Sorafenib

Catalog No.S7397 Synonyms: BAY 43-9006

Sorafenib Chemical Structure

Molecular Weight(MW): 464.82

Sorafenib 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.

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Cited by 71 Publications

10 Customer Reviews

  • Western blotting of Mcl-1 in HCT116 cells treated with indicated agents for 24 hours. ABT-263, 5 μmol/L; ABT-737, 5 μmol/L; SAHA, 4 μmol/L; MS-275, 5 μmol/L; regorafenib, 40 μmol/L; sorafenib, 20 μmol/L; UCN-01, 1 μmol/L; sunitinib, 15 μmol/L.

    Cancer Res, 2018, 78(16):4704-4715. Sorafenib purchased from Selleck.

    Sorafenib in combination with metformin or the AMPK activator salicylate enhances AMPK activation. a, b, AMPK activation with the combination of sorafenib and metformin in LKB1 mutant KRAS mutant (A549 and H460) NSCLC cells (a), LKB1 wild-type KRAS mutant (H358) (b, left panel) or LKB1 mutant KRAS wild-type (H838) NSCLC cells (b, right panel). Cells were treated for 48 hr with sorafenib (1-3 uM), metformin (1–1.5 mM) or the combination of sorafenib and metformin with the same concentrations as were used for the individual treatments. c, AMPK activation with the combination of sorafenib and salicylate in LKB1 mutant KRAS mutant (A549 and H460) or LKB1 mutant KRAS wild-type (H838) NSCLC cells. Cells were treated for 48 hr with sorafenib (1–3 uM), salicylate (1–1.5 mM) or the combination of sorafenib and salicylate with the same concentrations as were used for the individual treatments. Cell lysates were harvested for western blot analysis and probed with the indicated antibodies.

    Int J Cancer 2012 10.1002/ijc.29113.. Sorafenib 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 purchased from Selleck.

    (A) were exposed to 200 uM gentamicin for various time periods. Immunoreactivity for phosphorylated JNK (green) and c-Jun (blue) in hair cells increased in a time-dependent manner. B. Hair cells from explants pre-treated with 500 nM sorafenib displayed a near complete inhibition of JNK activation at all time points analyzed.

    J Neurosci 2013 33(7), 3079-93. Sorafenib purchased from Selleck.

  • Involvement of EV linc-VLDLR in tumor cell responses to chemotherapy. Cells were incubated with sorafenib, camptothecin, or doxorubicin. EVs were obtained after 24 hours, and qRT-PCR was performed for linc-VLDLR. The bars represent the mean ?SEM of the increase in cell viability from 3 independent studies. *, P < 0.05.

    Mol Cancer Res 2014 12(10), 1377-87. Sorafenib purchased from Selleck.

    HCC cell-derived exosomes reverse sorafenib-induced apoptosis in hepatoma carcinoma cells in vivo. a Tumors from mice treated with PBS (Control), sorafenib (Sora), sorafenib + LO2-exosomes (Sora + LO2 exo), sorafenib + MHCC-97 L-exosomes (Sora + 97 L exo), and sorafenib + MHCC-97H-exosomes (Sora + 97H exo) were paraffin-embedded and sectioned, followed by staining of apoptotic cell by using TUNEL assays.

    J Exp Clin Cancer Res, 2016, 35(1):159. Sorafenib purchased from Selleck.

  • Sorafenib and PX-866 interact to suppress tumor growth in vivo. Mice were PO administered vehicle diluent, sorafenib (25 mg/kg), PX-866 (2 mg/kg), or the drug combination QD for 3 days. Animals were monitored daily and tumor volume determined every fifth day. Tumors from animals were isolated at day 15 and fixed, sectioned (10-um), and stained against proliferation (Ki67 staining), phospho-ERK1/2 and phospho-AKT staining, the levels of tumor cell apoptosis/cleaved caspase 3, as well as with H&E and 4′,6-diamidino-2-phenylindole (DAPI).

    Mol Pharmacol 2013 84(4), 562-71. Sorafenib purchased from Selleck.

    Effects of sorafenib or sunitinib on LicA-induced cell death, ER stress responses, PLCc1, Ca2+, and ROS in HepG2 cells. HepG2 cells were pretreated with sorafenib or sunitinib for 1 h, then treated with LicA or TG for 1 h (for P-eIF2a and P-PLCc1) or 24 h (for CHOP, ATF6a(p90), and caspase-4). The cell lysates were subjected to Western blot analyses using antibodies against CHOP, ATF6a(p90), caspase-4(C), P-eIF2a, and b-actin.

    Apoptosis 2014 19(4), 682-97. Sorafenib purchased from Selleck.

  • PLoS One 2013 8(1), e54595. Sorafenib purchased from Selleck.

    (C) Western blotting revealed the expression levels of p-AKT, p-ERK1/2 and cleaved PARP in HUH-7 and R-HUH-7 HCC cell lines, these cell lines were treated with three different concentrations of sorafenib (0, 5, and 10 μM) for 24 h. (D) Western blotting revealed the expression levels of p-AKT, p-ERK1/2 and cleaved PARP in SK-HEP-1 and R-SK-HEP-1 HCC cell lines, these cell lines were treated with three different concentrations of sorafenib (0, 5, and 10 μM) for 24 h. (E) HUH-7 hepatoma cells treated with three different concentrations of sorafenib (0, 5, and 10 μM) for 24 h; proportions of apoptotic cells were calculated after cell cytotoxicity assay. (F) SK-HEP-1 hepatoma cells treated with three different concentrations of sorafenib (0, 5, and 10 μM) for 24 h; proportions of apoptotic cells were calculated after cell cytotoxicity assay. Data were expressed as mean ± standard deviation of each experiment in triplicate. (*P < 0.05, HUH-7, SK-HEP-1 are control groups, R-HUH-7, R-SK-HEP-1 are resistant groups).

    J Surg Res, 2016, 206(2):371-379. Sorafenib purchased from Selleck.

Purity & Quality Control

Choose Selective Raf Inhibitors

Biological Activity

Description Sorafenib 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.
Targets
Raf-1 [1]
(Cell-free assay)
mVEGFR2(Flk1) [1]
(Cell-free assay)
mVEGFR3 [1]
(Cell-free assay)
B-Raf [1]
(Cell-free assay)
B-Raf (V599E) [1]
(Cell-free assay)
6 nM 15 nM 20 nM 22 nM 38 nM
In vitro

Sorafenib inhibits both wild-type and V599E mutant B-Raf activity with IC50 of 22 nM and 38 nM, respectively. Sorafenib 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 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 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 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 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 significantly inhibits the phosphorylation of eIF4E and down-regulates Mcl-1 levels in hepatocellular carcinoma (HCC) cells in a MEK/ERK-independent manner. Sorafenib 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 Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
MV-4-11 M{TkUmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M4LB[GlEPTB;MD6wNFAxODNyMzFOwG0> NIDvZZdUSU6JRWK=
MONO-MAC-6 NYnrNJdVT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NEHNSXNKSzVyPUCuNFA1OThizszN NWH4T|FbW0GQR1XS
ALL-PO NGTtbGpIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M3PLNWlEPTB;MD6wN|E5PCEQvF2= MljyV2FPT0WU
NKM-1 NV6wTmx5T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NXXrdGVYUUN3ME2wMlA4PDF4IN88US=> MmD6V2FPT0WU
CGTH-W-1 MmHCS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MWfJR|UxRTBwMkWwNlIh|ryP NHn4ZYtUSU6JRWK=
BB65-RCC MmnUS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M1vTWWlEPTB;MD60O|A4OyEQvF2= NXzoV2tSW0GQR1XS
NOS-1 NXvES|dET3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NHLFOlZKSzVyPUCuOVY{PiEQvF2= NUD4UohPW0GQR1XS
SH-4 M3jpdWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M3PYSGlEPTB;MD62OVYyOyEQvF2= M3\N[HNCVkeHUh?=
HOP-62 MW\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MYPJR|UxRTBwOEWwPFgh|ryP MXHTRW5ITVJ?
HCC2998 MWHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M1raS2lEPTB;MD64PFgyQCEQvF2= M4OxdXNCVkeHUh?=
GDM-1 MljxS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NXq4W3hLUUN3ME2wMlkxPjl6IN88US=> M2TWPXNCVkeHUh?=
KM12 NHv1XFlIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NFrSSplKSzVyPUGuNFIxQThizszN M2nEVnNCVkeHUh?=
LB2518-MEL M4TsNmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NVGxWpZUUUN3ME2xMlIxQDB7IN88US=> MkDKV2FPT0WU
NCI-H1436 MUnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MULJR|UxRTFwMkG2O|gh|ryP M{DZfXNCVkeHUh?=
EM-2 MlLuS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NHm2[XFKSzVyPUGuN|U2PzhizszN NW\mdJJ{W0GQR1XS
LAMA-84 NVTxbmsxT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NV\YbHRSUUN3ME2xMlM4PjR6IN88US=> MmHOV2FPT0WU
KG-1 M3vmfWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MXXJR|UxRTFwNEe5N|Uh|ryP MVnTRW5ITVJ?
A388 M3;PR2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M1\ufmlEPTB;MT61PVE3PSEQvF2= MlPPV2FPT0WU
no-10 NGnUV5hIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NGfNV4pKSzVyPUGuOlE4OjZizszN NFvvPWpUSU6JRWK=
SF126 MYfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MXnJR|UxRTFwNkO4NVIh|ryP MWPTRW5ITVJ?
MEG-01 NUnhd4FKT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= Mn6xTWM2OD1zLkiwPVgh|ryP MVrTRW5ITVJ?
A3-KAW MXXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MYHJR|UxRTFwOEi0NkDPxE1? NI[yUXFUSU6JRWK=
D-247MG M1XvdGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MYPJR|UxRTJwMUS0PEDPxE1? NXWyWoQ{W0GQR1XS
OVCAR-4 M4PSNWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MmDiTWM2OD1{LkKxN|k{KM7:TR?= NFTZbpFUSU6JRWK=
NCI-SNU-1 Mn\tS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NX\yW2lDUUN3ME2yMlMyPjJizszN MXTTRW5ITVJ?
NCI-H2171 NVToO4ZKT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M1HTW2lEPTB;Mj6zPVc3PCEQvF2= M4\JSXNCVkeHUh?=
SIG-M5 M4rmR2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MWTJR|UxRTJwNEKyOFIh|ryP NWXybWwyW0GQR1XS
BE-13 MnLUS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MY\JR|UxRTJwNkm2NFkh|ryP NWK4TGY{W0GQR1XS
K052 NFX6TVNIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NYKxWIN4UUN3ME2yMlc1PjF4IN88US=> MVvTRW5ITVJ?
L-540 MYHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MlnsTWM2OD1{Lke1O|g6KM7:TR?= Ml\EV2FPT0WU
KMOE-2 MnG1S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M1PFfmlEPTB;Mj64NVM2KM7:TR?= MYnTRW5ITVJ?
MFH-ino Mn7VS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MU\JR|UxRTJwOUKxPFUh|ryP MoTDV2FPT0WU
HL-60 NIXVNW9Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MVTJR|UxRTNwME[yPVkh|ryP MniyV2FPT0WU
HCC2218 MoW0S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NFvaUZJKSzVyPUOuNVIxODNizszN NYfEeFlRW0GQR1XS
TE-5 NIX1S4NIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MnvpTWM2OD1|LkGzNVYzKM7:TR?= NIrRdXNUSU6JRWK=
MZ1-PC NFfkZWlIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NYPjTYltUUN3ME2zMlQ4PTB7IN88US=> MnW4V2FPT0WU
MRK-nu-1 MV7Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NUnnUVVMUUN3ME2zMlYyPDZ6IN88US=> M1rVVnNCVkeHUh?=
MZ7-mel M1;QXWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NWrGOY1WUUN3ME2zMlY3ODl7IN88US=> NVn3dlFYW0GQR1XS
BC-1 MnzXS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MmrWTWM2OD1|Lke0NFIh|ryP M2LnS3NCVkeHUh?=
ST486 MVrHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M4HIWWlEPTB;Mz64N|Y4OyEQvF2= MYPTRW5ITVJ?
KS-1 MYnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MX;JR|UxRTNwOEixPVgh|ryP MUTTRW5ITVJ?
SK-NEP-1 MXvHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MUfJR|UxRTRwMU[4NVUh|ryP MnPuV2FPT0WU
BC-3 NYPwVXRTT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NGjYcpBKSzVyPUSuNlM{QTFizszN Mlu0V2FPT0WU
NCI-H1581 NYPv[mNvT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M3XjN2lEPTB;ND6yPFc6QCEQvF2= MoKxV2FPT0WU
MHH-PREB-1 NHHYZopIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NFPVdYlKSzVyPUSuOFA1QDRizszN MXzTRW5ITVJ?
NOMO-1 MVTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NXW3XldOUUN3ME20MlQ5QTB3IN88US=> NVrsVZpDW0GQR1XS
QIMR-WIL MnPmS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MnriTWM2OD13LkC3Nlk1KM7:TR?= NYLhUpJRW0GQR1XS
SF539 NYXGR5JDT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M{n2dGlEPTB;NT6xN|IzPyEQvF2= NWnKPFZDW0GQR1XS
TE-12 MlPUS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M4HBT2lEPTB;NT6yOFkzQSEQvF2= NY\3Nnp7W0GQR1XS
NCI-H510A M2n6WGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MVjJR|UxRTVwNEG2PFUh|ryP MU\TRW5ITVJ?
JAR NYLnW5ZET3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NY\OfodlUUN3ME21MlUxQDJ2IN88US=> MkLjV2FPT0WU
no-11 MV;Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NIfXNnNKSzVyPUWuO|M2PjhizszN MkDtV2FPT0WU
BV-173 NWTXfVk5T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NFvoZphKSzVyPUWuPVU3QDJizszN NYXvfI8yW0GQR1XS
SR NITEemZIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= Mo\3TWM2OD14LkCwOlc5KM7:TR?= MUTTRW5ITVJ?
MOLT-16 NIHQOmJIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NIXvTYxKSzVyPU[uNlUzPjZizszN M2rQ[XNCVkeHUh?=
MZ2-MEL MYfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MUjJR|UxRTZwM{G4N|kh|ryP MlrqV2FPT0WU
SW954 MknCS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MmL0TWM2OD14LkS1PFY3KM7:TR?= MXvTRW5ITVJ?
ML-2 NVnvdXZnT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M2nidWlEPTB;Nj61Nlg1QSEQvF2= MXXTRW5ITVJ?
OCI-AML2 NFP6SI5Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NHnCTlNKSzVyPU[uOlExPjJizszN M1yyS3NCVkeHUh?=
SIMA MV\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NXLOU5dWUUN3ME23MlAxOTBzIN88US=> MUDTRW5ITVJ?
DOHH-2 NFW3dlFIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NHyxdotKSzVyPUeuNFU3PzZizszN MknZV2FPT0WU
697 MkD2S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MlLYTWM2OD15LkC1PVg6KM7:TR?= MlLwV2FPT0WU
NB1 NUiwT2Z4T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MofYTWM2OD15LkSwOFA4KM7:TR?= M{fzdHNCVkeHUh?=
D-392MG MULHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MljqTWM2OD15Lk[yOlY{KM7:TR?= M1f3V3NCVkeHUh?=
ES8 NFHWXWJIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NEfWb4dKSzVyPUeuO|Y2ODNizszN MoCyV2FPT0WU
RPMI-8226 MWnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MoPQTWM2OD15Lki0OVEyKM7:TR?= NWrndG1rW0GQR1XS
IST-MEL1 NYG0VYFvT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NH3LTWZKSzVyPUiuOFAxODJizszN NF36fZVUSU6JRWK=
NB14 NX;vdGlmT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MXXJR|UxRThwNkOxN|Mh|ryP M3PuT3NCVkeHUh?=
HD-MY-Z MVjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M37TW2lEPTB;OD62N|c1PiEQvF2= Mn7IV2FPT0WU
TE-10 M17mfmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MlXITWM2OD16Lke2N|U{KM7:TR?= MnTsV2FPT0WU
LC-1F NFmzNJhIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M{\NU2lEPTB;OT6xNFg{PCEQvF2= NUfzWo9JW0GQR1XS
OS-RC-2 M4Xid2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NYHNW2xWUUN3ME25MlEyOjR|IN88US=> NVviTJJ4W0GQR1XS
NCI-SNU-16 MVTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MnSxTWM2OD17LkKxNFI3KM7:TR?= MUXTRW5ITVJ?
SHP-77 NEe4bHdIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NYDtTIFqUUN3ME25MlcyPjZ{IN88US=> NEHrXlZUSU6JRWK=
A4-Fuk MmjaS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MoLwTWM2OD17Lke1OlEh|ryP MVXTRW5ITVJ?
NB6 NEj1dYJIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NUPCeHl7UUN3ME25Mlc3ODJ7IN88US=> NI\QTopUSU6JRWK=
JiyoyeP-2003 MnrMS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MmX3TWM2OD1zMD60O|Q2KM7:TR?= NV;wT5hjW0GQR1XS
DMS-114 NYPKfopwT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MYDJR|UxRTFyLkW0OFEh|ryP M1;0ZnNCVkeHUh?=
NB7 MlfSS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NUjuNpdsUUN3ME2xNE44PTJ4IN88US=> NWflOlI1W0GQR1XS
NCI-H747 MmXoS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M2jCT2lEPTB;MUGuNVIyPiEQvF2= M3u0[HNCVkeHUh?=
HH MVLHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NEjxT4NKSzVyPUGxMlM5PzZizszN NVHTdlVHW0GQR1XS
EW-18 M2S0XWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MVTJR|UxRTFzLkmwOFQh|ryP M2fTOXNCVkeHUh?=
CHP-126 M{jnc2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MYnJR|UxRTFzLkm3N|gh|ryP M3X2V3NCVkeHUh?=
NTERA-S-cl-D1 NF3vVYJIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M2nH[2lEPTB;MUKuNFI4QCEQvF2= MoTvV2FPT0WU
DEL NFfIZmlIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MUHJR|UxRTF{LkC5PFUh|ryP M{XvcnNCVkeHUh?=
LU-139 NH\PZZpIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M2fCVWlEPTB;MUKuOVQyOyEQvF2= M1v3OnNCVkeHUh?=
P30-OHK M1G2c2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 Ml3pTWM2OD1zMj61OFc6KM7:TR?= NW\jbotZW0GQR1XS
NCI-H1522 M3XnWGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 Mke0TWM2OD1zMj63OFYh|ryP M3\DdXNCVkeHUh?=
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LC-2-ad NI[0[41Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= Mmr2TWM2OD1{Nz62NlMyKM7:TR?= MYDTRW5ITVJ?
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LS-513 M13xTmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MlfhTWM2OD1|Mz64OlM5KM7:TR?= M{DuSXNCVkeHUh?=
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NCI-H1963 Moe3S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MXjJR|UxRTN3LkOwO|Ih|ryP MVPTRW5ITVJ?
MMAC-SF NF2wSYhIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NWHaN402UUN3ME2zOU45Pzh3IN88US=> MlG0V2FPT0WU
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WSU-NHL MXvHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? Mm\HTWM2OD1|Nj6xOlQh|ryP Mm[1V2FPT0WU
CESS MXTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NWHlOZNsUUN3ME2zOk4zQDR6IN88US=> MnW5V2FPT0WU
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CP66-MEL NI\1SohIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NH;ISm1KSzVyPUO5MlA4OzNizszN NX\XRY51W0GQR1XS
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IST-MES1 NF\3cmhIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M3nRbmlEPTB;NECuN|A6PiEQvF2= MVfTRW5ITVJ?
EC-GI-10 Mk[4S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MorWTWM2OD12MT61PFA2KM7:TR?= MWXTRW5ITVJ?
CTV-1 M4XTO2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NUnPVFNwUUN3ME20Nk45PDB4IN88US=> MVXTRW5ITVJ?
DG-75 MXzHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MUHJR|UxRTR|Lke1PVUh|ryP Mkn5V2FPT0WU
KNS-81-FD MUHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MVHJR|UxRTR3LkSwOVgh|ryP MnTLV2FPT0WU
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RPMI-8866 MYPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MYjJR|UxRTR4LkG4O|Mh|ryP NIPMSnBUSU6JRWK=
ACN NV;xNpdET3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= Mk[0TWM2OD12Nj60N|Qh|ryP MkKxV2FPT0WU
NCI-H1395 NHLITZJIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MYnJR|UxRTR4LkS3OVYh|ryP M3KxOnNCVkeHUh?=
NCI-H209 MXXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MVjJR|UxRTR5LkG0NFUh|ryP MlT1V2FPT0WU
TGW NYrKdnZpT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MmH5TWM2OD12OT6wO|kyKM7:TR?= MV7TRW5ITVJ?
NCI-H748 M3q0UGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NXizeoZzUUN3ME20PU41PzV|IN88US=> MYDTRW5ITVJ?
EKVX M1fsUmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NV:4SZpCUUN3ME20PU43PjJ6IN88US=> NXjT[2trW0GQR1XS

... Click to View More Cell Line Experimental Data

In vivo Oral administration of Sorafenib (~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 treatment 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 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] 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 TRAIL-resistant HCT116 bax-/- and HT29 tumor xenografts. [3]

Protocol

Kinase Assay:

[1]

+ Expand

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.
Cell Research:

[1]

+ Expand
  • Cell lines: MDA-MB-231, and HAoSMC
  • Concentrations: Dissolved in DMSO, final concentrations ~10 μM
  • Incubation Time: 72 hours
  • Method:

    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.


    (Only for Reference)
Animal Research:

[1]

+ Expand
  • Animal Models: Female NCr-nu/nu mice implanted s.c. with MDA-MB-231, Colo-205, HT-29, H460, or A549 cells
  • Formulation: Dissolved in Cremophor EL/ethanol (50:50) as 4-fold (4 × stock solution, and diluted to 1 × with water
  • Dosages: ~60 mg/kg
  • Administration: Orally once daily
    (Only for Reference)

Solubility (25°C)

In vitro DMSO 63 mg/mL warmed (135.53 mM)
Water Insoluble
Ethanol Insoluble
In vivo Add solvents to the product individually and in order(Data is from Selleck tests instead of citations):
5% DMSO+45% PEG 400+ddH2O
For best results, use promptly after mixing.
3mg/mL

* 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.

Chemical Information

Molecular Weight 464.82
Formula

C21H16ClF3N4O3

CAS No. 284461-73-0
Storage powder
in solvent
Synonyms BAY 43-9006

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Clinical Trial Information

NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT03730675 Not yet recruiting Hepatocellular Carcinoma|Portal Vein Tumor Thrombosis Zhongda Hospital November 2018 Not Applicable
NCT03645980 Recruiting Hepatocellular Carcinoma Johannes Gutenberg University Mainz|Leap Therapeutics Inc. October 10 2018 Phase 1|Phase 2
NCT03644511 Not yet recruiting Hepatocellular Carcinoma Bayer October 30 2018 --
NCT03606590 Recruiting Hepatocellular Carcinoma NovoCure Ltd. September 2018 Phase 2
NCT03630120 Recruiting Thyroid Cancer|Thyroid Cancer Medullary|Differentiated Thyroid Cancer|Papillary Thyroid Cancer|Follicular Thyroid Cancer|Poorly Differentiated Thyroid Gland Carcinoma H. Lee Moffitt Cancer Center and Research Institute August 6 2018 Phase 2
NCT03582618 Recruiting Hepatocellular Carcinoma|Advanced Cancer TaiRx Inc. July 12 2018 Phase 2

Tech Support

Answers to questions you may have can be found in the inhibitor handling instructions. Topics include how to prepare stock solutions, how to store inhibitors, and issues that need special attention for cell-based assays and animal experiments.

Handling Instructions

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID