Sorafenib Tosylate

Catalog No.S1040 Synonyms: Bay 43-9006

Sorafenib Tosylate Chemical Structure

Molecular Weight(MW): 637.03

Sorafenib Tosylate is a multikinase inhibitor of Raf-1, B-Raf and VEGFR-2 with IC50 of 6 nM, 22 nM and 90 nM in cell-free assays, respectively.

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In DMSO USD 352 In stock
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Cited by 41 Publications

5 Customer Reviews

  • Inhibition of the MAPK signaling pathway results in downregulation of Plk-1 protein expression. (a) WB analysis for Plk-1 protein after treatment of human melanoma cell lines M14 and WM-115 with MEK 1/2 inhibitor PD98059 (10 μM), JNK inhibitor (16 μM), p38 inhibitor SB203580 (20 μM), and multikinase inhibitor sorafenib (10 μM) for 48 h showing significant reduction in the expression of Plk-1 protein after 48 hours. (b) Annexin V/PI staining of cells treated with MAPK inhibitors and induction of apoptosis. JNK, c-Jun N-terminal kinase; MAPK, mitogen-activated protein kinase; MEK 1/2, mitogen-activated protein kinase kinase 1/2; Plk-1, polo-like kinase 1; WB, western blot.

    J Invest Dermatol 2011 131, 1886–1895. Sorafenib Tosylate purchased from Selleck.

    A549 and H1975 NSCLC cells were treated for 2 h–12 h as indicated with vehicle control or with pemetrexed (1.0 μM), sildenafil (2.0 μM), sorafenib (2.0 μM), alone or in combination as indicated. Cells were fixed in place and immuno-fluorescence staining performed to determine the phosphorylation and expression of the indicated proteins.

    Oncotarget, 2017, 8(8):13464-13475. Sorafenib Tosylate purchased from Selleck.

  • Autophagic activation in sunitinib- and sorafenib- but not AZD6244-treated cells. Medullary thyroid cancer-1.1 (MTC-1.1; A) and TT ( B) cells were treated with dimethyl sulfoxide (DMSO), sunitinib (50 nM), sorafenib (10 nM), AZD6244 (30 nM), or everolimus (20 nM) for 48 hours. Cell lysates were prepared, and light chain 3 (LC3)-I and -II cleaved caspase-3 protein levels were monitored by Western blotting. Reprobing against actin was per formed to ensure equal protein loading. ( C ) MTC-1.1 and TT cells were transiently transfected with autophagy protein 5 (Atg-5) small inter fering RNA. Transfection with scrambled small inter fering RNA was used as a control. After transfection, cells with and without Atg-5 knockdown were exposed to DMSO or 20 nM of everolimus for 48 hours. Cell lysates were pre- pared and LC3-I and -II protein expression levels were monitored by Western blotting. Reprobing against Atg-5 was per formed to monitor Atg-5 knockdown efficiency. Reprobing against actin was per formed to ensure equal protein.

    Surgery 2012 152(6), 1142-9. Sorafenib Tosylate purchased from Selleck.

    Autophagy inhibition blocks the antiproliferative effects of sunitinib and sorafenib but not AZD6244. Medullary thyroid cancer–1.1 (MTC-1.1) and TT cells were transfected transiently with scrambled or autophagy protein 5 (Atg-5) small inter fering RNA. After transfection, cells with and without Atg-5 knockdown were exposed to sunitinib (50 nM), sorafenib (10 nM), and AZD6244 (30 nM) for 48 hours. Treated cells were subjected to a 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium proliferation assay. Similar experiments were repeated 3 times. Histograms represent the relative percent of OD490 nM absorbance. The asterisk indicates significance versus scrambled small inter fering RNA–treated control ( P < .05). All data are relative multiples of expression compared to untreated cells. The data are representative of 3 experiments and are expressed as the mean ± the standard error.

    Surgery 2012 152(6), 1142-9. Sorafenib Tosylate purchased from Selleck.


    Inhibition of breast cancer cell growth using sorafenib. MCF-7 breast cancer cells were treated with increasing concentrations of sorafenib for 5 days. Cell number was measured  using a colorimetric growth assay (crystal violet stain) and expressed relative to DMSO treated control cells.

    2013 Christina W Yde/CDM Danish Cancer Society Research Center Denmark. Sorafenib Tosylate purchased from Selleck.

Purity & Quality Control

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Biological Activity

Description Sorafenib Tosylate is a multikinase inhibitor of Raf-1, B-Raf and VEGFR-2 with IC50 of 6 nM, 22 nM and 90 nM in cell-free assays, respectively.
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
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 NX;IR2dlT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MoLDOFghcA>? NGPHeY5IUTVyPUKg{txO M2HaNFIzPTZyNkK3
MCF7 NX;FbWhGT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NFTuS3c1QCCq NYTsbFhYT0l3ME2yMlUh|ryP NEXN[4czOjV4ME[yOy=>
EKVX NV3PRod[T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NFfkSlI1QCCq NXXtNG1{T0l3ME2yMlUh|ryP MlHGNlI2PjB4Mke=
HT-29 NFTNXopIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M3XGSlQ5KGh? NVP3WJR{T0l3ME2yMlUh|ryP MVSyNlU3ODZ{Nx?=
SNB19 NUflTlNKT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NX3VN3VkPDhiaB?= MnrJS2k2OD1|LkKg{txO MofaNlI2PjB4Mke=
OVCAR3 NE\nOmhIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MVW0PEBp NWTkZnppT0l3ME2zMlIh|ryP NWDDR4I3OjJ3NkC2Nlc>
CAKI-1 MorBS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NGfDW2Q1QCCq MUnHTVUxRTNwMjFOwG0> Mo\CNlI2PjB4Mke=
SW620 NFXBWpdIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MmLsOFghcA>? NEP2NIhIUTVyPUOuNkDPxE1? MnHYNlI2PjB4Mke=
TK10 NYC2e2Y3T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MlLWOFghcA>? NETGeopIUTVyPUWg{txO MUCyNlU3ODZ{Nx?=

... Click to View More Cell Line Experimental Data

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]


Kinase Assay:[1]
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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]
+ Expand
  • 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]
+ Expand
  • Animal Models: Female NCr-nu/nu mice implanted s.c. with MDA-MB-231, Colo-205, HT-29, H460, or A549 cells
  • Formulation: Dissolved in Cremophor EL/ethanol (50:50) as 4-fold (4 × stock solution, and diluted to 1 × with w
  • 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


CAS No. 475207-59-1
Storage powder
in solvent
Synonyms Bay 43-9006

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Clinical Trial Information

NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT02143401 Recruiting Cirrhosis|Hepatitis B Infection|Hepatitis C Infection|Metastatic Malignant Solid Neoplasm|Recurrent Hepatocellular Carcinoma|Recurrent Malignant Solid Neoplasm|Refractory Malignant Neoplasm|Stage IV Hepatocellular Carcinoma AJCC v7|Unresectable Solid Neoplasm National Cancer Institute (NCI) November 7 2014 Phase 1
NCT01666756 Active not recruiting Adult Primary Hepatocellular Carcinoma|Advanced Adult Primary Liver Cancer|Advanced Adult Hepatocellular Carcinoma|BCLC Stage B Adult Hepatocellular Carcinoma|BCLC Stage C Adult Hepatocellular Carcinoma City of Hope Medical Center|National Cancer Institute (NCI) May 6 2013 Phase 1
NCT01531361 Active not recruiting Advanced Malignant Neoplasm|BRAF Gene Mutation|Metastatic Malignant Neoplasm|Recurrent Malignant Neoplasm|Refractory Malignant Neoplasm M.D. Anderson Cancer Center|National Cancer Institute (NCI) February 6 2012 Phase 1
NCT02050919 Active not recruiting Pleomorphic Rhabdomyosarcoma|Stage IIB Adult Soft Tissue Sarcoma AJCC v7|Stage III Adult Soft Tissue Sarcoma AJCC v7|Stage IV Adult Soft Tissue Sarcoma AJCC v7 OHSU Knight Cancer Institute|Bayer|National Cancer Institute (NCI) December 3 2013 Phase 2
NCT01861314 Active not recruiting Acute Myeloid Leukemia|Recurrent Adult Acute Myeloid Leukemia|Secondary Acute Myeloid Leukemia|Therapy-Related Acute Myeloid Leukemia|Untreated Adult Acute Myeloid Leukemia National Cancer Institute (NCI) July 3 2013 Phase 1
NCT01004978 Active not recruiting Hepatocellular Carcinoma|Unresectable Hepatocellular Carcinoma National Cancer Institute (NCI) October 28 2009 Phase 3

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID