1. MAPK/ERK Pathway
    Protein Tyrosine Kinase/RTK
    Autophagy
    Apoptosis
  2. Raf
    VEGFR
    FLT3
    Autophagy
    Apoptosis
    Ferroptosis
  3. Sorafenib

Sorafenib (Synonyms: Bay 43-9006)

製品番号: HY-10201 純度: 99.92%
取扱説明書

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 構造式

Sorafenib 構造式

CAS 番号 : 284461-73-0

容量 価格(税別) 在庫状況 数量
無料サンプル (0.5-1 mg)   今すぐ申し込む  
Solution
10 mM * 1 mL in DMSO USD 66 在庫あり
Estimated Time of Arrival: December 31
Solid + Solvent
10 mM * 1 mL
ready for reconstitution
USD 66 在庫あり
Estimated Time of Arrival: December 31
Solid
100 mg USD 60 在庫あり
Estimated Time of Arrival: December 31
500 mg USD 78 在庫あり
Estimated Time of Arrival: December 31
1 g   お問い合わせ  
5 g   お問い合わせ  

* アイテムを追加する前、数量をご選択ください

カスタマーレビュー

Based on 96 publication(s) in Google Scholar

Other Forms of Sorafenib:

Top Publications Citing Use of Products

顧客検証

    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.

    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)/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).

    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)/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 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 Nov 29;64(11):1115-1123.

    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 Nov 29;64(11):1115-1123.

    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: Int J Biol Sci. 2018 Apr 25;14(5):577-585.

    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 MCE. Usage Cited in: Oncol Rep. 2018 Sep;40(3):1525-1532.

    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 MCE. Usage Cited in: Am J Cancer Res. 2017 Dec 1;7(12):2503-2514.

    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.

    Raf アイソフォーム固有の製品をすべて表示:

    • 生物活性

    • プロトコル

    • 純度とドキュメンテーション

    • 参考文献

    • カスタマーレビュー

    製品説明

    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)

    体外実験

    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].

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

    体内実験

    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].

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

    臨床実験
    分子量

    464.83

    分子式

    C₂₁H₁₆ClF₃N₄O₃

    CAS 番号
    輸送条件

    Room temperature in continental US; may vary elsewhere.

    保管条件
    Powder -20°C 3 years
      4°C 2 years
    In solvent -80°C 6 months
      -20°C 1 month
    溶剤 & 溶解度
    体外: 

    DMSO : ≥ 45 mg/mL (96.81 mM)

    *"≥" 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
    10 mM 0.2151 mL 1.0757 mL 2.1513 mL
    *Please refer to the solubility information to select the appropriate solvent.
    体内:
    • 1.

      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

    • 2.

      Add each solvent one by one:  10% DMSO    90% (20% SBE-β-CD in saline)

      Solubility: ≥ 2.08 mg/mL (4.47 mM); Clear solution

    • 3.

      Add each solvent one by one:  10% DMSO    90% corn oil

      Solubility: ≥ 2.08 mg/mL (4.47 mM); Clear solution

    *All of the co-solvents are provided by MCE.
    参考文献
    キナーゼ実験
    [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 はこれらの方法の精度を確認していません。 こちらは参照専用です。

    細胞実験
    [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 はこれらの方法の精度を確認していません。 こちらは参照専用です。

    動物実験
    [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 はこれらの方法の精度を確認していません。 こちらは参照専用です。

    参考文献

    純度: 99.92%

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    製品名:
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    製品番号:
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