Home MAPK Raf inhibitor - PDGFR inhibitor - VEGFR inhibitor - FLT3 inhibitor - c-Kit inhibitor - FGFR inhibitor - Ferroptosis activator - Autophagy activator - Apoptosis related activator Sorafenib (BAY 43-9006) tosylate

Sorafenib (BAY 43-9006) tosylate

Catalog No.S1040

For research use only.

Sorafenib (BAY 43-9006) tosylate is a multikinase inhibitor of Raf-1 and B-Raf with IC50 of 6 nM and 22 nM in cell-free assays, respectively. Sorafenib Tosylate inhibits VEGFR-2, VEGFR-3, PDGFR-β, Flt-3 and c-KIT with IC50 of 90 nM, 20 nM, 57 nM, 59 nM and 68 nM, respectively. Sorafenib Tosylate induces autophagy and apoptosis and activates ferroptosis with anti-tumor activity.

Sorafenib (BAY 43-9006) tosylate Chemical Structure

CAS No. 475207-59-1

Selleck's Sorafenib (BAY 43-9006) tosylate has been cited by 211 publications

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Description Sorafenib (BAY 43-9006) tosylate is a multikinase inhibitor of Raf-1 and B-Raf with IC50 of 6 nM and 22 nM in cell-free assays, respectively. Sorafenib Tosylate inhibits VEGFR-2, VEGFR-3, PDGFR-β, Flt-3 and c-KIT with IC50 of 90 nM, 20 nM, 57 nM, 59 nM and 68 nM, respectively. Sorafenib Tosylate induces autophagy and apoptosis and activates ferroptosis with anti-tumor activity.
Targets
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)		 Click to View More Targets
6 nM 15 nM 22 nM 38 nM 57 nM
In vitro

Sorafenib tosylate inhibits both wild-type and V599E mutant B-Raf activity with IC50 of 22 nM and 38 nM, respectively. Sorafenib tosylate also potently inhibits mVEGFR2 (Flk-1), mVEGFR3, mPDGFRβ, Flt3, and c-Kit with IC50 of 15 nM, 20 nM, 57 nM, 58 nM, and 68 nM, respectively. Sorafenib tosylate weakly inhibits FGFR-1 with IC50 of 580 nM. Sorafenib tosylate is not active against ERK-1, MEK-1, EGFR, HER-2, IGFR-1, c-Met, PKB, PKA, cdk1/cyclinB, PKCα, PKCγ, and pim-1. Sorafenib tosylate markedly inhibits VEGFR2 phosphorylation in NIH 3T3 cells with IC50 of 30 nM, and Flt-3 phosphorylation in HEK-293 cells with IC50 of 20 nM. Sorafenib tosylate potently blocks MEK 1/2 and ERK 1/2 phosphorylation in most cell lines but not in A549 or H460 cells, while having no effect on inhibition of the PKB pathway. Sorafenib tosylate inhibits the proliferation of HAoSMC and MDA-MB-231 cells with IC50 of 0.28 μM and 2.6 μM, respectively. [1] In addition to inhibition of the RAF/MEK/ERK signaling pathway, Sorafenib tosylate significantly inhibits the phosphorylation of eIF4E and down-regulates Mcl-1 levels in hepatocellular carcinoma (HCC) cells in a MEK/ERK-independent manner. Sorafenib tosylate inhibits the proliferation of PLC/PRF/5 and HepG2 cells with IC50 of 6.3 μM and 4.5 μM, respectively, and leads to the significant induction of apoptosis. [2]
Cell Data
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
MDA-MB-435 NFXxclNIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MlyxOFghcA>? MX\HTVUxRTJizszN MlrQQIEhfGG{Z3X0QUdg[myjbnunJIhz\WZ;J3j0eJB{Qi9xcIXicYVlNm6lYnmucoxuNm6raD7nc5YwOjJ3NkC2NlcoRjJ{NU[wOlI4RC:jPh?=
UACC257 NXXrbphXT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M{PadVQ5KGh? NGPwZlBIUTVyPUKg{txO M{n2OFxiKHSjcnfleF0oZ2KuYX7rK{BpemWoPTfoeJRxezpxL4D1Zo1m\C6wY3LpMo5tdS6waXiu[493NzJ{NU[wOlI4Lz5{MkW2NFYzPzxxYU6=
MCF7 MWHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MVS0PEBp NV\YcWZHT0l3ME2yMlUh|ryP NWi0VVNzRGFidHHy[4V1RSehYnzhcosoKGi{ZX[9K4h1fHC|Oj:vdJVjdWWmLn7jZokvdmyvLn7pbE5od3ZxMkK1OlA3OjdpPkKyOVYxPjJ5PD;hQi=>
EKVX M4frNmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M2XC[FQ5KGh? NIXpW2dIUTVyPUKuOUDPxE1? Mlq1QIEhfGG{Z3X0QUdg[myjbnunJIhz\WZ;J3j0eJB{Qi9xcIXicYVlNm6lYnmucoxuNm6raD7nc5YwOjJ3NkC2NlcoRjJ{NU[wOlI4RC:jPh?=
HT-29 M3W5V2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NVrqZ41PPDhiaB?= NHzCNmVIUTVyPUKuOUDPxE1? NYn6Tm1KRGFidHHy[4V1RSehYnzhcosoKGi{ZX[9K4h1fHC|Oj:vdJVjdWWmLn7jZokvdmyvLn7pbE5od3ZxMkK1OlA3OjdpPkKyOVYxPjJ5PD;hQi=>
SNB19 M{PhNGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MkPjOFghcA>? MmLCS2k2OD1|LkKg{txO MnW1QIEhfGG{Z3X0QUdg[myjbnunJIhz\WZ;J3j0eJB{Qi9xcIXicYVlNm6lYnmucoxuNm6raD7nc5YwOjJ3NkC2NlcoRjJ{NU[wOlI4RC:jPh?=
OVCAR3 NVrEcHo4T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NEHTUHc1QCCq NY\SNItjT0l3ME2zMlIh|ryP MnHvQIEhfGG{Z3X0QUdg[myjbnunJIhz\WZ;J3j0eJB{Qi9xcIXicYVlNm6lYnmucoxuNm6raD7nc5YwOjJ3NkC2NlcoRjJ{NU[wOlI4RC:jPh?=
CAKI-1 NVPQNWZlT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MlWzOFghcA>? MlfMS2k2OD1|LkKg{txO NW\TdFFIRGFidHHy[4V1RSehYnzhcosoKGi{ZX[9K4h1fHC|Oj:vdJVjdWWmLn7jZokvdmyvLn7pbE5od3ZxMkK1OlA3OjdpPkKyOVYxPjJ5PD;hQi=>
SW620 NWHoWGtTT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MnzKOFghcA>? NEDmOoJIUTVyPUOuNkDPxE1? NXzsOmRrRGFidHHy[4V1RSehYnzhcosoKGi{ZX[9K4h1fHC|Oj:vdJVjdWWmLn7jZokvdmyvLn7pbE5od3ZxMkK1OlA3OjdpPkKyOVYxPjJ5PD;hQi=>
TK10 MVPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NH;qVow1QCCq NHPJXphIUTVyPUWg{txO NYC3U4lSRGFidHHy[4V1RSehYnzhcosoKGi{ZX[9K4h1fHC|Oj:vdJVjdWWmLn7jZokvdmyvLn7pbE5od3ZxMkK1OlA3OjdpPkKyOVYxPjJ5PD;hQi=>
endothelial precursor cells Mmn0SpVv[3Srb36gZZN{[Xl? NHfOWppKdmirYnn0bY9vKG:oIHXu[I91cGWuaXHsJINwemRiYYLlZUBnd3KvYYTpc44hcW5iZX7kc5Rp\WyrYXygdJJm[3W{c3;yJINmdGy|IHL5JGNFOzFiY3;y[EBiemWjIHTleIVkfGmxbjDiZZNm\CCyaHXuc5R6eGmlIHTyeYch\Gm|Y3;2[ZJ6KGKjc3XkJIF{e2G7LDDJR|UxKD1iMD6wNFQzOSEQvF2u NWnkXopmRGFidHHy[4V1RSehYnzhcosoKGi{ZX[9K4h1fHC|Oj:vdJVjdWWmLn7jZokvdmyvLn7pbE5od3ZxMkK0NFk3PjZpPkKyOFA6PjZ4PD;hQi=>
Sf9 NUnp[3BOTnWwY4Tpc44h[XO|YYm= M2\EfGlvcGmkaYTpc44hd2ZiR2PUMZRi\2enZDDy[YNwdWKrbnHueEBpfW2jbjDWSWdHWjJiZYjwdoV{e2WmIHnuJHNnQSClZXzsd{BjgSC{YXTpc41mfHKrYzDhd5NigSxiSVO1NEA:KDBwMEGyOUDPxE1w NWq4[mNXRGFidHHy[4V1RSehYnzhcosoKGi{ZX[9K4h1fHC|Oj:vdJVjdWWmLn7jZokvdmyvLn7pbE5od3ZxMkSzOlgzODlpPkK0N|Y5OjB7PD;hQi=>
endothelial precursor cells/ADSC cells NFHyd21Vd3irY3n0fUBie3OjeR?= MVTUc5hq[2m2eTDpckBmdmSxdHjlcIlidCCycnXjeZJ{d3JiY3XscJMh[29vY4XseJVz\WRid3n0bEB{fHKxbXHsJJBz\WO3coPvdkBCTFOFIHPlcIx{KGK7IITveIFtKG63Y3zlbUBkd3WwdDDk[ZRm[3Srb36gZoF{\WRicHjlco91gXCrYzDkdpVoKGSrc3PveoVzgSCkYYPl[EBie3OjeTygSWM2OCB;IEWuOFYh|ryPLh?= NWn4XYV2RGFidHHy[4V1RSehYnzhcosoKGi{ZX[9K4h1fHC|Oj:vdJVjdWWmLn7jZokvdmyvLn7pbE5od3ZxMkK0NFk3PjZpPkKyOFA6PjZ4PD;hQi=>
endothelial precursor cells MlLZSpVv[3Srb36gZZN{[Xl? NHPPe4tKdmirYnn0bY9vKG:oIHPlcIwhdWmpcnH0bY9vKGmwIHXu[I91cGWuaXHsJJBz\WO3coPvdkBk\WyuczDifUBQemm|IHPlcIwhdWmpcnH0bY9vKGurdDDiZZNm\CCyaHXuc5R6eGmlIHTyeYch\Gm|Y3;2[ZJ6KGKjc3XkJIF{e2G7LDDJR|UxKD1iMU[uO{DPxE1w M1vmfFxiKHSjcnfleF0oZ2KuYX7rK{BpemWoPTfoeJRxezpxL4D1Zo1m\C6wY3LpMo5tdS6waXiu[493NzJ{NEC5OlY3Lz5{MkSwPVY3PjxxYU6=
RD Mon2dWhVWyCjc4PhfS=> MoH0dWhVWyCxZjDw[YRq[XS{aXOgZ4Fv[2W{IHPlcIwhdGmwZYOgeI8hcWSnboTp[pkhdXWudHnwcIUhd3Cyb4L0eY5qfGmnczDmc5Ih\HK3ZzDy[ZB2enCxc3nu[|ohWHKrbXHyfUB{[3KnZX6g[o9zKFKGIHPlcIx{ M3XodVxiKHSjcnfleF0oZ2KuYX7rK{BpemWoPTfoeJRxezpxL4D1Zo1m\C6wY3LpMo5tdS6waXiu[493NzJ7NEO1NVM6Lz5{OUSzOVE{QTxxYU6=
SK-N-SH MUXxTHRUKGG|c3H5 NEK5b3lyUFSVIH;mJJBm\GmjdILpZ{Bk[W6lZYKgZ4VtdCCuaX7ld{B1dyCrZHXueIlngSCvdXz0bZBt\SCxcIDvdpR2dmm2aXXzJIZweiCmcoXnJJJmeHW{cH;zbY5oQiCScnntZZJ6KHOlcnXlckBnd3JiU1utUk1UUCClZXzsdy=> MXy8ZUB1[XKpZYS9K39jdGGwazegbJJm\j1paIT0dJM7Ny:ydXLt[YQvdmOkaT7ucI0vdmmqLnfvek8zQTR|NUGzPUc,Ojl2M{WxN|k9N2F-
OHS-50 MUjxTHRUKGG|c3H5 M1zZ[pFJXFNib3[gdIVlcWG2cnnjJINidmOncjDj[YxtKGyrbnXzJJRwKGmmZX70bYZ6KG23bITpdIxmKG:ycH;yeJVvcXSrZYOg[o9zKGS{dXegdoVxfXKyb4Ppcoc7KFC{aX3hdpkhe2O{ZXXuJIZweiCRSGOtOVAh[2WubIO= MnfqQIEhfGG{Z3X0QUdg[myjbnunJIhz\WZ;J3j0eJB{Qi9xcIXicYVlNm6lYnmucoxuNm6raD7nc5YwOjl2M{WxN|koRjJ7NEO1NVM6RC:jPh?=
Click to View More Cell Line Experimental Data
Assay
Methods Test Index PMID
Western blot LC3-I / LC-3II / ATG5 ; p-STAT3 / STAT3/ Mcl-1 ; β-catenin / Survivin / Mcl-1 / PTMA ; pERK / ERK ; p-PKM2(Y105) / PMK2 / Caspase-9 ; RET(pY1016) / VEGFR2(pY1214) / MEK1(pT292) / ERK(pY204) ; Cyclin D1 23392173 26517516 22286758 26959741 22941289 26039995
Immunofluorescence p65 ; cytochrome c 22286758 22278289
Growth inhibition assay Cell viability 26039995
ELISA TGF-beta / CD206 ; Caspase-9 / Caspase-3 26158762 30923462
In vivo Oral administration of Sorafenib tosylate (~60 mg/kg) demonstrates broad spectrum, dose-dependent anti-tumor activity against a variety of human tumor xenograft models including MDA-MB-231, Colo-205, HT-29, DLD-1, NCI-H460, and A549, with no evidence of toxicity. In association with the anti-tumor efficacy, Sorafenib tosylatetreatment potently inhibits MEK 1/2 phosphorylation and pERK 1/2 levels in HT-29 and MDA-MB-231 xenografts but not in Colo-205 xenografts, and significantly suppresses tumor microvessel area (MVA) and microvessel density (MVD) in MDA MB-231, HT-29 and Colo-205 tumor xenografts. [1] Sorafenib tosylate treatment produces dose-dependent growth inhibition of PLC/PRF/5 tumor xenografts in SCID mice with TGIs of 49% and 78% at 10 mg/kg and 30 mg/kg, respectively, consistent with the inhibition of ERK and eIF4E phosphorylation, reduction of the microvessel area, and induction of tumor cell apoptosis. [2]

Protocol (from reference)

Kinase Assay:[1]
  • Biochemical assays:

    Recombinant baculoviruses expressing Raf-1 (residues 305–648) and B-Raf (residues 409–765) are purified as fusion proteins. Full-length human MEK-1 is generated by PCR and purified as a fusion protein from Escherichia coli lysates. Sorafenib tosylate is added to a mixture of Raf-1 (80 ng), or B-Raf (80 ng) with MEK-1 (1 μg) in assay buffer [20 mM Tris (pH 8.2), 100 mM NaCl, 5 mM MgCl2, and 0.15% β-mercaptoethanol] at a final concentration of 1% DMSO. The Raf kinase assay (final volume of 50 μL) is initiated by adding 25 μL of 10 μM γ[33P]ATP (400 Ci/mol) and incubated at 32 °C for 25 minutes. Phosphorylated MEK-1 is harvested by filtration onto a phosphocellulose mat, and 1% phosphoric acid is used to wash away unbound radioactivity. After drying by microwave heating, a β-plate counter is used to quantify filter-bound radioactivity. Human VEGFR2 (KDR) kinase domain is expressed and purified from Sf9 lysates. Time-resolved fluorescence energy transfer assays for VEGFR2 are performed in 96-well opaque plates in the time-resolved fluorescence energy transfer format. Final reaction conditions are as follows: 1 to 10 μM ATP, 25 nM poly GT-biotin, 2 nM Europium-labeled phospho (p)-Tyr antibody (PY20), 10 nM APC, 1 to 7 nM cytoplasmic kinase domain in final concentrations of 1% DMSO, 50 mM HEPES (pH 7.5), 10 mM MgCl2, 0.1 mM EDTA, 0.015% Brij-35, 0.1 mg/mL BSA, and 0.1% β-mercaptoethanol. Reaction volumes are 100 μL and are initiated by addition of enzyme. Plates are read at both 615 and 665 nM on a Perkin-Elmer VictorV Multilabel counter at ~1.5 to 2.0 hours after reaction initiation. Signal is calculated as a ratio: (665 nm/615 nM) × 10,000 for each well. For IC50 generation, Sorafenib tosylate is added before the enzyme initiation. A 50-fold stock plate is made with Sorafenib tosylate serially diluted 1:3 in a 50% DMSO/50% distilled water solution. Final Sorafenib tosylate concentrations range from 10 μM to 4.56 nM in 1% DMSO.
Cell Research:[1]
  • Cell lines: MDA-MB-231, and HAoSMC
  • Concentrations: Dissolved in DMSO, final concentrations ~10 μM
  • Incubation Time: 72 hours
  • Method: Cells are exposed to increasing concentrations of Sorafenib tosylate for 72 hours. Cell number is quantitated using the Cell TiterGlo ATP Luminescent assay kit. This assay measures the number of viable cells per well by measurement of luminescent signal based on amount of cellular ATP.
  • (Only for Reference)
Animal Research:[1]
  • Animal Models: Female NCr-nu/nu mice implanted s.c. with MDA-MB-231, Colo-205, HT-29, H460, or A549 cells
  • Dosages: ~60 mg/kg
  • Administration: Orally once daily
  • (Only for Reference)

Solubility (25°C)

In vitro

 DMSO 127 mg/mL
(199.36 mM)
Water 0.01 mg/mL
(0.01 mM)
Ethanol Insoluble

In vivo

Add solvents to the product individually and in order
(Data is from Selleck tests instead of citations):
2% Cremophor EL, 2% N,N-dimethylacetamide
For best results, use promptly after mixing.

 30 mg/mL (suspension)

* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.

Chemical Information

Molecular Weight 637.03
Formula

C21H16ClF3N4O3.C7H8O3S
CAS No. 475207-59-1
Storage 3 years -20°C powder
2 years -80°C in solvent
Smiles CC1=CC=C(C=C1)S(=O)(=O)O.CNC(=O)C1=NC=CC(=C1)OC2=CC=C(C=C2)NC(=O)NC3=CC(=C(C=C3)Cl)C(F)(F)F

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Molarity Calculator

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Clinical Trial Information

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

(data from https://clinicaltrials.gov, updated on 2021-09-06)

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