Sorafenib (BAY 43-9006) tosylate

For research use only. Not for use in humans.

目录号:S1040 中文名称:甲苯磺酸索拉非尼

Sorafenib (BAY 43-9006) tosylate Chemical Structure

CAS No. 475207-59-1

Sorafenib (BAY 43-9006) tosylate是Raf-1B-Raf的多重激酶抑制剂,无细胞试验中IC50分别为6 nM和22 nM。Sorafenib 还可抑制VEGFR-2VEGFR-3PDGFR-βFlt-3c-KIT,对应的IC50值分别为90 nM、20 nM、57 nM、59 nM和68 nM。Sorafenib Tosylate 可诱导autophagyapoptosis并激活ferroptosis,并具有抗肿瘤活性。

规格 价格 库存 购买数量  
10mM (1mL in DMSO) RMB 2882.17 现货
RMB 1206.06 现货
RMB 1801.93 现货
RMB 5475.69 现货
RMB 13079.43 现货
RMB 13898.43 现货
RMB 16355.43 现货
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客户使用Selleck生产的Sorafenib (BAY 43-9006) tosylate发表文献199篇:

产品安全说明书

Raf抑制剂选择性比较

生物活性

产品描述 Sorafenib (BAY 43-9006) tosylate是Raf-1B-Raf的多重激酶抑制剂,无细胞试验中IC50分别为6 nM和22 nM。Sorafenib 还可抑制VEGFR-2VEGFR-3PDGFR-βFlt-3c-KIT,对应的IC50值分别为90 nM、20 nM、57 nM、59 nM和68 nM。Sorafenib Tosylate 可诱导autophagyapoptosis并激活ferroptosis,并具有抗肿瘤活性。
靶点
Raf-1 [1]
(Cell-free assay)
VEGFR2/Flk1 [1]
(Cell-free assay)
B-Raf [1]
(Cell-free assay)
B-Raf (V599E) [1]
(Cell-free assay)
PDGFRβ [1]
(Cell-free assay)
6 nM 15 nM 22 nM 38 nM 57 nM
体外研究

Sorafenib作用于这些细胞系(如 Mia PaCa 2, HCT 116, A549,和NCI-H460),抑制ERK磷酸化,引起RAS/RAF通路的异常激活。Sorafenib作用于MDA-MB-231乳腺癌细胞系,完全抑制 MAPK 通路的激活。 Sorafenib 抑制 MEK 1/2 和ERK 1/2 磷酸化,这种作用存在剂量依赖性,IC50分别为40 nM和 100 nM。Sorafenib 作用于MDA-MB-231细胞,对 PKB通路没有效果,说明Sorafenib 选择性抑制MAPK, 而不抑制PKB通路。Sorafenib 作用于人胰脏(Mia PaCa 2)和结肠 (HCT 116和 HT-29)肿瘤细胞系,抑制pERK。Sorafenib 抑制EGFR,IGFR-1,c-met,和 HER-2 RTKs ,IC50>10,000 nM。此外, Sorafenibis 有效抑制细胞中VEGFR-2信号。Sorafenib 抑制mVEGFR-2 (flk-1), mVEGFR-3, 和mPDGFR-β,IC50 分别为15 nM, 20 nM,和 57 nM。[1]

Cell Data
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
MDA-MB-435 MW\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M{P1blQ5KGh? MVXHTVUxRTJizszN MWG8ZUB1[XKpZYS9K39jdGGwazegbJJm\j1paIT0dJM7Ny:ydXLt[YQvdmOkaT7ucI0vdmmqLnfvek8zOjV4ME[yO{c,OjJ3NkC2Nlc9N2F-
UACC257 Mnr6S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NFrNe5Q1QCCq MX\HTVUxRTJizszN NIjj[pI9[SC2YYLn[ZQ:L1:kbHHub{chcHKnZk2nbJR1eHN8Lz;weYJu\WRwbnPibU5vdG1wbnnoModwfi9{MkW2NFYzPyd-MkK1OlA3Ojd:L3G+
MCF7 MlvjS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M3\TTlQ5KGh? NE\teIFIUTVyPUKuOUDPxE1? M2PLZVxiKHSjcnfleF0oZ2KuYX7rK{BpemWoPTfoeJRxezpxL4D1Zo1m\C6wY3LpMo5tdS6waXiu[493NzJ{NU[wOlI4Lz5{MkW2NFYzPzxxYU6=
EKVX MWLHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NYjXUZgxPDhiaB?= MnPLS2k2OD1{LkWg{txO NXzreHZFRGFidHHy[4V1RSehYnzhcosoKGi{ZX[9K4h1fHC|Oj:vdJVjdWWmLn7jZokvdmyvLn7pbE5od3ZxMkK1OlA3OjdpPkKyOVYxPjJ5PD;hQi=>
HT-29 Mmq3S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M3m1d|Q5KGh? NIHwT4xIUTVyPUKuOUDPxE1? M{XZWlxiKHSjcnfleF0oZ2KuYX7rK{BpemWoPTfoeJRxezpxL4D1Zo1m\C6wY3LpMo5tdS6waXiu[493NzJ{NU[wOlI4Lz5{MkW2NFYzPzxxYU6=
SNB19 MX;Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MVi0PEBp MWfHTVUxRTNwMjFOwG0> MUS8ZUB1[XKpZYS9K39jdGGwazegbJJm\j1paIT0dJM7Ny:ydXLt[YQvdmOkaT7ucI0vdmmqLnfvek8zOjV4ME[yO{c,OjJ3NkC2Nlc9N2F-
OVCAR3 M4PzWGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M3;zd|Q5KGh? M{\qemdKPTB;Mz6yJO69VQ>? MYm8ZUB1[XKpZYS9K39jdGGwazegbJJm\j1paIT0dJM7Ny:ydXLt[YQvdmOkaT7ucI0vdmmqLnfvek8zOjV4ME[yO{c,OjJ3NkC2Nlc9N2F-
CAKI-1 NF7EPZRIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MmjyOFghcA>? NWfFdpRiT0l3ME2zMlIh|ryP MkLjQIEhfGG{Z3X0QUdg[myjbnunJIhz\WZ;J3j0eJB{Qi9xcIXicYVlNm6lYnmucoxuNm6raD7nc5YwOjJ3NkC2NlcoRjJ{NU[wOlI4RC:jPh?=
SW620 M4\RTWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 Mn71OFghcA>? NFLpUnRIUTVyPUOuNkDPxE1? MV68ZUB1[XKpZYS9K39jdGGwazegbJJm\j1paIT0dJM7Ny:ydXLt[YQvdmOkaT7ucI0vdmmqLnfvek8zOjV4ME[yO{c,OjJ3NkC2Nlc9N2F-
TK10 MVPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NIPrVJk1QCCq NVXSWGIyT0l3ME21JO69VQ>? NE\P[ZE9[SC2YYLn[ZQ:L1:kbHHub{chcHKnZk2nbJR1eHN8Lz;weYJu\WRwbnPibU5vdG1wbnnoModwfi9{MkW2NFYzPyd-MkK1OlA3Ojd:L3G+
endothelial precursor cells NVLiZWtwTnWwY4Tpc44h[XO|YYm= NXTuU3FnUW6qaXLpeIlwdiCxZjDlcoRwfGinbHnhcEBkd3KmIHHy[YEh\m:{bXH0bY9vKGmwIHXu[I91cGWuaXHsJJBz\WO3coPvdkBk\WyuczDifUBETDNzIHPvdoQh[XKnYTDk[ZRm[3Srb36gZoF{\WRicHjlco91gXCrYzDkdpVoKGSrc3PveoVzgSCkYYPl[EBie3OjeTygTWM2OCB;IECuNFA1OjFizszNMi=> M{fuTVxiKHSjcnfleF0oZ2KuYX7rK{BpemWoPTfoeJRxezpxL4D1Zo1m\C6wY3LpMo5tdS6waXiu[493NzJ{NEC5OlY3Lz5{MkSwPVY3PjxxYU6=
Sf9 NXPkZnBjTnWwY4Tpc44h[XO|YYm= M3nr[GlvcGmkaYTpc44hd2ZiR2PUMZRi\2enZDDy[YNwdWKrbnHueEBpfW2jbjDWSWdHWjJiZYjwdoV{e2WmIHnuJHNnQSClZXzsd{BjgSC{YXTpc41mfHKrYzDhd5NigSxiSVO1NEA:KDBwMEGyOUDPxE1w MorjQIEhfGG{Z3X0QUdg[myjbnunJIhz\WZ;J3j0eJB{Qi9xcIXicYVlNm6lYnmucoxuNm6raD7nc5YwOjR|NkiyNFkoRjJ2M{[4NlA6RC:jPh?=
endothelial precursor cells/ADSC cells M1H2cnRwgGmlaYT5JIF{e2G7 MUnUc5hq[2m2eTDpckBmdmSxdHjlcIlidCCycnXjeZJ{d3JiY3XscJMh[29vY4XseJVz\WRid3n0bEB{fHKxbXHsJJBz\WO3coPvdkBCTFOFIHPlcIx{KGK7IITveIFtKG63Y3zlbUBkd3WwdDDk[ZRm[3Srb36gZoF{\WRicHjlco91gXCrYzDkdpVoKGSrc3PveoVzgSCkYYPl[EBie3OjeTygSWM2OCB;IEWuOFYh|ryPLh?= NELGdIU9[SC2YYLn[ZQ:L1:kbHHub{chcHKnZk2nbJR1eHN8Lz;weYJu\WRwbnPibU5vdG1wbnnoModwfi9{MkSwPVY3Pid-MkK0NFk3PjZ:L3G+
endothelial precursor cells MVTGeY5kfGmxbjDhd5NigQ>? NEXtSZBKdmirYnn0bY9vKG:oIHPlcIwhdWmpcnH0bY9vKGmwIHXu[I91cGWuaXHsJJBz\WO3coPvdkBk\WyuczDifUBQemm|IHPlcIwhdWmpcnH0bY9vKGurdDDiZZNm\CCyaHXuc5R6eGmlIHTyeYch\Gm|Y3;2[ZJ6KGKjc3XkJIF{e2G7LDDJR|UxKD1iMU[uO{DPxE1w NEmxbZo9[SC2YYLn[ZQ:L1:kbHHub{chcHKnZk2nbJR1eHN8Lz;weYJu\WRwbnPibU5vdG1wbnnoModwfi9{MkSwPVY3Pid-MkK0NFk3PjZ:L3G+
RD NWfYeYVpeUiWUzDhd5NigQ>? NHrXZXFyUFSVIH;mJJBm\GmjdILpZ{Bk[W6lZYKgZ4VtdCCuaX7ld{B1dyCrZHXueIlngSCvdXz0bZBt\SCxcIDvdpR2dmm2aXXzJIZweiCmcoXnJJJmeHW{cH;zbY5oQiCScnntZZJ6KHOlcnXlckBnd3JiUlSgZ4VtdHN? M1K3XFxiKHSjcnfleF0oZ2KuYX7rK{BpemWoPTfoeJRxezpxL4D1Zo1m\C6wY3LpMo5tdS6waXiu[493NzJ7NEO1NVM6Lz5{OUSzOVE{QTxxYU6=
SK-N-SH M1;wZZFJXFNiYYPzZZk> NEPRUnpyUFSVIH;mJJBm\GmjdILpZ{Bk[W6lZYKgZ4VtdCCuaX7ld{B1dyCrZHXueIlngSCvdXz0bZBt\SCxcIDvdpR2dmm2aXXzJIZweiCmcoXnJJJmeHW{cH;zbY5oQiCScnntZZJ6KHOlcnXlckBnd3JiU1utUk1UUCClZXzsdy=> M4DtUVxiKHSjcnfleF0oZ2KuYX7rK{BpemWoPTfoeJRxezpxL4D1Zo1m\C6wY3LpMo5tdS6waXiu[493NzJ7NEO1NVM6Lz5{OUSzOVE{QTxxYU6=
OHS-50 NHvwZ3pyUFSVIHHzd4F6 MmXsdWhVWyCxZjDw[YRq[XS{aXOgZ4Fv[2W{IHPlcIwhdGmwZYOgeI8hcWSnboTp[pkhdXWudHnwcIUhd3Cyb4L0eY5qfGmnczDmc5Ih\HK3ZzDy[ZB2enCxc3nu[|ohWHKrbXHyfUB{[3KnZX6g[o9zKE:KUz21NEBk\Wyucx?= NGe0c4o9[SC2YYLn[ZQ:L1:kbHHub{chcHKnZk2nbJR1eHN8Lz;weYJu\WRwbnPibU5vdG1wbnnoModwfi9{OUSzOVE{QSd-Mkm0N|UyOzl:L3G+

