1. MAPK/ERK Pathway
    Protein Tyrosine Kinase/RTK
    Autophagy
  2. Raf
    VEGFR
    PDGFR
    FLT3
    c-Kit
    Autophagy

Sorafenib (Synonyms: Bay 43-9006)

Cat. No.: HY-10201 Purity: 99.83%
Data Sheet SDS Handling Instructions

Sorafenib is a potent multikinase inhibitor with IC50s of 6 nM, 20 nM, and 22 nM for Raf-1, B-Raf, and VEGFR-3, respectively.

For research use only. We do not sell to patients.
Sorafenib Chemical Structure

Sorafenib Chemical Structure

CAS No. : 284461-73-0

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Customer Review

Other Forms of Sorafenib:

    Sorafenib purchased from MCE. Usage Cited in: Int J Clin Exp Pathol. 2015 Apr 1;8(4):3871-81.

    The relationship between SOX9 and Raf/MEK/ERK signaling pathway. Co-treatment of si-SOX9-1 and Sorafenib (10uM, 15uM)/Sunitinib (2 uM, 3 uM) significantly decreases expression of MEK1 and its phosphorylated protein (p-MEK1/2, p-ERK1/2) as assayed by Western blot (with GAPDH as internal control).

    Sorafenib purchased from MCE. Usage Cited in: Int J Clin Exp Pathol. 2015 Apr 1;8(4):3871-81.

    The relationship between SOX9 and Raf/MEK/ERK signaling pathway. Co-treatment of si-SOX9-1 and Sorafenib (10uM, 15uM)/Sunitinib (2 uM, 3 uM) significantly decreases expression of MEK1 and its phosphorylated protein (p-MEK1/2, p-ERK1/2) as assayed by RT-PCR (with β-actin as internal control).

    Sorafenib purchased from MCE. Usage Cited in: Oncotarget. 2017 May 2;8(18):29771-29784.

    Sorafenib inhibits Pin1 biosynthesis and accumulation in Huh7 and HepG2 cells. Cells are treated with 5 or 10 μM Sorafenib for indicated times. Pin1 protein expression is determined by Western Blot.

    Sorafenib purchased from MCE. Usage Cited in: J Pharmacol Exp Ther. 2017 Aug;362(2):219-229.

    The combination of sorafenib and CAI induces apoptosis in NSCLC. Effect of 10 μM CAI and/or 5 μM Sorafenib on the expression of cleaved PARP and cleaved caspase-. Protein levels of cleaved PARP and cleaved caspase-3 from treated cell lysates are normalized against GAPDH levels.

    Sorafenib purchased from MCE. Usage Cited in: Endocr J. 2017 Aug 31.

    Effect of Sorafenib on phosphorylation of ERK and AKT. Thyroid cancer cells are treated for 30 minutes with 10 μM Sorafenib, 10 μM Forskolin, and combination therapy of 10 μM Sorafenib with 10 μM Forskolin. The levels of ERK and AKT phosphorylation are examined by immunoblot analysis. β-actin is used as the control. Sorafenib suppresses phosphorylation of ERK, but not of AKT.

    Sorafenib purchased from MCE. Usage Cited in: Endocr J. 2017 Aug 31.

    Effect of Sorafenib and Forskolin on expression of CDK4 and CDK regulatory proteins. Thyroid cancer cells are treated for 24 hours with 10 μM Sorafenib, 10 μM Forskolin, and combination therapy of 10 μM Sorafenib with 10 μM Forskolin. The expression of cyclin D1, CDK4, and phosphorylation of RB are examined by immunoblot analysis. β-actin is used as the control. The combination therapy suppresses expression of cyclin D1, and Forskolin monotherapy suppresses expression of cyclin D1 in TPC-1 and W

    Sorafenib purchased from MCE. Usage Cited in: Br J Cancer. 2017 Sep 26;117(7):974-983.

    The effect of the AKT inhibitor MK2206 (10 μM) on the expression levels of phosphor-AKT, AKT, and STMN1 in TKI-pretreated NCI-H460 cells. β-actin is used as a loading control.
    • Biological Activity

    • Protocol

    • Technical Information

    • Purity & Documentation

    • References

    Description

    Sorafenib is a potent multikinase inhibitor with IC50s of 6 nM, 20 nM, and 22 nM for Raf-1, B-Raf, and VEGFR-3, respectively.

    IC50 & Target

    IC50: 6 nM (Raf-1), 20 nM (VEGFR-3), 22 nM (BRAF), 57 nM (PDGFR-β), 58 nM (Flt3), 68 nM (c-KIT), 90 nM (VEGFR-2)[1]

    In Vitro

    Sorafenib (BAY 43-9006) also inhibits BRAFwt (IC50=22 nM), BRAFV599E (IC50=38 nM), VEGFR-2 (IC50=90 nM), VEGFR-3 (IC50=20 nM), PDGFR-β (IC50=57 nM), c-KIT (IC50=68 nM), and Flt3 (IC50=58 nM) in biochemical assays. In MDA-MB-231 breast cancer cells, Sorafenib completely blocks activation of the MAPK pathway. Cells are preincubated with Sorafenib (0.01 to 3 μM), and dose-dependent inhibition of basal MEK 1/2 and ERK 1/2 phosphorylation (IC50, 40 and 100 nM, respectively)[1].

    In Vivo

    Sorafenib demonstrates broad oral antitumor efficacy in panel of human tumor xenograft models. Sorafenib is given orally at 7.5 to 60 mg/kg. There is no lethality and no increase in weight loss in any treated group relative to the corresponding control group. Daily oral administration of Sorafenib (30 to 60 mg/kg) produces complete tumor stasis during treatment in five of the six models[1]. The survival rate is 73.3 % in Diethyl nitrosamine (DENA) group and 83.3 % in Sorafenib group compared to 100 % in the normal control group. DENA group shows a significant increase in liver index (1.51-fold increase, p<0.05) compared to normal control group, while treatment with Sorafenib shows significant decrease (p<0.05) in liver index when compared to DENA group. The liver index in Sorafenib group significantly decreases to lower than its value in the normal control[2].

    Clinical Trial
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    References
    Preparing Stock Solutions
    Concentration Volume Mass 1 mg 5 mg 10 mg
    1 mM 2.1513 mL 10.7566 mL 21.5132 mL
    5 mM 0.4303 mL 2.1513 mL 4.3026 mL
    10 mM 0.2151 mL 1.0757 mL 2.1513 mL
    Please refer to the solubility information to select the appropriate solvent.
    Kinase Assay
    [1]

    To test compound inhibition against various RAF kinase isoforms, Sorafenib is added to a mixture of Raf-1 (80 ng), wt BRAF, or V599E BRAF (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[1]. MCE has not independently confirmed the accuracy of these methods. They are for reference only.

    Cell Assay
    [1]

    Sorafenib is dissolved in DMSO and stored, and then diluted with appropriate media before use[1].

    The MDA-MB-231 human mammary adenocarcinoma cell lines are plated at 2×105 cells per well in 12-well tissue culture plates in DMEM growth media (10% heat-inactivated FCS) overnight. Cells are washed once with serum-free media and incubated in DMEM supplemented with 0.1% fatty acid-free BSA containing various concentrations of BAY 43-9006 (0.01, 0.03 , 0.1, 0.3, 1, 3 μM) in 0.1% DMSO for 120 minutes to measure changes in basal pMEK 1/2, pERK 1/2, or pPKB. Cells are washed with cold PBS (PBS containing 0.1 mM vanadate) and lysed in a 1% (v/v) Triton X-100 solution containing protease inhibitors. Lysates are clarified by centrifugation, subjected to SDS-PAGE, transferred to nitrocellulose membranes, blocked in TBS-BSA, and probed with 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), or anti-PKB primary antibodies. Blots are developed with horseradish peroxidase (HRP)-conjugated secondary antibodies and developed with Amersham ECL reagent on Amersham Hyperfilm[1]. MCE has not independently confirmed the accuracy of these methods. They are for reference only.

    Animal Administration
    [1][2]

    Sorafenib is dissolved in Cremophor EL/ethanol (50:50; Cremophor EL, 95% ethyl alcohol) at 4-fold (4×) of the highest dose, foil wrapped, and stored at room temperature (Mice)[1].

    Mice[1]
    Female NCr-nu/nu mice are used. Mice bearing 75 to 150 mg tumors are treated orally with Sorafenib (7.5 to 60 mg/kg), administered daily for 9 days. In each model, Sorafenib produces dose-dependent tumor growth inhibition with no evidence of toxicity, as measured by increased weight loss relative to control animals or drug-related lethality. In parallel to the antitumor efficacy studies, additional groups of four mice bearing 100 to 200 mg tumors are treated orally with vehicle or Sorafenib (30 to 60 mg/kg), administered daily for 5 days, which is the shortest treatment duration producing complete tumor stasis in the treated groups.
    Rat[2]
    In the study, 100- to 120-g male albino rats are utilized. After acclimatization period, rats are weighed and randomly divided into three groups: Group 1 (normal control group; n=10) is given the vehicle daily for 8 weeks. Group 2 (DENA group; n=15) receive i.p. single dose of 200 mg/kg DENA. Group 3 (Sorafenib group; n=12) is given Sorafenib orally at a dose of 10 mg/kg daily for 2 weeks, 6 weeks after DENA i.p. injection. At the end of the experiment (8 weeks), rats are weighed, anesthetized by ether, and killed, and their livers are dissected. Fresh liver is washed twice with ice-cold saline, dried on clean paper towel, and weighed. Liver index is calculated as liver weight (g)/final body weight (g)×100. The liver is divided into five portions: one portion is preserved in 10 % formalin for histopathological examination and the other portions are immediately frozen in liquid nitrogen and stored at −80°C. MCE has not independently confirmed the accuracy of these methods. They are for reference only.

    References
    Molecular Weight

    464.83

    Formula

    C₂₁H₁₆ClF₃N₄O₃

    CAS No.

    284461-73-0

    Storage
    Powder -20°C 3 years
      4°C 2 years
    In solvent -80°C 6 months
      -20°C 1 month
    Shipping

    Room temperature in continental US; may vary elsewhere

    Solvent & Solubility

    DMSO: ≥ 45 mg/mL

    Sorafenib is dissolved in DMSO and then diluted with saline (the final DMSO concentration is <0.1%)[3].
    Sorafenib is prepared in vehicle (saline)[4].

    * "<1 mg/mL" means slightly soluble or insoluble. "≥" means soluble, but saturation unknown.

    References

    Purity: 99.83%

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    Product Name:
    Sorafenib
    Cat. No.:
    HY-10201
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