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 62 Publications

9 Customer Reviews

  • 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.

  • 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.

    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 NVfteXlWT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NXPvU4pWUUN3ME2wMlAxODByM{CzJO69VQ>? MVjTRW5ITVJ?
MONO-MAC-6 NV;QbVluT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NUXIcXRGUUN3ME2wMlAxPDF6IN88US=> M3TGcXNCVkeHUh?=
ALL-PO Ml;sS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NHjHT5ZKSzVyPUCuNFMyQDRizszN MoDrV2FPT0WU
NKM-1 NHPnO3lIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MlvrTWM2OD1yLkC3OFE3KM7:TR?= NXLJN3FZW0GQR1XS
CGTH-W-1 NFjuN41Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NULYUmlOUUN3ME2wMlI2ODJ{IN88US=> NYTwSXdzW0GQR1XS
BB65-RCC MUPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NFXxV|RKSzVyPUCuOFcxPzNizszN NXrTUXlXW0GQR1XS
NOS-1 MofYS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NUXH[GpRUUN3ME2wMlU3OzZizszN MVTTRW5ITVJ?
SH-4 NHjNcIhIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NIfIOHVKSzVyPUCuOlU3OTNizszN M3\1WHNCVkeHUh?=
HOP-62 MXfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MX3JR|UxRTBwOEWwPFgh|ryP M{TMTnNCVkeHUh?=
HCC2998 NFq3foxIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NV25RmhCUUN3ME2wMlg5QDF6IN88US=> MXPTRW5ITVJ?
GDM-1 M3G1dGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MVrJR|UxRTBwOUC2PVgh|ryP MlWyV2FPT0WU
KM12 NFPkb5RIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NYLCVHJDUUN3ME2xMlAzODl6IN88US=> M3vU[XNCVkeHUh?=
LB2518-MEL NX\vflhUT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NHLQRYxKSzVyPUGuNlA5ODlizszN MY\TRW5ITVJ?
NCI-H1436 MVjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NEmzU3NKSzVyPUGuNlE3PzhizszN MnLwV2FPT0WU
EM-2 NIfLWFlIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MkPqTWM2OD1zLkO1OVc5KM7:TR?= M1XTd3NCVkeHUh?=
LAMA-84 NXrH[IsxT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NIHVWJNKSzVyPUGuN|c3PDhizszN M4jO[nNCVkeHUh?=
KG-1 MVTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NFHvUFBKSzVyPUGuOFc6OzVizszN MYnTRW5ITVJ?
A388 M1\ob2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MofQTWM2OD1zLkW5NVY2KM7:TR?= Mof1V2FPT0WU
no-10 MXPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NWrvU4VpUUN3ME2xMlYyPzJ4IN88US=> NGmxcHZUSU6JRWK=
SF126 NHiyNFlIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NEjjTY1KSzVyPUGuOlM5OTJizszN NGTGeWJUSU6JRWK=
MEG-01 M4PiV2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MUfJR|UxRTFwOEC5PEDPxE1? NHjEclFUSU6JRWK=
A3-KAW NYPmbJQ{T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NI\lc4ZKSzVyPUGuPFg1OiEQvF2= NUjGcHlyW0GQR1XS
D-247MG NH:wdXlIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NEjjU2pKSzVyPUKuNVQ1QCEQvF2= MVrTRW5ITVJ?
OVCAR-4 NIX2TphIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NHThPHlKSzVyPUKuNlE{QTNizszN MlXpV2FPT0WU
NCI-SNU-1 MoD2S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? Ml20TWM2OD1{LkOxOlIh|ryP M3XKUHNCVkeHUh?=
NCI-H2171 M{LVSWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M17uRmlEPTB;Mj6zPVc3PCEQvF2= NE\mUXFUSU6JRWK=
SIG-M5 NGfTdJpIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NVjXXVNZUUN3ME2yMlQzOjR{IN88US=> MmPpV2FPT0WU
BE-13 MXjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NFLyeFdKSzVyPUKuOlk3ODlizszN NFLXO4NUSU6JRWK=
K052 M2fpSmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NUi4WXBQUUN3ME2yMlc1PjF4IN88US=> MoS2V2FPT0WU
L-540 MnT1S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NV3aZXJ1UUN3ME2yMlc2Pzh7IN88US=> NVXkNZRjW0GQR1XS
KMOE-2 NVfCSYs3T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NUTXZlFDUUN3ME2yMlgyOzVizszN Mk\YV2FPT0WU
MFH-ino NH3hNoRIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NX24NZhOUUN3ME2yMlkzOTh3IN88US=> M4D4NnNCVkeHUh?=
HL-60 MUnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NV;1VVZyUUN3ME2zMlA3Ojl7IN88US=> MmXxV2FPT0WU
HCC2218 MUTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NVe1eotiUUN3ME2zMlEzODB|IN88US=> NUDuTGZoW0GQR1XS
TE-5 NGS3T4ZIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NHvjSpFKSzVyPUOuNVMyPjJizszN NXjBd|I6W0GQR1XS
MZ1-PC MmXMS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NG\GWFhKSzVyPUOuOFc2ODlizszN NE\1RndUSU6JRWK=
MRK-nu-1 M4fxfmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NWrIUmJCUUN3ME2zMlYyPDZ6IN88US=> MVrTRW5ITVJ?
MZ7-mel M2DoRmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 Mlf4TWM2OD1|Lk[2NFk6KM7:TR?= NHPFcnVUSU6JRWK=
BC-1 MkPKS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MX3JR|UxRTNwN{SwNkDPxE1? NF7hWVVUSU6JRWK=
ST486 NHfu[3BIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MUPJR|UxRTNwOEO2O|Mh|ryP NUTZfoJxW0GQR1XS
KS-1 M3\Bdmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MV;JR|UxRTNwOEixPVgh|ryP MVzTRW5ITVJ?
SK-NEP-1 NVfWWnFZT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NVrUbZVoUUN3ME20MlE3QDF3IN88US=> MUfTRW5ITVJ?
BC-3 M1vMbmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NYLBeJhNUUN3ME20MlI{OzlzIN88US=> MVrTRW5ITVJ?
NCI-H1581 NH;DWHFIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MmPKTWM2OD12LkK4O|k5KM7:TR?= MVnTRW5ITVJ?
MHH-PREB-1 MXzHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M3TzV2lEPTB;ND60NFQ5PCEQvF2= NUjic2FUW0GQR1XS
NOMO-1 MYTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NYHCeXBqUUN3ME20MlQ5QTB3IN88US=> M2j1c3NCVkeHUh?=
QIMR-WIL NXTJd2x{T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NWTVXItYUUN3ME21MlA4Ojl2IN88US=> NGPh[GpUSU6JRWK=
SF539 MWnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NUDOR45OUUN3ME21MlE{OjJ5IN88US=> NIGwZ|ZUSU6JRWK=
TE-12 M4HLZmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MWrJR|UxRTVwMkS5Nlkh|ryP MoL0V2FPT0WU
NCI-H510A MmLvS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NIi4dFNKSzVyPUWuOFE3QDVizszN M3rwcHNCVkeHUh?=
JAR MlHhS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M{W4bGlEPTB;NT61NFgzPCEQvF2= NFHK[W5USU6JRWK=
no-11 NEiwSphIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M3H0XGlEPTB;NT63N|U3QCEQvF2= NIH0TWFUSU6JRWK=
BV-173 M{DMcWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NHLHPIZKSzVyPUWuPVU3QDJizszN NX;iboU1W0GQR1XS
SR MUXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NG\UT3hKSzVyPU[uNFA3PzhizszN NGXPeJNUSU6JRWK=
MOLT-16 NWjQSmhvT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M{nWdWlEPTB;Nj6yOVI3PiEQvF2= NXLxWWlUW0GQR1XS
MZ2-MEL M4XaNmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NVvaTG9sUUN3ME22MlMyQDN7IN88US=> M3TqVnNCVkeHUh?=
SW954 M4TBT2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M3PCfmlEPTB;Nj60OVg3PiEQvF2= MWHTRW5ITVJ?
ML-2 M3TUdGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NYiwbpY{UUN3ME22MlUzQDR7IN88US=> NV\pd3A5W0GQR1XS
OCI-AML2 MXzHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MXvJR|UxRTZwNkGwOlIh|ryP M{XUZXNCVkeHUh?=
SIMA MVfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M{LubmlEPTB;Nz6wNFExOSEQvF2= MlzFV2FPT0WU
DOHH-2 NVzHS2xYT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MWrJR|UxRTdwMEW2O|Yh|ryP M{TwcXNCVkeHUh?=
697 NWjCfnQ3T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NIL6fFNKSzVyPUeuNFU6QDlizszN M4PsUnNCVkeHUh?=
NB1 NU\L[2NoT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NFnQUohKSzVyPUeuOFA1ODdizszN NH:wXmJUSU6JRWK=
D-392MG MWXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NWDDPXkyUUN3ME23MlYzPjZ|IN88US=> MXLTRW5ITVJ?
ES8 M1HFW2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NHLxNlBKSzVyPUeuO|Y2ODNizszN MonpV2FPT0WU
RPMI-8226 NHu5bllIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NV;DXm9JUUN3ME23Mlg1PTFzIN88US=> NF[3NIZUSU6JRWK=
IST-MEL1 NVvOXZlST3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MnnaTWM2OD16LkSwNFAzKM7:TR?= NXHsO4Y3W0GQR1XS
NB14 MXrHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MnPlTWM2OD16Lk[zNVM{KM7:TR?= M1W1UXNCVkeHUh?=
HD-MY-Z NWj2OI9ZT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MULJR|UxRThwNkO3OFYh|ryP NWTNe3VIW0GQR1XS
TE-10 NWPjd4c4T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MmHaTWM2OD16Lke2N|U{KM7:TR?= Ml2zV2FPT0WU
LC-1F MmnzS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MVPJR|UxRTlwMUC4N|Qh|ryP NGTje2RUSU6JRWK=
OS-RC-2 NHzablRIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MWfJR|UxRTlwMUGyOFMh|ryP NGW4VWFUSU6JRWK=
NCI-SNU-16 NWizXlhIT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MX;JR|UxRTlwMkGwNlYh|ryP MnnkV2FPT0WU
SHP-77 NVP6VlNuT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MVvJR|UxRTlwN{G2OlIh|ryP NFfHN5RUSU6JRWK=
A4-Fuk NX3qdpRvT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NY\lcmtiUUN3ME25Mlc2PjFizszN MUPTRW5ITVJ?
NB6 MoHwS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? Mo[zTWM2OD17Lke2NFI6KM7:TR?= M{i1UHNCVkeHUh?=
JiyoyeP-2003 MX\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NXPhUlZ5UUN3ME2xNE41PzR3IN88US=> NFHlUHFUSU6JRWK=
DMS-114 MnjoS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NITxT2lKSzVyPUGwMlU1PDFizszN MlfGV2FPT0WU
NB7 MUTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NWjaZ|hjUUN3ME2xNE44PTJ4IN88US=> MXzTRW5ITVJ?
NCI-H747 NWfwcmhJT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NXS5emxyUUN3ME2xNU4yOjF4IN88US=> MnH3V2FPT0WU
HH NUiwbmh5T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M{\mTmlEPTB;MUGuN|g4PiEQvF2= NXX4fIh4W0GQR1XS
EW-18 MV;Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MXPJR|UxRTFzLkmwOFQh|ryP MUPTRW5ITVJ?
CHP-126 MVzHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MVXJR|UxRTFzLkm3N|gh|ryP MonBV2FPT0WU
NTERA-S-cl-D1 Mnz4S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M123UmlEPTB;MUKuNFI4QCEQvF2= NVr4VXZ3W0GQR1XS
DEL MWHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NFu4PXdKSzVyPUGyMlA6QDVizszN MoTvV2FPT0WU
LU-139 MlTVS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NH7DZ2ZKSzVyPUGyMlU1OTNizszN NFjSbXpUSU6JRWK=
P30-OHK MV7Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MmnBTWM2OD1zMj61OFc6KM7:TR?= NFq1OWhUSU6JRWK=
NCI-H1522 NW\QUGR{T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MoPzTWM2OD1zMj63OFYh|ryP M13XZnNCVkeHUh?=
NCI-H1299 MnzVS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? Mle5TWM2OD1zMz6yPVEyKM7:TR?= NI\QeVFUSU6JRWK=
UACC-257 MnTkS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MnHOTWM2OD1zMz61NVI3KM7:TR?= Mn31V2FPT0WU
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EW-13 MXPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MnHpTWM2OD1{OT6xO|Q3KM7:TR?= NUi4Xm9VW0GQR1XS
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MC116 M{TMV2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M1HQUGlEPTB;M{KuNFgzPiEQvF2= MlTkV2FPT0WU
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NCI-H2196 NFz1T3BIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M2j2cmlEPTB;M{OuNlU2PyEQvF2= NXG1V4trW0GQR1XS
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LP-1 M2H1V2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MUXJR|UxRTN|Lkm5OVYh|ryP M2HQNHNCVkeHUh?=
A253 MXjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NWDlR2FIUUN3ME2zOE4zOjl4IN88US=> NU\YfoRbW0GQR1XS
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NCI-H1963 NXrTZ5Z7T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NITOZlFKSzVyPUO1MlMxPzJizszN M1jCZXNCVkeHUh?=
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LB831-BLC NE\DOWxIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MUXJR|UxRTN4LkC2OVQh|ryP NXHyZlBYW0GQR1XS
WSU-NHL NH22bYFIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MVTJR|UxRTN4LkG2OEDPxE1? M4f0ZnNCVkeHUh?=
CESS NUXzeXZ{T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NYq2T4p6UUN3ME2zOk4zQDR6IN88US=> NF7aNHdUSU6JRWK=
NEC8 NXrjd2pyT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MVXJR|UxRTN4LkW4N|Uh|ryP MVrTRW5ITVJ?
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MHH-CALL-2 M{HyXWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 Mny3TWM2OD1|Nz6xPFIyKM7:TR?= M2PZenNCVkeHUh?=
K5 NXnncGU{T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MY\JR|UxRTN6LkSzJO69VQ>? MXjTRW5ITVJ?
CP66-MEL NXO3Spc1T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NUD1fYxYUUN3ME2zPU4xPzN|IN88US=> NIDRWZlUSU6JRWK=
OPM-2 MXHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MkDoTWM2OD1|OT64OFMzKM7:TR?= Mo\xV2FPT0WU
IST-MES1 NHfkZWxIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M4XjRmlEPTB;NECuN|A6PiEQvF2= M{nLNXNCVkeHUh?=
EC-GI-10 MoPIS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MULJR|UxRTRzLkW4NFUh|ryP NWn3Rm5{W0GQR1XS
CTV-1 NHyyfIFIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MnjITWM2OD12Mj64OFA3KM7:TR?= MnnJV2FPT0WU
DG-75 M3i3[2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MV3JR|UxRTR|Lke1PVUh|ryP NXrSUVFQW0GQR1XS
KNS-81-FD NF\6WnRIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MnHpTWM2OD12NT60NFU5KM7:TR?= NGriVFhUSU6JRWK=
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RPMI-8866 NUTsS4k5T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M2HIdGlEPTB;NE[uNVg4OyEQvF2= MVTTRW5ITVJ?
ACN M2DmZWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NHPWVoNKSzVyPUS2MlQ{PCEQvF2= NV;ZNpl5W0GQR1XS
NCI-H1395 NUnMbVl2T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NHHDUmRKSzVyPUS2MlQ4PTZizszN NUTTUZB1W0GQR1XS
NCI-H209 NFn2cFBIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MVTJR|UxRTR5LkG0NFUh|ryP M3nkOXNCVkeHUh?=
TGW NHvuSIhIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NI\EZ3ZKSzVyPUS5MlA4QTFizszN MYjTRW5ITVJ?
NCI-H748 NVzwPGt5T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MoqxTWM2OD12OT60O|U{KM7:TR?= Ml7lV2FPT0WU
EKVX M{SxSGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NHfJe3VKSzVyPUS5MlY3OjhizszN MlTUV2FPT0WU

... 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:
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
Synonyms BAY 43-9006

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Clinical Trial Information

NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT00727233 Completed Neurofibromatosis Type I|Plexiform Neurofibroma National Cancer Institute (NCI)|National Institutes of Health Clinical Center (CC) July 8, 2008 Phase 1
NCT02989870 Not yet recruiting HepatoCellular Carcinoma|Unresectable HepatoCellular Carcinoma|Liver Cancer H. Lee Moffitt Cancer Center and Research Institute|National Comprehensive Cancer Network April 30, 2017 Phase 1
NCT01445080 Completed Leukemia|With AML and FLT3-ITD Mutations National Cancer Institute (NCI)|National Institutes of Health Clinical Center (CC) August 23, 2006 Phase 1
NCT01434602 Recruiting Brain Tumor|Glioblastoma|Anaplastic Glioma National Cancer Institute (NCI)|National Institutes of Health Clinical Center (CC) October 21, 2015 Phase 1|Phase 2
NCT02988440 Not yet recruiting Hepatocellular Carcinoma Novartis Pharmaceuticals|Novartis May 2017 Phase 1
NCT03037437 Not yet recruiting Hepatocellular Cancer The University of Texas Health Science Center at San Antonio January 2017 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