Sorafenib Tosylate 化学構造
分子量: 637.03




Quality Control & MSDS


  • Compare Raf Inhibitors
  • 研究分野



製品説明 Sorafenib Tosylateは、Raf-1、B-RafとVEGFR-2のマルチキナーゼ阻害剤で、IC50 がそれぞれ 6 nM、 22 nM、90 nMです。
ターゲット Raf-1 B-Raf VEGFR2 PDGFRβ
IC50 6 nM 22 nM 90 nM 57 nM [1]
In vitro試験 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 LinesAssay TypeConcentrationIncubation TimeFormulationActivity DescriptionPMID
MDA-MB-435 M3;N[Wdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M{jRXFQ5KGh? MYfHTVUxRTJizszN NGi0fYEzOjV4ME[yOy=>
UACC257 NUXyNIo3T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MVG0PEBp MljYS2k2OD1{IN88US=> M4W3[VIzPTZyNkK3
MCF7 Mn7vS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M1LGVFQ5KGh? M36wd2dKPTB;Mj61JO69VQ>? M{fr[VIzPTZyNkK3
EKVX NGnJOFBIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MUm0PEBp M3n4PGdKPTB;Mj61JO69VQ>? M3KwUVIzPTZyNkK3
HT-29 NF;5coxIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MWG0PEBp NIr2Z4JIUTVyPUKuOUDPxE1? MlvLNlI2PjB4Mke=
SNB19 MUnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MWK0PEBp Mm\MS2k2OD1|LkKg{txO NI\meYkzOjV4ME[yOy=>
OVCAR3 M4OyXmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MnjSOFghcA>? MYnHTVUxRTNwMjFOwG0> MXuyNlU3ODZ{Nx?=
CAKI-1 MX;Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MVW0PEBp NEL3W3BIUTVyPUOuNkDPxE1? MnnZNlI2PjB4Mke=
SW620 NUmyVXRqT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NEewNJM1QCCq MXLHTVUxRTNwMjFOwG0> Mk\1NlI2PjB4Mke=
TK10 NX3aXGlnT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NUjpOJZmPDhiaB?= NHLRd3RIUTVyPUWg{txO NELTUo4zOjV4ME[yOy=>

... Click to View More Cell Line Experimental Data

In vivo試験 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]
臨床試験 Sorafenib sensitizes bax-/- cells to TRAIL in a dose-dependent manner, through a mechanism involving down-regulating NF-κB mediated Mcl-1 and cIAP2 expression. Combining Sorafenib (30-60 mg/kg) with TRAIL (5 mg/kg) show dramatic efficacy in TRA

プロトコル (参考用のみ)

キナーゼアッセイ: [1]

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.

細胞アッセイ: [1]

細胞株 MDA-MB-231, and HAoSMC
濃度 Dissolved in DMSO, final concentrations ~10 μM
反応時間 72 hours
実験の流れ 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.

動物実験: [1]

動物モデル Female NCr-nu/nu mice implanted s.c. with MDA-MB-231, Colo-205, HT-29, H460, or A549 cells
製剤 Dissolved in Cremophor EL/ethanol (50:50) as 4-fold (4 × stock solution, and diluted to 1 × with w
投薬量 ~60 mg/kg
投与方法 Orally once daily

Conversion of different model animals based on BSA (Value based on data from FDA Draft Guidelines)

SpeciesMouseRatRabbitGuinea pigHamsterDogMonkeyBaboon
Weight (kg)
Body Surface Area (m2)0.0070.0250.
Km factor361285201220
Animal A (mg/kg) = Animal B (mg/kg) multiplied by  Animal B Km
Animal A Km

For example, to modify the dose of resveratrol used for a mouse (22.4 mg/kg) to a dose based on the BSA for a rat, multiply 22.4 mg/kg by the Km factor for a mouse and then divide by the Km factor for a rat. This calculation results in a rat equivalent dose for resveratrol of 11.2 mg/kg.

Rat dose (mg/kg) = mouse dose (22.4 mg/kg) ×  mouse Km(3)  = 11.2 mg/kg
rat Km(6)



Download Sorafenib Tosylate SDF
分子量 637.03


CAS No. 475207-59-1
保管 2年-20℃
6月-80℃in solvent
別名 Bay 43-9006
溶解度 (25°C) * In vitro DMSO 127 mg/mL (199.36 mM)
0.01 mg/mL (0.01 mM)
エタノール <1 mg/mL (<1 mM)
In vivo 2% Cremophor EL, 2% N,N-dimethylacetamide 30 mg/mL
* <1 mg/ml means slightly soluble or insoluble.
* 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.
化学名 2-Pyridinecarboxamide, 4-[4-[[[[4-chloro-3-(trifluoromethyl)phenyl]amino]carbonyl]amino]phenoxy]-N-methyl-, 4-methylbenzenesulfonate (1:1)

カスタマーフィードバック (4)

Click to enlarge
Source J Invest Dermatol , 2011, 131, 1886–1895. Sorafenib Tosylate purchased from Selleck
Method Western blot
Cell Lines human melanoma cell lines M14 and WM-115
Concentrations 10 µM
Incubation Time 48 h
Results To see whether inhibition of this pathway has an impact on the expression of Plk-1 in human melanoma, we used specific inhibitors of mitogen-activated protein kinase kinase (MEK) 1/2 (PD98059), multikinase inhibitor (sorafenib), c-Jun N-terminal kinase (JNK) (JNK inhibitor II), and the p38 MAPK (SB203580). Treatment of human melanoma cell lines WM-115 and M14 with these inhibitors was accompanied with significant reduction of Plk-1 protein levels (Figure a). This phenomenon was accompanied by induction of apoptosis(Figure b).

Click to enlarge
Source Surgery, 2012, 152(6), 1142-9. Sorafenib Tosylate purchased from Selleck
Method Western blot
Cell Lines MTC-1.1/TT cells
Concentrations 10 nM
Incubation Time 48 h
Results Sunitinb and sorafenib treatment at the IC50 increased LC3-II protein levels in both MTC-1 .1 and TT cells (Fig A and B). The siRNA-mediated knock-down of Atg- 5, a key molecule for autophagosome formation, abrogated the induction of LC3-II after sunitinib and sorafenib exposure ( Fig C ). These results indicated that both sunitinib and sorafenib promote autophagic activation in MTC cells. Sunitinib and sorafenib exposure also increased the expression level of cleaved caspase-3, a marker of apoptosis, indicating that these TKIs also activate apoptosis.

Click to enlarge
Source Surgery, 2012, 152(6), 1142-9. Sorafenib Tosylate purchased from Selleck
Method MTS cell proliferation assay
Cell Lines MTC-1.1/TT cells
Concentrations 10 nM
Incubation Time 48 h
Results Atg-5 siRNA treatment decreased the antiproliferative effects of sunitinib and sorafenib by 44% ( P < .05) and 41% ( P < .05 ), respectively, in MTC-1 .1 cells and by 43% ( P < .01) and 39% ( P < .05 ), respectively, in TT cells.

Click to enlarge
Source 2013, Christina W Yde/CDM Danish Cancer Society Research Center Denmark. Sorafenib Tosylate purchased from Selleck
Method Cell growth assay
Cell Lines MCF-7 breast cancer cells
Concentrations 0-1 μM
Incubation Time 5 d
Results Sorafenib potently inhibited the survival of MCF7 cells in a dose-dependent manner.

文献中の引用 (38)



電話番号: +1-832-582-8158 Ext:3月曜日〜金曜日 9:00 AM–5:00 PM (米国中部標準時)


* 必須

Related Raf 阻害剤

  • LY3009120

    LY03009120 is a potent pan-Raf inhibitor with IC50 of 44 nM, 31-47 nM, and 42 nM for A-raf, B-Raf, and C-Raf in A375 cells, respectively. Phase 1.

  • GDC-0994

    GDC-0994 is a potent, orally available ERK1/2 inhibitor. Phase 1.

  • Ulixertinib (BVD-523, VRT752271)

    Ulixertinib (BVD-523, VRT752271) is a potent and reversible ERK1/ERK2 inhibitor with IC50 of <0.3 nM for ERK2. Phase 1.

  • Cobimetinib (GDC-0973, RG7420)

    Cobimetinib (GDC-0973, RG7420) is a potent and highly selective MEK1 inhibitor with IC50 of 4.2 nM. Phase 3.

  • Vemurafenib (PLX4032, RG7204)

    Vemurafenib (PLX4032, RG7204)新しくて強力な阻害剤で、 B-RAFV600Eに作用すると、IC50 が 31 nMになる。

    Features:A novel and potent inhibitor of the B-RAFV600E oncoprotein.

  • Dabrafenib (GSK2118436)

    Dabrafenib(GSK2118436)は、B-Rafの強力なATP競争的阻害剤で、 B-Raf、 B-RafV600E 、c-Rafに作用する時、 IC50 がそれぞれ 3.2 nM、 0.8 nM 、 5.0 nMです。

  • Sorafenib

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

  • PLX-4720

    PLX-4720は、B-Raf(V600E)とc-Raf-1(Y340D/Y341D)の「実行中の」形の強力で選択的な阻害剤で、IC50 がそれぞれ 13 nM と 6.7 nMです。

  • TAK-632

    TAK-632 is a potent pan-Raf inhibitor with IC50 of 8.3 nM and 1.4 nM for B-Raf(wt) and C-Raf, respectively, showing less or no inhibition against other tested kinases.


Tags: Sorafenib Tosylateを買う | Sorafenib Tosylate供給者 | Sorafenib Tosylateを購入する | Sorafenib Tosylate費用 | Sorafenib Tosylate生産者 | オーダーSorafenib Tosylate | Sorafenib Tosylate代理店
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID