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> Sorafenib [284461-73-0]

Sorafenib [284461-73-0]

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Referência HY-10201-1ml

Tamanho : 10mM/1mL

Marca : MedChemExpress

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Sorafénib (Bay 43-9006) est un inhibiteur de Raf qui est puissant et actif par voie orale avec des IC50 de 6 nM et 20 nM pour Raf-1 et B-Raf, respectivement. Sorafénib est un inhibiteur multikinase avec des IC50 de 90 nM, 15 nM, 20 nM, 57 nM et 58 nM pour VEGFR2, VEGFR3, PDGFRβ, FLT3 et c-Kit, respectivement. Sorafénib induit l'autophagie etl'apoptose. Sorafénib a une activité anti-tumorale. Sorafenib est un activateur de la ferroptose.

Sorafenib (Bay 43-9006) ist ein potenter und oral wirksamer Raf-Inhibitor mit IC50s von 6 nM bzw. 20 nM für Raf-1 und B-Raf. Sorafenib ist ein Multikinase-Inhibitor mit IC50s von 90 nM, 15 nM, 20 nM, 57 nM und 58 nM für VEGFR2, VEGFR3, PDGFRβ, FLT3 und c-Kit. Sorafenib induziert autophagy und apoptosis. Sorafenib hat antitumorale Aktivität. Sorafenib ist ein ferroptosis-Aktivator.

Sorafenib (Bay 43-9006) is a potent and orally active Raf inhibitor with IC50s of 6 nM and 20 nM for Raf-1 and B-Raf, respectively. Sorafenib is a multikinase inhibitor with IC50s of 90 nM, 15 nM, 20 nM, 57 nM and 58 nM for VEGFR2, VEGFR3, PDGFRβ, FLT3 and c-Kit, respectively. Sorafenib induces autophagy and apoptosis. Sorafenib has anti-tumor activity. Sorafenib is a ferroptosis activator.

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Sorafenib Chemical Structure

Sorafenib Chemical Structure

CAS No. : 284461-73-0

This product is a controlled substance and not for sale in your territory.

Based on 197 publication(s) in Google Scholar

Other Forms of Sorafenib:

  • Sorafenib Tosylate In-stock
  • Sorafenib-d3 In-stock
  • Sorafenib-13C,d3 In-stock
  • Sorafenib-d4 Obtenir un devis

    Sorafenib purchased from MedChemExpress. Usage Cited in: Discov Oncol. 2023 May 27;14(1):83.  [Abstract]

    Sorafenib (3 µM; 24 h) significantly inhibits the cell proliferation of HepG2 and Hep3B.

    Sorafenib purchased from MedChemExpress. Usage Cited in: Discov Oncol. 2023 May 27;14(1):83.  [Abstract]

    Sorafenib (0.25, 0.5, 1, 2, 4, 6 µM; 24 h) significantly inhibits the cell viability of HepG2 and Hep3B.

    Sorafenib purchased from MedChemExpress. Usage Cited in: Int J Biol Sci. 2018 Apr 25;14(5):577-585.  [Abstract]

    Hep3B, HepG2 and Huh7 cells are treated with 5 μM Sorafenib. The expressing levels of JAK1, JAK2, STAT3, SHP1, SHP2, actin and phosphorylation levels of STAT3 are determined by western blot using the antibodies, respectively.

    Sorafenib purchased from MedChemExpress. Usage Cited in: Oncol Rep. 2018 Sep;40(3):1525-1532.  [Abstract]

    SMMC-7721 and HepG2 cells are treated with 4 µM Sorafenib and 100 µM Berberine alone or in combination (4 µM Sorafenib+100 µM Berberine) for 72 h, and the expression levels of apoptosis-associated proteins are measured by western blot analysis.

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

    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.

    Sorafenib purchased from MedChemExpress. Usage Cited in: Am J Cancer Res. 2017 Dec 1;7(12):2503-2514.  [Abstract]

    VPA potentiates anti-tumor effects of Sorafenib tosylate in vivo. The expression of cleaved caspase9, cleaved caspase3, cleaved PARP from tumor tissue homogenates are analyzed by western blot.

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

    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 MedChemExpress. Usage Cited in: Endocr J. 2017 Nov 29;64(11):1115-1123.  [Abstract]

    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 MedChemExpress. Usage Cited in: Endocr J. 2017 Nov 29;64(11):1115-1123.  [Abstract]

    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 MedChemExpress. Usage Cited in: Oncotarget. 2017 May 2;8(18):29771-29784.  [Abstract]

    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 MedChemExpress. Usage Cited in: Int J Clin Exp Pathol. 2015 Apr 1;8(4):3871-81.  [Abstract]

    The relationship between SOX9 and Raf/MEK/ERK signaling pathway. Co-treatment of si-SOX9-1 and Sorafenib (10uM, 15uM)/SU 11248 (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 MedChemExpress. Usage Cited in: Int J Clin Exp Pathol. 2015 Apr 1;8(4):3871-81.  [Abstract]

    The relationship between SOX9 and Raf/MEK/ERK signaling pathway. Co-treatment of si-SOX9-1 and Sorafenib (10uM, 15uM)/SU 11248 (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).

    Voir tous les produits spécifiques à Isoform Raf:

    Voir toutes les isoformes
    BRaf c-Raf Raf

    Voir tous les produits spécifiques à Isoform VEGFR:

    Voir toutes les isoformes
    VEGFR1/Flt-1 VEGFR2/KDR/Flk-1 VEGFR3/Flt-4
    Description

    Sorafenib (Bay 43-9006) is a potent and orally active Raf inhibitor with IC50s of 6 nM and 20 nM for Raf-1 and B-Raf, respectively. Sorafenib is a multikinase inhibitor with IC50s of 90 nM, 15 nM, 20 nM, 57 nM and 58 nM for VEGFR2, VEGFR3, PDGFRβ, FLT3 and c-Kit, respectively. Sorafenib induces autophagy and apoptosis. Sorafenib has anti-tumor activity. Sorafenib is a ferroptosis activator[1].

    IC50 & Target[1]

    VEGFR3

    20 nM (IC50)

    Braf

    22 nM (IC50)

    Raf-1

    6 nM (IC50)

    VEGFR2

    90 nM (IC50)

    PDGFRβ

    57 nM (IC50)

    BrafV599E

    38 nM (IC50)

    c-Kit

    68 nM (IC50)

    Flt3

    58 nM (IC50)

    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].

    MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

    Sorafenib Related Antibodies
    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].

    MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
    Essai clinique
    Masse moléculaire

    464.83

    Formule

    C21H16ClF3N4O3
    CAS No.

    284461-73-0
    Appearance

    Solid

    Color

    White to off-white

    SMILES

    O=C(NC(C=C1)=CC=C1OC2=CC(C(NC)=O)=NC=C2)NC3=CC=C(Cl)C(C(F)(F)F)=C3
    Livraison

    Room temperature in continental US; may vary elsewhere.
    Stockage
    Powder -20°C 3 years
    4°C 2 years
    In solvent -80°C 1 year
    -20°C 6 months
    Solvant et solubilité
    In Vitro: 

    DMSO : ≥ 45 mg/mL (96.81 mM; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)

    *"≥" means soluble, but saturation unknown.

    Preparing
    Stock Solutions
    Concentration Solvent 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
    View the Complete Stock Solution Preparation Table

    * Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
    Storage method and period of stock solution: -80°C, 1 year; -20°C, 6 months. When stored at -80°C, please use it within 1 year. When stored at -20°C, please use it within 6 months.

    • Calculateur de molarité

    • Calculateur de dilution

    Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)

    Mass
    =
    Concentration
    ×
    Volume
    ×
    Molecular Weight *

    Concentration (start) × Volume (start) = Concentration (final) × Volume (final)

    This equation is commonly abbreviated as: C1V1 = C2V2

    Concentration (start)

    C1

    ×
    Volume (start)

    V1

    =
    Concentration (final)

    C2

    ×
    Volume (final)

    V2

    In Vivo:

    Select the appropriate dissolution method based on your experimental animal and administration route.

    For the following dissolution methods, please ensure to first prepare a clear stock solution using an In Vitro approach and then sequentially add co-solvents:
    To ensure reliable experimental results, the clarified stock solution can be appropriately stored based on storage conditions. As for the working solution for in vivo experiments, it is recommended to prepare freshly and use it on the same day.
    The percentages shown for the solvents indicate their volumetric ratio in the final prepared solution. If precipitation or phase separation occurs during preparation, heat and/or sonication can be used to aid dissolution.

    • Protocol 1

      Add each solvent one by one:  2% DMSO    40% PEG300    5% Tween-80    53% Saline

      Solubility: 4 mg/mL (8.61 mM); Suspended solution; Need ultrasonic

    • Protocol 2

      Add each solvent one by one:  10% DMSO    40% PEG300    5% Tween-80    45% Saline

      Solubility: 2.08 mg/mL (4.47 mM); Suspended solution; Need ultrasonic

      This protocol yields a suspended solution of 2.08 mg/mL. Suspended solution can be used for oral and intraperitoneal injection.

      Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (20.8 mg/mL) to 400 μL PEG300, and mix evenly; then add 50 μL Tween-80 and mix evenly; then add 450 μL Saline to adjust the volume to 1 mL.

      Preparation of Saline: Dissolve 0.9 g sodium chloride in ddH₂O and dilute to 100 mL to obtain a clear Saline solution.
    In Vivo Dissolution Calculator
    Please enter the basic information of animal experiments:

    Dosage

    mg/kg

    Animal weight
    (per animal)

    g

    Dosing volume
    (per animal)

    μL

    Number of animals

    Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.
    Please enter your animal formula composition:
    %
    DMSO +
    % 
    +
    %
    Tween-80 +
    %
    Saline
    Recommended: Keep the proportion of DMSO in working solution below 2% if your animal is weak.
    The co-solvents required include: DMSO, . All of co-solvents are available by MedChemExpress (MCE). , Tween 80. All of co-solvents are available by MedChemExpress (MCE).
    Calculation results:
    Working solution concentration: mg/mL
    Method for preparing stock solution: mg drug dissolved in μL  DMSO (Stock solution concentration: mg/mL).
    The concentration of the stock solution you require exceeds the measured solubility. The following solution is for reference only. If necessary, please contact MedChemExpress (MCE).
    Method for preparing in vivo working solution for animal experiments: Take μL DMSO stock solution, add μL . μL , mix evenly, next add μL Tween 80, mix evenly, then add μL Saline.
     If the continuous dosing period exceeds half a month, please choose this protocol carefully.
    Please ensure that the stock solution in the first step is dissolved to a clear state, and add co-solvents in sequence. You can use ultrasonic heating (ultrasonic cleaner, recommended frequency 20-40 kHz), vortexing, etc. to assist dissolution.
    Pureté et documentation

    Purity: 99.92%

    COA (244 KB) HNMR (242 KB) LCMS (120 KB) Elemental Analysis Report (102 KB)

    Instruction de manipulation (2659 KB)
    Références

    • [1]. Wilhelm SM, et al. BAY 43-9006 exhibits broad spectrum oral antitumor activity and targets the RAF/MEK/ERK pathway and receptor tyrosine kinases involved in tumor progression and angiogenesis. Cancer Res. 2004 Oct 1;64(19):7099-109.  [Content Brief]

      [2]. El-Ashmawy NE, et al. Sorafenib effect on liver neoplastic changes in rats: more than a kinase inhibitor. Clin Exp Med. 2016 Apr 16.  [Content Brief]

      [3]. Jin W, et al. Long non-coding RNA TUC338 is functionally involved in sorafenib-sensitized hepatocarcinoma cells by targeting RASAL1. Oncol Rep. 2017 Jan;37(1):273-280.  [Content Brief]

      [4]. Li M, et al. Activation of an AKT/FOXM1/STMN1 pathway drives resistance to tyrosine kinase inhibitors in lung cancer. Br J Cancer. 2017 Aug 29.  [Content Brief]

    Essai de kinase
    [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 n'a pas confirmé de manière indépendante l'exactitude de ces méthodes. Ils sont pour référence seulement.
    Test cellulaire
    [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 n'a pas confirmé de manière indépendante l'exactitude de ces méthodes. Ils sont pour référence seulement.
    Administration animale
    [1][2]

    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.
    Rats[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 n'a pas confirmé de manière indépendante l'exactitude de ces méthodes. Ils sont pour référence seulement.
    Références

    • [1]. Wilhelm SM, et al. BAY 43-9006 exhibits broad spectrum oral antitumor activity and targets the RAF/MEK/ERK pathway and receptor tyrosine kinases involved in tumor progression and angiogenesis. Cancer Res. 2004 Oct 1;64(19):7099-109.  [Content Brief]

      [2]. El-Ashmawy NE, et al. Sorafenib effect on liver neoplastic changes in rats: more than a kinase inhibitor. Clin Exp Med. 2016 Apr 16.  [Content Brief]

      [3]. Jin W, et al. Long non-coding RNA TUC338 is functionally involved in sorafenib-sensitized hepatocarcinoma cells by targeting RASAL1. Oncol Rep. 2017 Jan;37(1):273-280.  [Content Brief]

      [4]. Li M, et al. Activation of an AKT/FOXM1/STMN1 pathway drives resistance to tyrosine kinase inhibitors in lung cancer. Br J Cancer. 2017 Aug 29.  [Content Brief]

    Complete Stock Solution Preparation Table

    * Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
    Storage method and period of stock solution: -80°C, 1 year; -20°C, 6 months. When stored at -80°C, please use it within 1 year. When stored at -20°C, please use it within 6 months.

    Optional Solvent Concentration Solvent Mass 1 mg 5 mg 10 mg 25 mg
    DMSO 1 mM 2.1513 mL 10.7566 mL 21.5132 mL 53.7831 mL
    5 mM 0.4303 mL 2.1513 mL 4.3026 mL 10.7566 mL
    10 mM 0.2151 mL 1.0757 mL 2.1513 mL 5.3783 mL
    15 mM 0.1434 mL 0.7171 mL 1.4342 mL 3.5855 mL
    20 mM 0.1076 mL 0.5378 mL 1.0757 mL 2.6892 mL
    25 mM 0.0861 mL 0.4303 mL 0.8605 mL 2.1513 mL
    30 mM 0.0717 mL 0.3586 mL 0.7171 mL 1.7928 mL
    40 mM 0.0538 mL 0.2689 mL 0.5378 mL 1.3446 mL
    50 mM 0.0430 mL 0.2151 mL 0.4303 mL 1.0757 mL
    60 mM 0.0359 mL 0.1793 mL 0.3586 mL 0.8964 mL
    80 mM 0.0269 mL 0.1345 mL 0.2689 mL 0.6723 mL
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    Sorafenib Related Classifications

    Help & FAQs

    Keywords:

    Sorafenib284461-73-0Bay 43-9006RafVEGFRFLT3AutophagyApoptosisFerroptosisRaf kinasesVascular endothelial growth factor receptorCluster of differentiation antigen 135CD135Fms like tyrosine kinase 3Inhibitorinhibitorinhibit

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