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

  • 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 Mo[wS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MoK0TWM2OD1yLkCwNFAxOzB|IN88US=> M2rMUXNCVkeHUh?=
MONO-MAC-6 NVLndZJwT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MVPJR|UxRTBwMEC0NVgh|ryP NHHtXnBUSU6JRWK=
ALL-PO NIrqfINIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M3rXNmlEPTB;MD6wN|E5PCEQvF2= NITrZ2pUSU6JRWK=
NKM-1 Ml\6S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MX\JR|UxRTBwMEe0NVYh|ryP M1vqZXNCVkeHUh?=
CGTH-W-1 MX\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NXrjeJZiUUN3ME2wMlI2ODJ{IN88US=> Ml6xV2FPT0WU
BB65-RCC NH[5OlVIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NVr2eHRiUUN3ME2wMlQ4ODd|IN88US=> NInSRpBUSU6JRWK=
NOS-1 MlXwS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M4\0fmlEPTB;MD61OlM3KM7:TR?= NXW3dZBVW0GQR1XS
SH-4 MknNS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NFz6Nm5KSzVyPUCuOlU3OTNizszN NH6yN2JUSU6JRWK=
HOP-62 NGX1SYNIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MYDJR|UxRTBwOEWwPFgh|ryP M1jlNXNCVkeHUh?=
HCC2998 MWfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MW\JR|UxRTBwOEi4NVgh|ryP MnT5V2FPT0WU
GDM-1 MlqwS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MlfXTWM2OD1yLkmwOlk5KM7:TR?= NWfIfnpxW0GQR1XS
KM12 MXfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MmPkTWM2OD1zLkCyNFk5KM7:TR?= M2\FRXNCVkeHUh?=
LB2518-MEL Ml;qS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M161NGlEPTB;MT6yNFgxQSEQvF2= NILTXGVUSU6JRWK=
NCI-H1436 NGLQTXlIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M{i3VWlEPTB;MT6yNVY4QCEQvF2= NEjwZY1USU6JRWK=
EM-2 MWnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NV;0TndmUUN3ME2xMlM2PTd6IN88US=> MWTTRW5ITVJ?
LAMA-84 Ml\pS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MX7JR|UxRTFwM{e2OFgh|ryP MVnTRW5ITVJ?
KG-1 NWj4TXk3T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M3[yUGlEPTB;MT60O|k{PSEQvF2= NWPnfpdPW0GQR1XS
A388 NWO3VGpyT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MmLyTWM2OD1zLkW5NVY2KM7:TR?= NXiwVZdQW0GQR1XS
no-10 MnLUS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? Mn7TTWM2OD1zLk[xO|I3KM7:TR?= M3LYV3NCVkeHUh?=
SF126 NIrPc|lIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MlnITWM2OD1zLk[zPFEzKM7:TR?= NUnHNZdRW0GQR1XS
MEG-01 NInyUGpIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NGrBdm9KSzVyPUGuPFA6QCEQvF2= M3jXbnNCVkeHUh?=
A3-KAW NYjC[ZdmT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M4T1U2lEPTB;MT64PFQzKM7:TR?= MXPTRW5ITVJ?
D-247MG NYLJTnZiT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M{TOU2lEPTB;Mj6xOFQ5KM7:TR?= MnPDV2FPT0WU
OVCAR-4 MorNS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MXLJR|UxRTJwMkGzPVMh|ryP MnfNV2FPT0WU
NCI-SNU-1 NWDpbWFST3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MXHJR|UxRTJwM{G2NkDPxE1? MXLTRW5ITVJ?
NCI-H2171 MlzPS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M1[3V2lEPTB;Mj6zPVc3PCEQvF2= NF7BWFFUSU6JRWK=
SIG-M5 NI\o[3VIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MWLJR|UxRTJwNEKyOFIh|ryP NIjWWIlUSU6JRWK=
BE-13 MlzTS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NGHoXlRKSzVyPUKuOlk3ODlizszN NGrT[XhUSU6JRWK=
K052 NF3mdnVIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= Moq5TWM2OD1{Lke0OlE3KM7:TR?= MmLiV2FPT0WU
L-540 NHjGWGVIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NGTzfXVKSzVyPUKuO|U4QDlizszN M2i5R3NCVkeHUh?=
KMOE-2 NVmw[FluT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NF3uelZKSzVyPUKuPFE{PSEQvF2= MnXwV2FPT0WU
MFH-ino MkjsS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NX;yTotvUUN3ME2yMlkzOTh3IN88US=> MlTpV2FPT0WU
HL-60 MlfiS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NGKx[GdKSzVyPUOuNFYzQTlizszN NHHaZWpUSU6JRWK=
HCC2218 M1q3O2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MkHaTWM2OD1|LkGyNFA{KM7:TR?= MXTTRW5ITVJ?
TE-5 NE\YSGxIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NXHL[ItvUUN3ME2zMlE{OTZ{IN88US=> M1G1W3NCVkeHUh?=
MZ1-PC NIr5SGhIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MYHJR|UxRTNwNEe1NFkh|ryP NEnYN2tUSU6JRWK=
MRK-nu-1 NFrWZZlIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MmHPTWM2OD1|Lk[xOFY5KM7:TR?= M1Kxd3NCVkeHUh?=
MZ7-mel NGLFcoJIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MWHJR|UxRTNwNk[wPVkh|ryP NVjnc5Q1W0GQR1XS
BC-1 Mk\mS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NWjTUmF[UUN3ME2zMlc1ODJizszN NULnfXlzW0GQR1XS
ST486 NEfje|FIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M{LmSWlEPTB;Mz64N|Y4OyEQvF2= MoHwV2FPT0WU
KS-1 NXLqOG5yT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NXXURm9EUUN3ME2zMlg5OTl6IN88US=> MlfsV2FPT0WU
SK-NEP-1 M3v2OGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MnS4TWM2OD12LkG2PFE2KM7:TR?= M4PkUXNCVkeHUh?=
BC-3 MlL6S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MXHJR|UxRTRwMkOzPVEh|ryP MVjTRW5ITVJ?
NCI-H1581 NYTETndCT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M2DBVGlEPTB;ND6yPFc6QCEQvF2= NWHCd|JRW0GQR1XS
MHH-PREB-1 NXTZcFk4T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NUXhXpBqUUN3ME20MlQxPDh2IN88US=> M1nGb3NCVkeHUh?=
NOMO-1 MmGzS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MoXLTWM2OD12LkS4PVA2KM7:TR?= NUn1TlhWW0GQR1XS
QIMR-WIL NYDmVlRjT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NF3ZRlZKSzVyPUWuNFczQTRizszN NX[5OWFIW0GQR1XS
SF539 Mn;mS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M3[wcWlEPTB;NT6xN|IzPyEQvF2= M{XyRnNCVkeHUh?=
TE-12 MXHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NYnQdYR7UUN3ME21MlI1QTJ7IN88US=> NYnm[ItYW0GQR1XS
NCI-H510A MUjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M13RPWlEPTB;NT60NVY5PSEQvF2= MY\TRW5ITVJ?
JAR M{LZbGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M4XVN2lEPTB;NT61NFgzPCEQvF2= NFjFXY9USU6JRWK=
no-11 M1H4Umdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 Mk\ITWM2OD13LkezOVY5KM7:TR?= M4XVRnNCVkeHUh?=
BV-173 M2W4[mdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NFvkN|ZKSzVyPUWuPVU3QDJizszN Ml2yV2FPT0WU
SR NHjXb5NIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NGTJZnlKSzVyPU[uNFA3PzhizszN MVrTRW5ITVJ?
MOLT-16 MkW5S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NWrTWW9QUUN3ME22MlI2OjZ4IN88US=> M{HV[nNCVkeHUh?=
MZ2-MEL NGDpbYFIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NYLPTpp[UUN3ME22MlMyQDN7IN88US=> NI\mOWFUSU6JRWK=
SW954 MUXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MkfLTWM2OD14LkS1PFY3KM7:TR?= M1LBNHNCVkeHUh?=
ML-2 MnzPS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NYCyNlJYUUN3ME22MlUzQDR7IN88US=> Ml\5V2FPT0WU
OCI-AML2 NInDPG1Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NV7tU|hJUUN3ME22MlYyODZ{IN88US=> MYPTRW5ITVJ?
SIMA NETxVolIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M17CVWlEPTB;Nz6wNFExOSEQvF2= NVXjeppOW0GQR1XS
DOHH-2 MV\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MV\JR|UxRTdwMEW2O|Yh|ryP MWrTRW5ITVJ?
697 MV\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M13VOGlEPTB;Nz6wOVk5QSEQvF2= MWrTRW5ITVJ?
NB1 NGDaZ4JIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NI\RO5lKSzVyPUeuOFA1ODdizszN NUfnUJlyW0GQR1XS
D-392MG NWLORm1XT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NHyyV5JKSzVyPUeuOlI3PjNizszN MUHTRW5ITVJ?
ES8 M4G5Nmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NFPGO5pKSzVyPUeuO|Y2ODNizszN NXOyZmR5W0GQR1XS
RPMI-8226 NXe2V|V1T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M{D0eWlEPTB;Nz64OFUyOSEQvF2= NV7w[I9sW0GQR1XS
IST-MEL1 MlHaS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? Mnv0TWM2OD16LkSwNFAzKM7:TR?= M{W5[nNCVkeHUh?=
NB14 MmDqS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NIHiWHVKSzVyPUiuOlMyOzNizszN Mkm4V2FPT0WU
HD-MY-Z MVHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MV\JR|UxRThwNkO3OFYh|ryP M2jv[XNCVkeHUh?=
TE-10 MljnS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NYDXO5VxUUN3ME24Mlc3OzV|IN88US=> NUnvenlIW0GQR1XS
LC-1F M{D2XGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NIL4Nm9KSzVyPUmuNVA5OzRizszN NWrZRWdxW0GQR1XS
OS-RC-2 NVv3cVNmT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M1zFVmlEPTB;OT6xNVI1OyEQvF2= M2faS3NCVkeHUh?=
NCI-SNU-16 MWrHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MmPBTWM2OD17LkKxNFI3KM7:TR?= MlqyV2FPT0WU
SHP-77 MlnES5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NILRXGhKSzVyPUmuO|E3PjJizszN Ml3hV2FPT0WU
A4-Fuk NHm2boNIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M2\1S2lEPTB;OT63OVYyKM7:TR?= MYDTRW5ITVJ?
NB6 M4HQS2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M4TXPWlEPTB;OT63OlAzQSEQvF2= M1mzV3NCVkeHUh?=
JiyoyeP-2003 NWjYVZZKT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= Ml\rTWM2OD1zMD60O|Q2KM7:TR?= MYjTRW5ITVJ?
DMS-114 MYnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MkD5TWM2OD1zMD61OFQyKM7:TR?= NXzzWVdLW0GQR1XS
NB7 M4PRemdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MmrpTWM2OD1zMD63OVI3KM7:TR?= NIPXUJJUSU6JRWK=
NCI-H747 MmHoS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NEDFOlhKSzVyPUGxMlEzOTZizszN MkfOV2FPT0WU
HH NULjXXhOT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NIH2cWlKSzVyPUGxMlM5PzZizszN MlfKV2FPT0WU
EW-18 MofzS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NYDwe4VRUUN3ME2xNU46ODR2IN88US=> MmTjV2FPT0WU
CHP-126 MUXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M17zZ2lEPTB;MUGuPVc{QCEQvF2= MnrVV2FPT0WU
NTERA-S-cl-D1 MnXES5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MmOyTWM2OD1zMj6wNlc5KM7:TR?= NXLwZXJEW0GQR1XS
DEL NX3MUJBIT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NHHvVYhKSzVyPUGyMlA6QDVizszN MWXTRW5ITVJ?
LU-139 MoXUS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MYjJR|UxRTF{LkW0NVMh|ryP NGfvOHBUSU6JRWK=
P30-OHK MofhS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MUPJR|UxRTF{LkW0O|kh|ryP M3r0c3NCVkeHUh?=
NCI-H1522 M{fnUGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NILUV4JKSzVyPUGyMlc1PiEQvF2= NWPZUmV1W0GQR1XS
NCI-H1299 MkDuS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MlTBTWM2OD1zMz6yPVEyKM7:TR?= NUjCN2w4W0GQR1XS
UACC-257 MV\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NHzweW9KSzVyPUGzMlUyOjZizszN M{HaSnNCVkeHUh?=
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NCI-H2196 NVHuSWc{T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NIrxb4lKSzVyPUOzMlI2PTdizszN MXvTRW5ITVJ?
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A253 NGrmZVJIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MVLJR|UxRTN2LkKyPVYh|ryP NF3aTGFUSU6JRWK=
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NCI-H1963 M{HFcGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MXPJR|UxRTN3LkOwO|Ih|ryP MoXJV2FPT0WU
MMAC-SF MWjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NXy2VGx2UUN3ME2zOU45Pzh3IN88US=> NFHJRXZUSU6JRWK=
LB831-BLC Mo[wS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MWXJR|UxRTN4LkC2OVQh|ryP M1jTSHNCVkeHUh?=
WSU-NHL NWLFNFdWT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MVrJR|UxRTN4LkG2OEDPxE1? MoDSV2FPT0WU
CESS M{Wzemdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M1ftdGlEPTB;M{[uNlg1QCEQvF2= M336[HNCVkeHUh?=
NEC8 Mm\4S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NY[zb5I3UUN3ME2zOk42QDN3IN88US=> NYPZ[HhsW0GQR1XS
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MHH-CALL-2 Mn\VS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M4jFNGlEPTB;M{euNVgzOSEQvF2= NEPKOYtUSU6JRWK=
K5 MWHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NFrrZYJKSzVyPUO4MlQ{KM7:TR?= Mm\KV2FPT0WU
CP66-MEL MmXwS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NGrMdIVKSzVyPUO5MlA4OzNizszN NEnmV2JUSU6JRWK=
OPM-2 Mmj0S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M{fzXWlEPTB;M{muPFQ{OiEQvF2= M2nTdnNCVkeHUh?=
IST-MES1 M1X1[mdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NViyVmpsUUN3ME20NE4{ODl4IN88US=> MnPkV2FPT0WU
EC-GI-10 Mnv0S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NXPMW294UUN3ME20NU42QDB3IN88US=> M3\nbnNCVkeHUh?=
CTV-1 NIf4fINIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MXrJR|UxRTR{Lki0NFYh|ryP NYfWc|BFW0GQR1XS
DG-75 M1LJ[2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MYXJR|UxRTR|Lke1PVUh|ryP NX3WUnc6W0GQR1XS
KNS-81-FD NGnhZWRIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M3voN2lEPTB;NEWuOFA2QCEQvF2= MV3TRW5ITVJ?
NCI-H82 NFf1SVZIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NYXRdVNbUUN3ME20OU42PzV6IN88US=> NFv6VWhUSU6JRWK=
RPMI-8866 MXzHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M4rTemlEPTB;NE[uNVg4OyEQvF2= M13PcXNCVkeHUh?=
ACN NEnYWFdIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NVTDfVdQUUN3ME20Ok41OzRizszN Mn7GV2FPT0WU
NCI-H1395 NEnyV4dIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NE\jTphKSzVyPUS2MlQ4PTZizszN M1fabnNCVkeHUh?=
NCI-H209 MXTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M4DmU2lEPTB;NEeuNVQxPSEQvF2= NV3UdFBiW0GQR1XS
TGW MUPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MWLJR|UxRTR7LkC3PVEh|ryP MUnTRW5ITVJ?
NCI-H748 Ml3yS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M{XVTGlEPTB;NEmuOFc2OyEQvF2= MoftV2FPT0WU
EKVX MXLHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NUDiUHdEUUN3ME20PU43PjJ6IN88US=> MmXZV2FPT0WU

... 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
NCT03468231 Recruiting Hepatocellular Carcinoma Sun Yat-sen University|First Affiliated Hospital Sun Yat-Sen University|Dongguan People''s Hospital|Kaiping Central Hospital|First Affiliated Hospital Xi''an Jiaotong University|Guangzhou Twelfth People ''s Hospital|The First Affiliated Hospital of University of South China March 9 2018 Phase 3
NCT02616692 Completed Hepatocellular Cancer Bayer May 9 2016 --
NCT01751763 Completed Carcinoma Hepatocellular Bayer July 9 2013 --
NCT02530476 Active not recruiting Leukemia|Acute Myeloid Leukemia M.D. Anderson Cancer Center|Karyopharm Therapeutics Inc|National Cancer Institute (NCI) December 8 2015 Phase 1|Phase 2
NCT02303444 Active not recruiting Thyroid Neoplasms Bayer April 8 2015 --
NCT01258608 Completed Carcinoma Hepatocellular Human Genome Sciences Inc. a GSK Company|GlaxoSmithKline February 8 2011 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