Catalog No.S1040 Synonyms: Bay 43-9006
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.
Cited by 42 Publications
6 Customer Reviews
Western blot analysis of proteins expression levels in pericytes at 5-hour treatment with DMSO (vehicle), 10 μmol/L vemurafenib (Vemu.), 2.5 μmol/L sorafenib (Sora.), and combined therapy with 10 μmol/L vemurafenib plus 2.5 μmol/L sorafenib. These results were validated by three independent replicate measurements. Cells were grown in 0.2% FBS DMEM growth medium during treatment.
Clin Cancer Res, 2018, 24(23):6078-6097. Sorafenib Tosylate purchased from Selleck.
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.
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|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.|
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.  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. 
|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.  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. |
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.
|In vitro||DMSO||127 mg/mL (199.36 mM)|
|Water||0.01 mg/mL (0.01 mM)|
|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)|
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Clinical Trial Information
|NCT Number||Recruitment||Conditions||Sponsor/Collaborators||Start Date||Phases|
|NCT03211416||Recruiting||Advanced Adult Hepatocellular Carcinoma|Child-Pugh Class A|Stage III Hepatocellular Carcinoma|Stage IIIA Hepatocellular Carcinoma|Stage IIIB Hepatocellular Carcinoma|Stage IIIC Hepatocellular Carcinoma|Stage IV Hepatocellular Carcinoma|Stage IVA Hepatocellular Carcinoma|Stage IVB Hepatocellular Carcinoma||Roswell Park Cancer Institute|National Cancer Institute (NCI)||September 13 2017||Phase 1|Phase 2|
|NCT03236649||Not yet recruiting||Hepatocellular Carcinoma (HCC)||Beijing Shenogen Biomedical Co. Ltd|Chinese Academy of Medical Sciences|NanJing PLA 81 Hospital|Beijing Cancer Hospital|Chinese PLA General Hospital|Beijing Hospital|General Hospital of Chinese Armed Police Forces|Guang''anmen Hospital of China Academy of Chinese Medical Sciences|Jinan Central Hospital|Linyi Tumour Hospital|The First Affiliated Hospital of Anhui Medical University|Anhui Provincial Hospital|The First Affiliated Hospital with Nanjing Medical University|The Affiliated Tumor Hospital of Nantong University Nantong Jiangsu Province China|Nanfang Hospital of Southern Medical University|Foshan First People ''s Hospital|Affiliated Cancer Hospital & Institute of Guangzhou Medical University|Tianjin Medical University Cancer Institute and Hospital|Hebei Medical University Fourth Hospital|Hunan Cancer Hospital|First Hospital of Jilin University|307 Hospital of PLA|Fudan University|Henan Cancer Hospital|Jilin Provincial Tumor Hospital|First Affiliated Hospital of Harbin Medical University|First Affiliated Hospital Bengbu Medical College|The First Affiliated Hospital of Soochow University|Tongji Hospital|Beijing YouAn Hospital||August 30 2017||Phase 3|
|NCT02728050||Recruiting||Acute Biphenotypic Leukemia|Acute Myeloid Leukemia|de Novo Myelodysplastic Syndrome|High Risk Myelodysplastic Syndrome|Myelodysplastic Syndrome|Myeloproliferative Neoplasm||University of Washington|National Cancer Institute (NCI)||December 1 2016||Phase 1|Phase 2|
|NCT02779283||Recruiting||Acute Lymphoblastic Leukemia|Acute Myeloid Leukemia||OHSU Knight Cancer Institute|National Cancer Institute (NCI)||January 13 2016||Phase 1|
|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|
|NCT02035527||Completed||Metastatic Squamous Neck Cancer With Occult Primary Squamous Cell Carcinoma|Recurrent Metastatic Squamous Neck Cancer With Occult Primary|Recurrent Salivary Gland Cancer|Recurrent Squamous Cell Carcinoma of the Hypopharynx|Recurrent Squamous Cell Carcinoma of the Larynx|Recurrent Squamous Cell Carcinoma of the Lip and Oral Cavity|Recurrent Squamous Cell Carcinoma of the Nasopharynx|Recurrent Squamous Cell Carcinoma of the Oropharynx|Recurrent Squamous Cell Carcinoma of the Paranasal Sinus and Nasal Cavity|Recurrent Verrucous Carcinoma of the Larynx|Recurrent Verrucous Carcinoma of the Oral Cavity|Salivary Gland Squamous Cell Carcinoma|Stage IV Squamous Cell Carcinoma of the Hypopharynx|Stage IV Squamous Cell Carcinoma of the Nasopharynx|Stage IVA Salivary Gland Cancer|Stage IVA Squamous Cell Carcinoma of the Larynx|Stage IVA Oral Cavity Squamous Cell Carcinoma|Stage IVA Squamous Cell Carcinoma of the Oropharynx|Stage IVA Squamous Cell Carcinoma of the Paranasal Sinus and Nasal Cavity|Stage IVA Verrucous Carcinoma of the Larynx|Stage IVA Verrucous Carcinoma of the Oral Cavity|Stage IVB Salivary Gland Cancer|Stage IVB Squamous Cell Carcinoma of the Larynx|Stage IVB Squamous Cell Carcinoma of the Lip and Oral Cavity|Stage IVB Squamous Cell Carcinoma of the Oropharynx|Stage IVB Squamous Cell Carcinoma of the Paranasal Sinus and Nasal Cavity|Stage IVB Verrucous Carcinoma of the Larynx|Stage IVB Verrucous Carcinoma of the Oral Cavity|Stage IVC Salivary Gland Cancer|Stage IVC Squamous Cell Carcinoma of the Larynx|Stage IVC Squamous Cell Carcinoma of the Lip and Oral Cavity|Stage IVC Squamous Cell Carcinoma of the Oropharynx|Stage IVC Squamous Cell Carcinoma of the Paranasal Sinus and Nasal Cavity|Stage IVC Verrucous Carcinoma of the Larynx|Stage IVC Verrucous Carcinoma of the Oral Cavity|Tongue Cancer|Untreated Metastatic Squamous Neck Cancer With Occult Primary||Ohio State University Comprehensive Cancer Center|National Comprehensive Cancer Network||April 14 2014||Phase 1|
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