG|ZYOgZ49td267IH71cYJmeiCmb4PlJIRmeGWwZHXueIx6 M2jVNlI{PTZ3MkS0
VCaP  MXLHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NI\GN24xNTNizszN M2frcVE1KGR? NGjvfoZFVVOR MUjk[YNz\WG|ZYOgZ49td267IH71cYJmeiCmb4PlJIRmeGWwZHXueIx6 M1n0PFI{PTZ3MkS0
LNCaP  MYfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MkLZNE0{KM7:TR?= MXWxOEBl MV7EUXNQ NXPZbnk2\GWlcnXhd4V{KGOxbH;ufUBvfW2kZYKg[I9{\SCmZYDlcoRmdnSueR?= M3PlUFI{PTZ3MkS0
MDA-MB-468 MYHD[YxtKF[rYXLpcIl1gSCDc4PhfS=> NYrMbI4zUUN3ME25Mlch|ryP Ml\KNlI3PzhzNkG=
MDA-MB-231 MVfD[YxtKF[rYXLpcIl1gSCDc4PhfS=> M1[0c2lEPTB;MUOg{txO M4jjRVIzPjd6MU[x
Cal-51 Mmr6R4VtdCCYaXHibYxqfHliQYPzZZk> MY\JR|UxRThwNjFOwG0> MXmyNlY4QDF4MR?=

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
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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細胞株 試験類型 濃度 培養時間 溶剤類型 活性叙述 PMID