... Click to View More Cell Line Experimental Data

Assay
Methods Test Index PMID
Western blot
LC3-I / LC-3II / ATG5; 

PubMed: 23392173     


Sorafenib induces the conversion of LC3 in a dose-dependent manner. PLC5, Hep3B, SK-Hep1 and HepG2 were exposed to sorafenib at the indicated doses for 16 h and the expression levels of LC3-II were analyzed by western blot.

p-STAT3 / STAT3/ Mcl-1; 

PubMed: 23392173     


Effects of sorafenib on STAT3-related proteins in HCC cells. The cells were treated with sorafenib at the indicated dose for 16 h. 

β-catenin / Survivin / Mcl-1 / PTMA; 

PubMed: 26517516     


Co-inhibition of β-catenin and PTMA by sorafenib in HCC cells. Cell lines indicated on top were treated or not with 10 μM sorafenib for 24 hrs and processed for immuno-blotting. IC50 values (the concentration of sorafenib that inhibits 50% of cell growth) for each cell line are indicated below the panels.

pERK / ERK; 

PubMed: 22286758     


Western blot analysis of p-ERK (T202/Y204) and ERK at indicated time points in HCT116 cells treated with 20 μmol/L sorafenib.

p-PKM2(Y105) / PMK2 / Caspase-9 ; 

PubMed: 26959741     


Sorafenib downregulates the p-PKM2(Y105) at the indicated doses after treatment for 24 h.

RET(pY1016) / VEGFR2(pY1214) / MEK1(pT292) / ERK(pY204) ; 

PubMed: 22941289     


Sorafenib affected the phosphorylation of receptor tyrosine kinase RET and VEGFR2, as well as MEK/ERK kinases signaling cascades in three cell lines. Three cell lines were treated by sorafenib with two concentration gradients, 1 and 5 μmol/L/L, and then collected after 2, 4, and 8 h, cells without sorafenib treatment were as the controls (0 h). Total proteins were extracted and quantified to be used in Western blot assays. (A) Sorafenib inhibited RET and VEGFR2 phosphorylation dose-dependently while activated MEK and ERK phosphorylation in A549 cells. (B) Sorafenib also inhibited RET and VEGFR2 phosphorylation, and slightly activated MEK and ERK phosphorylation in HeLa cells. (C) Sorafenib activated the phosphorylation of RET, VEGFR2, and MEK, but inhibited ERK phosphorylation in HepG2 cells.

Cyclin D1; 

PubMed: 26039995     


Dose-escalation effects of sorafenib or SC-1 for 24 h on STAT3-related proteins in HSC-T6 and LX2 cells.

23392173 26517516 22286758 26959741 22941289 26039995
Immunofluorescence
p65; 

PubMed: 22286758     


HCT116 cells were treated with 20 μmol/L sorafenib or 10 ng/mL TNF-α for 3 hours then fixed. Immunofluorescence was carried out as described in the Materials and Methods for p65 (green) and DAPI (blue). Representative pictures (400×) are shown

cytochrome c; 

PubMed: 22278289     


Immunoflourescent staining and quantification of mitochondrial membrane potential (appearing in red, mitotracker) and cytochrome c (appearing in green, FITC) in 22Rv1 and PC3 treated with 20 μM sorafenib for 24 h

22286758 22278289
Growth inhibition assay
Cell viability; 

PubMed: 26039995     


Dose-escalation and time-dependent effects of sorafenib for 24 or 48 h on cell viability in HSC-T6, LX2, and mouse primary HSCs. Circles, mean; bars, SE (n = 3). 

26039995
ELISA
TGF-beta / CD206; 

PubMed: 26158762     


In Macrophage, TGF-β secretion and CD206 were confirmed by ELISA.

Caspase-9 / Caspase-3; 

PubMed: 30923462     


Caspase-9 and caspase-3 activities were measured via ELISA assay. FCCP, an activator of mitophagy, was added into the medium of sorafenib-treated cells to activate mitophagy. Adenovirus-loaded LATS2 (Ad-LATS2) was transfected into HepG2 cells in the presence of sorafenib. *p < 0.05 vs. control group; #p < 0.05 vs. Sorafenib + Ad-cont group; #p < 0.05 vs. Sorafenib + Ad-LATS2 group

26158762 30923462
体内研究 Sorafenib 按30 mg/kg或60 mg/kg 剂量每天口服处理HT-29肿瘤,与对照组相比,实验组50到80% MVA和 MVD受抑制。Sorafenib作用于Colo-205肿瘤, 可观察到MVA 和MVD明显受抑制,而不抑制MAPK。[1]

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:[1]
- 合并

生化实验:

测定抑制多种RAF激酶亚型的效果, Sorafenib加到反应buffer[20 mM Tris (pH 8.2), 100 mM NaCl, 5 mM MgCl2, 和0.15% β-巯基乙醇] 中Raf-1(80 ng), wtBRAF, 或V599EBRAF (80 ng) 及MEK-1 (1 μg)的混合物中,DMSO终浓度为1%。加入25 μL 10 μM γ-[33P]ATP(400 Ci/mol),开始 RAF 激酶实验(终体积为 50 μL),在32 oC下温育25分钟。过滤到磷酸纤维素垫上收集磷酸化的MEK-1,使用 1% 磷酸冲洗未结合的放射性。微波加热烘干, 使用β-计数板测定过滤结合的放射性。
细胞实验:[1]
- 合并
  • Cell lines: Colo-205, HT-29, 和DLD-1人结肠癌细胞
  • Concentrations: 0 μM -10 μM
  • Incubation Time: 2 小时
  • Method: Colo-205, HT-29, 和 DLD-1人结肠癌细胞系按每孔 2 × 105个细胞接种在12孔组织培养板上,过夜,孔中含DMEM 生长培养基(10% 热灭活FCS)。使用无血清培养基冲洗细胞一次,然后在含0.1% 无脂肪酸BSA的DMEM培养基中 与溶于 0.1% DMSO的不同浓度Sorafenib温育120分钟,测定pMEK 1/2, pERK 1/2,或pPKB的改变量。使用冰冻 PBS (含0.1 mM钒酸盐的PBS ) 冲洗细胞,然后溶于含蛋白酶抑制剂的1% (v/v) Triton X-100溶液中。离心净化裂解物,然后进行SDS-PAGE,再转移到硝化棉膜上, 然后在 TBS-BSA中阻断,再使用anti-pMEK 1/2 (Ser217/Ser221; 1:1000), anti-MEK 1/2, anti-pERK 1/2 (Thr202/Tyr204; 1:1000), anti-ERK 1/2, anti-pPKB (Ser473; 1:1000), 或anti-PKB一抗做探针。使用辣根过氧化物酶(HRP)标记的二抗进行印迹,然后使用Amersham ECL试剂在Amersham Hyperfilm上进行显影。
    (Only for Reference)
动物实验: [1]
- 合并
  • Animal Models: 携带HT-29和Colo-205细胞的雌性NCr-nu/nu小鼠
  • Dosages: 30 mg/kg或60 mg/kg
  • Administration: 口服处理
    (Only for Reference)

溶解度 (25°C)

体外 DMSO 127 mg/mL (199.36 mM)
Water 0.01 mg/mL (0.01 mM)
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% Cremophor EL, 2% N,N-dimethylacetamide
30 mg/mL (suspension)

* 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 637.03
化学式

C21H16ClF3N4O3.C7H8O3S

CAS号 475207-59-1
储存条件 粉状
溶于溶剂
别名 N/A

动物体内配方计算器 (澄清溶液)

第一步:请输入基本实验信息(考虑到实验过程中的损耗,建议多配一只动物的药量)
给药剂量 mg/kg 动物平均体重 g 每只动物给药体积 ul 动物数量
第二步:请输入动物体内配方组成(配方适用于不溶于水的药物;不同批次药物配方比例不同,请联系Selleck为您提供正确的澄清溶液配方)
% DMSO % % Tween 80 % ddH2O
计算重置

计算器

摩尔浓度计算器

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 (mg) = 浓度 (mM) x 体积 (mL) 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、SDS / 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、SDS / 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 interventions Conditions Sponsor/Collaborators Start Date Phases
NCT04710641 Not yet recruiting Drug: MTL-CEBPA|Drug: Sorafenib Hepatocellular Carcinoma|Hepatitis B|Hepatitis C Mina Alpha Limited May 1 2021 Phase 2
NCT04763408 Not yet recruiting Drug: Lenvatinib|Drug: Sorafenib Carcinoma Hepatocellular Eisai Inc. March 15 2021 --
NCT04000737 Recruiting Drug: YIV-906+Sorafenib|Drug: Placebo+Sorafenib Advanced Hepatocellular Carcinoma Yiviva Inc. January 10 2020 Phase 2
NCT03958669 Recruiting -- Hepatocellular Carcinoma|Sorafenib University Hospital Tuebingen|German Federal Ministry of Education and Research November 1 2019 --
NCT03764293 Recruiting Drug: SHR-1210|Drug: Apatinib|Drug: Sorafenib Locally Advanced or Metastatic and Unresectable HCC Jiangsu HengRui Medicine Co. Ltd. June 10 2019 Phase 3
NCT03582618 Recruiting Drug: Sorafenib|Drug: CVM-1118 Hepatocellular Carcinoma|Advanced Cancer TaiRx Inc. July 12 2018 Phase 2

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID