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 MX3Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MWfJR|UxRTBwMECwNFA{ODNizszN NYOzcY9YW0GQR1XS
MONO-MAC-6 MXjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MlrpTWM2OD1yLkCwOFE5KM7:TR?= NI\QSGRUSU6JRWK=
ALL-PO M3L3dWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NXHGR4o1UUN3ME2wMlA{OTh2IN88US=> NWP0OZZIW0GQR1XS
NKM-1 M2LtXmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MVXJR|UxRTBwMEe0NVYh|ryP NFXqXGZUSU6JRWK=
CGTH-W-1 MmXGS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NYfGRXE4UUN3ME2wMlI2ODJ{IN88US=> MW\TRW5ITVJ?
BB65-RCC MYfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MWfJR|UxRTBwNEewO|Mh|ryP NGLzPYFUSU6JRWK=
NOS-1 MljwS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NULrdm8{UUN3ME2wMlU3OzZizszN MYjTRW5ITVJ?
SH-4 NYHQdlRTT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NF3VfotKSzVyPUCuOlU3OTNizszN MWnTRW5ITVJ?
HOP-62 MXfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MmrYTWM2OD1yLki1NFg5KM7:TR?= M{L4bXNCVkeHUh?=
HCC2998 NInPVVhIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MojSTWM2OD1yLki4PFE5KM7:TR?= MVfTRW5ITVJ?
GDM-1 M3n5bGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NHrmVJNKSzVyPUCuPVA3QThizszN NYTYe5FGW0GQR1XS
KM12 M3PJT2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NUTjdXFLUUN3ME2xMlAzODl6IN88US=> NGj2[3FUSU6JRWK=
LB2518-MEL MVTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MXrJR|UxRTFwMkC4NFkh|ryP Ml\BV2FPT0WU
NCI-H1436 NVHMTYFJT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NXXSU2U5UUN3ME2xMlIyPjd6IN88US=> NYjHVZhHW0GQR1XS
EM-2 NUO3fYJ[T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NET1doFKSzVyPUGuN|U2PzhizszN MWrTRW5ITVJ?
LAMA-84 NVrrd|lwT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M162bmlEPTB;MT6zO|Y1QCEQvF2= MWfTRW5ITVJ?
KG-1 NFfWUoVIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NX:xN41lUUN3ME2xMlQ4QTN3IN88US=> M17kSnNCVkeHUh?=
A388 NFriUZNIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M3vu[WlEPTB;MT61PVE3PSEQvF2= NEPMelNUSU6JRWK=
no-10 M2PWcWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MmT2TWM2OD1zLk[xO|I3KM7:TR?= M2myWHNCVkeHUh?=
SF126 M{PQTmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M2fjRWlEPTB;MT62N|gyOiEQvF2= M1;CW3NCVkeHUh?=
MEG-01 MVjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NH7jPY9KSzVyPUGuPFA6QCEQvF2= NUjmW4tDW0GQR1XS
A3-KAW NVLGW4FUT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NUi0c5FQUUN3ME2xMlg5PDJizszN M2DSc3NCVkeHUh?=
D-247MG NF\zb5VIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NVzsRmNqUUN3ME2yMlE1PDhizszN M2rOTHNCVkeHUh?=
OVCAR-4 MYLHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M1fYZmlEPTB;Mj6yNVM6OyEQvF2= Moi1V2FPT0WU
NCI-SNU-1 NVW3WocyT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NW\OcHMyUUN3ME2yMlMyPjJizszN M{fPZnNCVkeHUh?=
NCI-H2171 MXLHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NHn2[JBKSzVyPUKuN|k4PjRizszN Mnm4V2FPT0WU
SIG-M5 NXHZO4t[T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MWfJR|UxRTJwNEKyOFIh|ryP MkXoV2FPT0WU
BE-13 M1P1[Wdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M4\pNmlEPTB;Mj62PVYxQSEQvF2= MXzTRW5ITVJ?
K052 M3v4Smdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MlHlTWM2OD1{Lke0OlE3KM7:TR?= MlrkV2FPT0WU
L-540 MnO4S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MlzITWM2OD1{Lke1O|g6KM7:TR?= MXLTRW5ITVJ?
KMOE-2 NYDPfIxPT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M37CbGlEPTB;Mj64NVM2KM7:TR?= NGDNNJVUSU6JRWK=
MFH-ino NH:zWnJIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= Mm\UTWM2OD1{LkmyNVg2KM7:TR?= NGK4elNUSU6JRWK=
HL-60 NVPTWlhST3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M2nGN2lEPTB;Mz6wOlI6QSEQvF2= MYPTRW5ITVJ?
HCC2218 NGe4SXRIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NF33[IVKSzVyPUOuNVIxODNizszN MXnTRW5ITVJ?
TE-5 MVvHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NETl[ldKSzVyPUOuNVMyPjJizszN NV7PN4VMW0GQR1XS
MZ1-PC MWLHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M2DONGlEPTB;Mz60O|UxQSEQvF2= MljEV2FPT0WU
MRK-nu-1 NXLCclRDT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MVnJR|UxRTNwNkG0Olgh|ryP MnTTV2FPT0WU
MZ7-mel MoriS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NW\DZpdmUUN3ME2zMlY3ODl7IN88US=> NWDHeIQ6W0GQR1XS
BC-1 M{HHNWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MVTJR|UxRTNwN{SwNkDPxE1? NYXMeo9FW0GQR1XS
ST486 NXLNSpFYT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NVq5UIJuUUN3ME2zMlg{Pjd|IN88US=> NYSxe3BRW0GQR1XS
KS-1 NIHVUIFIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M2XmNmlEPTB;Mz64PFE6QCEQvF2= NF73U3ZUSU6JRWK=
SK-NEP-1 M{DhW2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 Mkn1TWM2OD12LkG2PFE2KM7:TR?= MXPTRW5ITVJ?
BC-3 NHH2ZnNIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= Ml\WTWM2OD12LkKzN|kyKM7:TR?= NXS5ZY1HW0GQR1XS
NCI-H1581 MWHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NWPDbHdrUUN3ME20MlI5Pzl6IN88US=> MnzUV2FPT0WU
MHH-PREB-1 M4DUb2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M3LuZWlEPTB;ND60NFQ5PCEQvF2= MVvTRW5ITVJ?
NOMO-1 NGXxR|JIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M4\4VmlEPTB;ND60PFkxPSEQvF2= NUHCXmRsW0GQR1XS
QIMR-WIL Mn3XS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M1vIUmlEPTB;NT6wO|I6PCEQvF2= Ml2wV2FPT0WU
SF539 M13hTWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MoSxTWM2OD13LkGzNlI4KM7:TR?= NFTCUGhUSU6JRWK=
TE-12 M{nTS2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M3f1TGlEPTB;NT6yOFkzQSEQvF2= MVjTRW5ITVJ?
NCI-H510A MWLHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MkTETWM2OD13LkSxOlg2KM7:TR?= M4T4THNCVkeHUh?=
JAR MlzpS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NEnLc2dKSzVyPUWuOVA5OjRizszN MlfVV2FPT0WU
no-11 NFjsSIVIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= Mk\PTWM2OD13LkezOVY5KM7:TR?= M1XjR3NCVkeHUh?=
BV-173 MWfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MWTJR|UxRTVwOUW2PFIh|ryP NUnqbGNkW0GQR1XS
SR MVLHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M2rBVGlEPTB;Nj6wNFY4QCEQvF2= MUjTRW5ITVJ?
MOLT-16 NGTvTZdIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M17BeGlEPTB;Nj6yOVI3PiEQvF2= NYL4SGFsW0GQR1XS
MZ2-MEL M4Hubmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MU\JR|UxRTZwM{G4N|kh|ryP MmLnV2FPT0WU
SW954 M{PDbmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MoLOTWM2OD14LkS1PFY3KM7:TR?= NFW3W21USU6JRWK=
ML-2 MnLSS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MWLJR|UxRTZwNUK4OFkh|ryP NWDDe4dHW0GQR1XS
OCI-AML2 NGLsTJVIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NHW2Om5KSzVyPU[uOlExPjJizszN MlrDV2FPT0WU
SIMA NUPVTnJiT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M4TTSmlEPTB;Nz6wNFExOSEQvF2= NXPp[4hmW0GQR1XS
DOHH-2 MWLHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M{jNfGlEPTB;Nz6wOVY4PiEQvF2= MlXXV2FPT0WU
697 MoDaS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NHTvb2ZKSzVyPUeuNFU6QDlizszN MlPsV2FPT0WU
NB1 MmX1S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? Ml3mTWM2OD15LkSwOFA4KM7:TR?= MmL5V2FPT0WU
D-392MG M4rORWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MkfJTWM2OD15Lk[yOlY{KM7:TR?= Mn\xV2FPT0WU
ES8 NFL2b4lIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M2HOZ2lEPTB;Nz63OlUxOyEQvF2= MVrTRW5ITVJ?
RPMI-8226 NUHueW5UT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M3nBfWlEPTB;Nz64OFUyOSEQvF2= NGfrVFVUSU6JRWK=
IST-MEL1 NV3kSWZ3T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NV\RdnlUUUN3ME24MlQxODB{IN88US=> NY\V[ZN[W0GQR1XS
NB14 NYXVVVA3T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NYO5S40xUUN3ME24MlY{OTN|IN88US=> M3:xc3NCVkeHUh?=
HD-MY-Z NGDlW2NIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NWnrcXlnUUN3ME24MlY{PzR4IN88US=> NY\Oc3dKW0GQR1XS
TE-10 NXfKSng3T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MoXXTWM2OD16Lke2N|U{KM7:TR?= Ml3FV2FPT0WU
LC-1F M4DiVGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M4jtcGlEPTB;OT6xNFg{PCEQvF2= M4f1[3NCVkeHUh?=
OS-RC-2 NH3OS4tIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M2TweWlEPTB;OT6xNVI1OyEQvF2= M1i2RXNCVkeHUh?=
NCI-SNU-16 NInDXoxIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NFK4bopKSzVyPUmuNlExOjZizszN M1z3SXNCVkeHUh?=
SHP-77 NEPVb3dIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NYLYSFl4UUN3ME25MlcyPjZ{IN88US=> M{S1V3NCVkeHUh?=
A4-Fuk Ml7DS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M4jabmlEPTB;OT63OVYyKM7:TR?= NFSyTo1USU6JRWK=
NB6 MmX6S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M{fPTGlEPTB;OT63OlAzQSEQvF2= MkLuV2FPT0WU
JiyoyeP-2003 Mk\4S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MmfmTWM2OD1zMD60O|Q2KM7:TR?= M4LUe3NCVkeHUh?=
DMS-114 M3G1bmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NH\WcXVKSzVyPUGwMlU1PDFizszN M2TLTXNCVkeHUh?=
NB7 NUDvfplKT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NGWyWFJKSzVyPUGwMlc2OjZizszN MV;TRW5ITVJ?
NCI-H747 MWnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M1rWc2lEPTB;MUGuNVIyPiEQvF2= M{DMVXNCVkeHUh?=
HH NXfpblBQT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NWHKXIRHUUN3ME2xNU4{QDd4IN88US=> NXvhVol{W0GQR1XS
EW-18 NWDDXmZKT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NWmzb|NDUUN3ME2xNU46ODR2IN88US=> NYSxUnpQW0GQR1XS
CHP-126 NWPYNZRMT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NXvRbIJmUUN3ME2xNU46PzN6IN88US=> MWHTRW5ITVJ?
NTERA-S-cl-D1 MUfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NVfhd2xwUUN3ME2xNk4xOjd6IN88US=> NHfNNG1USU6JRWK=
DEL NHvYb3NIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MVvJR|UxRTF{LkC5PFUh|ryP M{j3PHNCVkeHUh?=
LU-139 NIn0S5pIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MoXNTWM2OD1zMj61OFE{KM7:TR?= NIX1eXVUSU6JRWK=
P30-OHK M2rMdGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NUPx[G5CUUN3ME2xNk42PDd7IN88US=> NX\wSlBGW0GQR1XS
NCI-H1522 NFvmbXNIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MkLoTWM2OD1zMj63OFYh|ryP NVjJXolLW0GQR1XS
NCI-H1299 MoLwS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NHXzR4dKSzVyPUGzMlI6OTFizszN MnnkV2FPT0WU
UACC-257 NX7kfXFoT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MUnJR|UxRTF|LkWxNlYh|ryP MYjTRW5ITVJ?
Calu-6 M{XJeGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M1ezZ2lEPTB;MUOuOlA1PiEQvF2= M2G3bnNCVkeHUh?=
NCI-H1882 MXHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MYrJR|UxRTF|Lki1OVUh|ryP MYDTRW5ITVJ?
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ES1 NWfOVmt6T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NWLnepNTUUN3ME2xOE4yPTVzIN88US=> Mn;vV2FPT0WU
NCI-H1694 M3\Wfmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M2\RS2lEPTB;MUSuOFgyOSEQvF2= MnnKV2FPT0WU
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C2BBe1 NHfqTnFIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NGTuVG5KSzVyPUK0MlMzOzlizszN M2rWdXNCVkeHUh?=
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DJM-1 MYfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MkXyTWM2OD1{ND61NlIyKM7:TR?= MlHkV2FPT0WU
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SK-N-DZ M3S4dGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MVLJR|UxRTJ4LkO0NVQh|ryP NF76[5ZUSU6JRWK=
COR-L88 M2C4[mdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NXvUe3E3UUN3ME2yOk42Pzl4IN88US=> MWHTRW5ITVJ?
LU-65 MmPmS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MX\JR|UxRTJ4Lki1N|Uh|ryP NHu4cYNUSU6JRWK=
TGBC1TKB MkjES5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NWXGfZpGUUN3ME2yOk46QDJ6IN88US=> MWrTRW5ITVJ?
THP-1 M{jVWWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NIHGN4RKSzVyPUK3MlIyPDFizszN MoTXV2FPT0WU
ONS-76 NWTsOFI6T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MXLJR|UxRTJ5LkOzNkDPxE1? MV\TRW5ITVJ?
LC-2-ad NX[2No1{T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NGi0eZZKSzVyPUK3MlYzOzFizszN NUD6clE6W0GQR1XS
EW-13 Mkn5S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NVnXNFlQUUN3ME2yPU4yPzR4IN88US=> M1fNcnNCVkeHUh?=
MS-1 NHnEVFdIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MYrJR|UxRTNyLkeyO|gh|ryP MkfoV2FPT0WU
NCI-H2227 NFWwTIpIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NInFTY1KSzVyPUOwMlk5ODZizszN MYXTRW5ITVJ?
LXF-289 NYXkNmNKT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M1jQfWlEPTB;M{GuOFQ6OiEQvF2= MkPPV2FPT0WU
MC116 M4KweWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MVPJR|UxRTN{LkC4NlYh|ryP MYnTRW5ITVJ?
EVSA-T NGPpdmdIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MYTJR|UxRTN{LkK1PFUh|ryP Mk[yV2FPT0WU
CTB-1 MVTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M1rwV2lEPTB;M{OuNVExOSEQvF2= MnzkV2FPT0WU
COLO-320-HSR NHfmb4xIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NGHucmlKSzVyPUOzMlE3ODNizszN NUHtfVF2W0GQR1XS
NCI-H2196 M{HITmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MVfJR|UxRTN|LkK1OVch|ryP MYfTRW5ITVJ?
LB2241-RCC Ml;ES5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M1TmOmlEPTB;M{OuN|E{PSEQvF2= NU\GZ5AxW0GQR1XS
LS-513 NYXPV|lIT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NVjjPI17UUN3ME2zN{45PjN6IN88US=> M3jDdHNCVkeHUh?=
LP-1 NHLQW2lIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NX36c5RiUUN3ME2zN{46QTV4IN88US=> NIPGXWdUSU6JRWK=
A253 MV3Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NHLqOYpKSzVyPUO0MlIzQTZizszN NHf3Rm5USU6JRWK=
SK-MM-2 NIr4UXdIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= Mln1TWM2OD1|ND65OFUyKM7:TR?= MkCyV2FPT0WU
NCI-H1963 Mme4S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NFO4coNKSzVyPUO1MlMxPzJizszN MoDaV2FPT0WU
MMAC-SF M2\ESWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M{jxW2lEPTB;M{WuPFc5PSEQvF2= MWLTRW5ITVJ?
LB831-BLC MY\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NX3LeVhoUUN3ME2zOk4xPjV2IN88US=> NE\PPVBUSU6JRWK=
WSU-NHL Ml;VS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M1rVd2lEPTB;M{[uNVY1KM7:TR?= NH34[ZlUSU6JRWK=
CESS MmHSS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NX3VWpRuUUN3ME2zOk4zQDR6IN88US=> MUDTRW5ITVJ?
NEC8 MUDHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NXjUcYMzUUN3ME2zOk42QDN3IN88US=> Ml23V2FPT0WU
KNS-42 NF3PRo1Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M3jG[2lEPTB;M{euNVI{PyEQvF2= NEK1SpdUSU6JRWK=
MHH-CALL-2 NGD0SlFIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NIXRVIdKSzVyPUO3MlE5OjFizszN MWXTRW5ITVJ?
K5 NUi1O2FpT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MmKyTWM2OD1|OD60N{DPxE1? MYTTRW5ITVJ?
CP66-MEL MojSS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NUGwb|RRUUN3ME2zPU4xPzN|IN88US=> MV3TRW5ITVJ?
OPM-2 NXvocIlCT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M3f1PWlEPTB;M{muPFQ{OiEQvF2= Mmm2V2FPT0WU
IST-MES1 NIS2PFRIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NXnQXWlLUUN3ME20NE4{ODl4IN88US=> MlPpV2FPT0WU
EC-GI-10 M36wbmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M37FW2lEPTB;NEGuOVgxPSEQvF2= M2Xuc3NCVkeHUh?=
CTV-1 NVnu[XhbT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NFuySIZKSzVyPUSyMlg1ODZizszN NHrmTXBUSU6JRWK=
DG-75 Mk\pS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MnrxTWM2OD12Mz63OVk2KM7:TR?= MXnTRW5ITVJ?
KNS-81-FD MYTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MoHGTWM2OD12NT60NFU5KM7:TR?= NWra[nJFW0GQR1XS
NCI-H82 NF;2dWlIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MX7JR|UxRTR3LkW3OVgh|ryP NFrDO2lUSU6JRWK=
RPMI-8866 MYrHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MVfJR|UxRTR4LkG4O|Mh|ryP MUPTRW5ITVJ?
ACN MmTNS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MWnJR|UxRTR4LkSzOEDPxE1? NUjYXIZ2W0GQR1XS
NCI-H1395 MoL6S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NHXQNFFKSzVyPUS2MlQ4PTZizszN NVHJVY1jW0GQR1XS
NCI-H209 NHfsSItIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MlHzTWM2OD12Nz6xOFA2KM7:TR?= NFv3PINUSU6JRWK=
TGW NI\ZRnNIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MnSwTWM2OD12OT6wO|kyKM7:TR?= NVT0Nms1W0GQR1XS
NCI-H748 NYm3SlQzT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MXvJR|UxRTR7LkS3OVMh|ryP NITpZVRUSU6JRWK=
EKVX MlzZS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MlfUTWM2OD12OT62OlI5KM7:TR?= MnjkV2FPT0WU

... 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
in solvent
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