Rucaparib (AG-014699,PF-01367338) phosphate

目录号:S1098

Rucaparib (AG-014699,PF-01367338) phosphate Chemical Structure

Molecular Weight(MW): 421.36

Rucaparib (AG-014699,PF-01367338)是一种PARP抑制剂,无细胞试验中作用于PARP1的Ki为1.4 nM,对其余8个PARP位点也有结合亲和力。Phase 3。

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客户使用该产品的6个实验数据:

  • 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.

  • 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.

    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.

  • 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.

产品安全说明书

PARP抑制剂选择性比较

生物活性

产品描述 Rucaparib (AG-014699,PF-01367338)是一种PARP抑制剂,无细胞试验中作用于PARP1的Ki为1.4 nM,对其余8个PARP位点也有结合亲和力。Phase 3。
特性 AG-014699是第一个用于人类癌症疗法的PARP 抑制剂。
靶点
PARP [1]
(Cell-free assay)
1.4 nM(Ki)
体外研究

AG-014699有效抑制纯化的全长人类PARP-1,作用于LoVo和SW620细胞显示出强PARP抑制效果。AG-014699是AG14447的磷酸盐形式,且是第一个和temozolomide联用用于临床实验的PARP抑制剂。[1] AG-014699的辐射增敏性是由于下游NF-κB激活的抑制,及SSB修复抑制。AG-014699可以作用于DNA损伤激活的NF-κB,且克服传统NF-κB抑制剂的毒性,不会损害其他重要的炎症反应。[2]1μM AG-014699作用于D283Med细胞时抑制PARP-1活性达97.1%。[3]在NB-1691, SH-SY-5Y, 和SKNBE(2c)细胞中AG-014699明显增强Topotecan和Temozolomide的细胞毒性。[4]

Cell Data
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
BT-474 NEHpWoRHfW6ldHnvckBCe3OjeR?= M120UVAvOS9zL{WwNE8yODByIH7N MnjGbY5pcWKrdIOgVGFTWCCjY4Tpeol1gSCjdDDzeIFzfGmwZzDjc45k\XKwdILheIlwdiCxZjC1NFAhdk1? NUjKTVZLOjVzMki0OVU>
BT474 MWDHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NEn6OGQ2ODBibl2= M{XvflEx6oDVMUZCpIQ> MYDy[YR2[2W|IHPlcIwh\3Kxd4ToJIlvKHSqZTDmc5VzKGyrbnXzJIFv\CC|aXfubYZq[2GwdHz5 M2nqPVI2OTJ6NEW1
SKBR3 MXzHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NUfEdFR3PTByIH7N NF3nS5EyOOLCk{G1xsBl MoD5doVlfWOnczDj[YxtKGe{b4f0bEBqdiC2aHWg[o92eiCuaX7ld{BidmRic3nncolncWOjboTsfS=> M2PzNVI2OTJ6NEW1
AU565 M{jpTGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 Mn\zOVAxKG6P MXWxNQKBmzF3wrDk M2XBbZJm\HWlZYOgZ4VtdCCpcn;3eIghcW5idHjlJIZwfXJibHnu[ZMh[W6mIIPp[45q\mmlYX70cJk> NUXP[mR5OjVzMki0OVU>
EFM192A NGHsN4lIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MX61NFAhdk1? NHfTWWUyOOLCk{G1xsBl NWrEWJFtemWmdXPld{Bk\WyuIHfyc5d1cCCrbjD0bIUh\m:3cjDsbY5meyCjbnSgd4lodmmoaXPhcpRtgQ>? NULUR4M4OjVzMki0OVU>
MDA-MB-231 MY\GeY5kfGmxbjDBd5NigQ>? NWPjZpVsOTBxMkCvOFAh|ryP NInvb4szPCCq NGXWUZVqdmO{ZXHz[ZMheC2DS2SgcIV3\Wy|IHnuJIEh\G:|ZT3k[ZBmdmSnboSgcYFvdmW{ MoL0NlQ1OjBzNUK=
MDA-MB-231 MkLaR4VtdCCYaXHibYxqfHliQYPzZZk> MWewMlEuPDBizszN NXjWNZFJOjRiaB?= M4LZZ2lEPTEkgJm95qCKOTdwN{hCpO69VQ>? MXiyOFQzODF3Mh?=
MDA-MB-231 NX;6[VJ7SXCxcITvd4l{KEG|c3H5 M1rsR|ExNzJyL{SwJO69VQ>? NY[zSZo5OjRiaB?= NHXPNnlqdmS3Y3XzJIFxd3C2b4Ppd{Bld3OnIHTldIVv\GWwdHz5 NILzNpgzPDR{MEG1Ni=>
MDA-MB-231 NX3SXXc2T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M1S5XFExNzJyL{SwJO69VQ>? NF3pNmQzPCCq M1PkVIJtd2OtczDj[YxtKGO7Y3zlJJBzd2e{ZYPzbY9vKGmwIFeyM20heGijc3W= MlziNlQ1OjBzNUK=
H460 M4riS2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NWjiUWNKPDByIH7N MlfQNlTDqGh? NUL0R4dYcW6lcnXhd4V{KGOnbHz1cIFzKHKjZHnvd4Vve2m2aY\peJk> M4WxclI1PDFzNkGx
A549  NFrtXXBIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= Mk[xOFAxKG6P MmjtNlTDqGh? MVHpcoNz\WG|ZYOgZ4VtdHWuYYKgdoFlcW:|ZX7zbZRqfmm2eR?= MVyyOFQyOTZzMR?=
DT40 MV;Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NH3WZlBKSzVyPUKxJI5O MXiyOFM2PjhzMx?=
DU145 MUTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NYX6OnplUUN3ME2xPEBvVQ>? NFLkcZgzPDN3NkixNy=>
COLO704 MYHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NVXOZ|hDUUN3ME2yMlUzKMLzIECuOlch|ryP NGjOTVczOzd{OUSwNi=>
OVMANAb NXfFb2tJT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NF30UZZKSzVyPUKuOVghyrFiMD6zPEDPxE1? M4jiRlI{PzJ7NECy
OV177 MXjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MkjFTWM2OD1{Lke4JOKyKDBwN{Gg{txO MWGyN|czQTRyMh?=
OAW28 MUTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MWXJR|UxRTNwNkGgxtEhOC5{ODFOwG0> NYnlXYttOjN5Mkm0NFI>
OVSAHO Mlq0S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MUjJR|UxRTNwNkSgxtEhOC5|MzFOwG0> NEiyUnUzOzd{OUSwNi=>
OVKATE NFnvUmdIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M4PlVGlEPTB;Mz62OEDDuSBzLke5JO69VQ>? NFf2cYkzOzd{OUSwNi=>
OVCAR3 MX7Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M2LUZ2lEPTB;Mz63OEDDuSByLkSwJO69VQ>? MnTnNlM4Ojl2MEK=
PEO14 MlfnS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NIXLdG5KSzVyPUOuPFQhyrFiMD63OkDPxE1? Mkm5NlM4Ojl2MEK=
A2780 NY\CfVNvT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NE\DOmtKSzVyPUOuPVQhyrFiMD6yOUDPxE1? NGD5VnczOzd{OUSwNi=>
OVTOKO MY\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NUHPdGo3UUN3ME20MlE1KMLzIEGuOVMh|ryP MUWyN|czQTRyMh?=
KURAMOCHIb NXvydoVWT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MVfJR|UxRTRwM{SgxtEhOC5{OTFOwG0> NGfIVJozOzd{OUSwNi=>
TOV21G NUS5d2xOT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MonBTWM2OD13LkC3JOKyKDFwM{Cg{txO MUmyN|czQTRyMh?=
OVISE NXzremNvT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MVPJR|UxRTVwNkigxtEhOC5{MzFOwG0> NV3JVWJROjN5Mkm0NFI>
KK NXG0VGU1T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NYnrPJc4UUN3ME22MlE2KMLzIEGuOFIh|ryP NGTjbnczOzd{OUSwNi=>
RMUGS MU\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NXnyNldjUUN3ME23MlA{KMLzIEGuPFMh|ryP NXLRXHV[OjN5Mkm0NFI>
PEO6 MnTjS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M4CySWlEPTB;Nz6wOkDDuSByLke0JO69VQ>? Moe3NlM4Ojl2MEK=
OVCA429 M3;Pfmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M3fjVWlEPTB;OD6yPUDDuSBzLk[0JO69VQ>? MVKyN|czQTRyMh?=
OV167 MlvUS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MnXtTWM2OD16LkOzJOKyKDFwMUig{txO MX:yN|czQTRyMh?=
RMG1 M4n2UWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MUHJR|UxRTlwM{KgxtEhOi5|NjFOwG0> M{jlbFI{PzJ7NECy
OVCAR5 MkTVS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MXPJR|UxRTlwNUCgxtEhOi53OTFOwG0> MmSxNlM4Ojl2MEK=
EFO21 NYezdVZwT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MXvJR|UxRTlwOUKgxtEhOS56NzFOwG0> NWLRZmxWOjN5Mkm0NFI>
ES2 MWHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MknLTWM2OD1zMD6xNkDDuSBzLkKzJO69VQ>? MUSyN|czQTRyMh?=
Tyk-nu NUDOTG1HT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NWeyeYNOUUN3ME2xNE4zOCEEsTCxMlEzKM7:TR?= NGLKTJEzOzd{OUSwNi=>
CAOV3 MVjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NXjpO3dYUUN3ME2xNE4{PyEEsTCwMlg4KM7:TR?= M1O5WlI{PzJ7NECy
OV207 Mkj4S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NFPTZpVKSzVyPUGyMlI4KMLzIECuN|Ih|ryP MmjUNlM4Ojl2MEK=
HEY MkXNS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MkXXTWM2OD1zMz6wNUDDuSByLke1JO69VQ>? NIjHO5ozOzd{OUSwNi=>
DOV13 NX\PNGlHT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NXXxcnppUUN3ME6xOUDPxE1? MViyN|czQTRyMh?=
EFO27 MWPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MnKxTWM2OD5zNTFOwG0> MYKyN|czQTRyMh?=
HEY C2 NEnnNmtIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M4KxdWlEPTB-MUWg{txO NEPKUGkzOzd{OUSwNi=>
KOC-7cc NH\USGlIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= Mn;tTWM2OD5zNTFOwG0> Ml7aNlM4Ojl2MEK=
MCASb NXfrRooyT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M1LCcGlEPTB-MUWg{txO NVTLV|gzOjN5Mkm0NFI>
OAW42 MUXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M3TjWGlEPTB-MUWg{txO MWeyN|czQTRyMh?=
OV2008 NIHUO3VIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MmrtTWM2OD5zNTFOwG0> NHSzTY0zOzd{OUSwNi=>
OV90 NEDyZnpIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NHzmV3hKSzVyPkG1JO69VQ>? Ml\KNlM4Ojl2MEK=
OVCA420b NXXWRVBIT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MkjuTWM2OD5zNTFOwG0> M2L1OFI{PzJ7NECy
OVCA432 MmnTS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MXPJR|UxRjF3IN88US=> NWW3e4x[OjN5Mkm0NFI>
PEA2 NUHlfGF[T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M{\ubWlEPTB-MUWg{txO M1\2c|I{PzJ7NECy
SKOV3 Mo\GS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MmXWTWM2OD5zNTFOwG0> NVPlfIpzOjN5Mkm0NFI>
TOV112D NGDvN5JIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NXTvfG17OC1|IN88US=> Ml;qTWM2OD5zNTFOwG0> NV;HO|dyOjN5Mkm0NFI>
C4-2 NXv6cVZxT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M133U|AuOyEQvF2= MnPuNVQh\A>? NVHYemNNTE2VTx?= MkDv[IVkemWjc3XzJINwdG:weTDueY1j\XJiZH;z[UBl\XCnbnTlcpRtgQ>? NVrSbog6OjN3NkWyOFQ>
PC3 NF23[|RIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NGLE[JQxNTNizszN M1rwblE1KGR? NInUT3ZFVVOR M4\YXoRm[3KnYYPld{Bkd2yxbomgcpVu[mW{IHTvd4Uh\GWyZX7k[Y51dHl? M4PWV|I{PTZ3MkS0
DU145 MXTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NWX6WotbOC1|IN88US=> NH3jfGIyPCCm NYjDRodRTE2VTx?= NXH4WZpq\GWlcnXhd4V{KGOxbH;ufUBvfW2kZYKg[I9{\SCmZYDlcoRmdnSueR?= M2\JcVI{PTZ3MkS0
VCaP  MUfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M2X3XFAuOyEQvF2= M2fkSFE1KGR? NUf5SmlPTE2VTx?= MWfk[YNz\WG|ZYOgZ49td267IH71cYJmeiCmb4PlJIRmeGWwZHXueIx6 MYiyN|U3PTJ2NB?=
LNCaP  NUH3PY1pT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MnXHNE0{KM7:TR?= M3fTSFE1KGR? MVzEUXNQ MYXk[YNz\WG|ZYOgZ49td267IH71cYJmeiCmb4PlJIRmeGWwZHXueIx6 NEGzO3czOzV4NUK0OC=>
MDA-MB-468 MmTQR4VtdCCYaXHibYxqfHliQYPzZZk> NF\T[GlKSzVyPUmuO{DPxE1? MVWyNlY4QDF4MR?=
MDA-MB-231 Mm\XR4VtdCCYaXHibYxqfHliQYPzZZk> NH3le2lKSzVyPUGzJO69VQ>? NHXVeWMzOjZ5OEG2NS=>
Cal-51 MYnD[YxtKF[rYXLpcIl1gSCDc4PhfS=> M1PtPWlEPTB;OD62JO69VQ>? MVeyNlY4QDF4MR?=

... Click to View More Cell Line Experimental Data

体内研究 AG-014699无毒,明显增强D384Med移植瘤DNA修复功能蛋白中temozolomide诱导的TGD。药物动力学研究显示在脑组织中也检测到AG-014699,说明AG-014699用于治疗颅内恶性肿瘤具有潜在可能。[3]活体模型(NB1691和SHSY5Y移植瘤)研究显示AG-014699增强temozolomide的抗癌活性,产生彻底且持久的肿瘤衰退现象。[4]

推荐的实验操作(此推荐来自于公开的文献所以Selleck并不保证其有效性)

激酶实验:[3]
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激酶实验:

不同浓度(0到1μ)AG-014699作用于5×103D283Med 细胞,与只用DMSO处理5×103D283Med细胞相比,来测定PARP活性抑制率。参考GCLP验证试验的PAR标准曲线,在和NAD+及寡核苷酸(底物和激活剂)温育的6分钟期间,使用10H PAR抗体,通过PAR形成量的免疫检测,在细胞样本中测量最大程度刺激的PARP活性。
细胞实验: [3]
+ 展开
  • Cell lines: D425Med, D283Med和D384Med细胞
  • Concentrations: 0.4 μM
  • Incubation Time: 3或5天
  • Method: 髓母细胞瘤细胞系包含D425Med, D283Med,和D384Med细胞,分别按1×103, 3×103,和3×103密度接种在96孔板上。接种24小时(D384Med细胞)或48小时(D283Med和D425Med细胞)后,细胞用不同浓度temozolomide处理。培养3天(D425Med和D384Med细胞)或5天(D283Med细胞)后,通过XTT细胞增殖检测试剂盒检测细胞活力。用DMSO处理的对照组和0.4μ AG-014699处理的实验组的百分比表示细胞生长。计算temozolomide单独使用或者和AG-014699联用时的GI50值。Temozolomide单独使用时的GI50值和与AG-014699联用时的GI50值之比就是趋化因子50(PF50)值。
    (Only for Reference)
动物实验:[3]
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  • Animal Models: 携带D283Med移植瘤的CD-1裸鼠
  • Formulation: 盐水溶液
  • Dosages: 1 mg/kg
  • Administration: 腹腔注射,每天1次或4次
    (Only for Reference)

溶解度 (25°C)

体外 DMSO 84 mg/mL (199.35 mM)
Water Insoluble
Ethanol Insoluble
体内 从左到右依次将纯溶剂加入产品,现配现用(数据来自Selleck实验检测而非文献):
2% DMSO+30% PEG 300+2% Tween 80+ddH2O
10mg/mL

* 溶解度检测是由Selleck技术部门检测的,可能会和文献中提供的溶解度有所差异,这是由于生产工艺和批次不同产生的正常现象。请按照顺序依次加入各个纯溶剂。

化学数据

分子量 421.36
化学式

C19H18FN3O.H3PO4

CAS号 459868-92-9
稳定性 powder
in solvent
别名 N/A

计算器

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摩尔浓度计算器

本计算器可帮助您计算出特定溶液中溶质的质量、溶液浓度和体积之间的关系,公式为:

质量 (g) = 浓度 (mol/L) x 体积 (L) x 分子量 (g/mol)

摩尔浓度计算公式

  • 质量
    浓度
    体积
    分子量

*在配置溶液时,请务必参考Selleck产品标签上、MSDS / COA(可在Selleck的产品页面获得)批次特异的分子量使用本工具。

稀释计算器

稀释计算器

用本工具协助配置特定浓度的溶液,使用的计算公式为:

开始浓度 x 开始体积 = 最终浓度 x 最终体积

稀释公式

稀释公式一般简略地表示为: C1V1 = C2V2 ( 输入 输出 )

  • C1
    V1
    C2
    V2

在配置溶液时,请务必参考Selleck产品标签上、MSDS / COA(可在Selleck的产品页面获得)批次特异的分子量使用本工具。.

连续稀释计算器方程

  • 连续稀释

  • 计算结果

  • 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):
分子量计算器

分子量计算器

通过输入化合物的化学式来计算其分子量:

总分子量:g/mol

注:化学分子式大小写敏感。C10H16N2O2 c10h16n2o2

摩尔浓度计算器

质量 浓度 体积 分子量
计算

临床试验信息

NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT03533946 Recruiting Prostate Cancer University of Utah|Clovis Oncology Inc. August 8 2018 Phase 2
NCT03499444 Recruiting Advanced Solid Tumor Clovis Oncology Inc. February 6 2018 Phase 1
NCT03101280 Recruiting Gynecologic Neoplasms Hoffmann-La Roche May 4 2017 Phase 1
NCT03337087 Not yet recruiting Biliary System Disorder|BRCA1 Gene Mutation|BRCA2 Gene Mutation|Gastroesophageal Junction Adenocarcinoma|Homologous Recombination Deficiency|Metastatic Pancreatic Adenocarcinoma|PALB2 Gene Mutation|Stage IV Colorectal Cancer AJCC v7|Stage IV Pancreatic Cancer AJCC v6 and v7|Stage IVA Colorectal Cancer AJCC v7|Stage IVB Colorectal Cancer AJCC v7 Academic and Community Cancer Research United|National Cancer Institute (NCI) August 31 2018 Phase 1|Phase 2
NCT03521037 Recruiting Neoplasms Clovis Oncology Inc. March 31 2018 Phase 1
NCT03140670 Recruiting Pancreatic Cancer Abramson Cancer Center of the University of Pennsylvania June 30 2017 Phase 2

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操作手册

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID