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 MlzGS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M4jVRmlEPTB;MD6wNFAxODNyMzFOwG0> NW\HXmdWW0GQR1XS
MONO-MAC-6 NWXKWWk5T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MmLWTWM2OD1yLkCwOFE5KM7:TR?= MVjTRW5ITVJ?
ALL-PO NUTnTJJxT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NFHNUYxKSzVyPUCuNFMyQDRizszN M3zjXHNCVkeHUh?=
NKM-1 NF3Z[29Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M1jvS2lEPTB;MD6wO|QyPiEQvF2= NWSxPIdFW0GQR1XS
CGTH-W-1 NH31cJBIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NWKwVpNyUUN3ME2wMlI2ODJ{IN88US=> MoHMV2FPT0WU
BB65-RCC NW\id|loT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NWL3RpRSUUN3ME2wMlQ4ODd|IN88US=> NXTzepZFW0GQR1XS
NOS-1 MoDXS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MnL1TWM2OD1yLkW2N|Yh|ryP NHjWZ41USU6JRWK=
SH-4 MYTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NXHFZ2tzUUN3ME2wMlY2PjF|IN88US=> NGWwVIdUSU6JRWK=
HOP-62 NFPLNYdIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= Mn3CTWM2OD1yLki1NFg5KM7:TR?= NXfsRXFDW0GQR1XS
HCC2998 M3T3Nmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NF:xbnVKSzVyPUCuPFg5OThizszN NXHSSVRRW0GQR1XS
GDM-1 NYDrOFR3T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MXnJR|UxRTBwOUC2PVgh|ryP MX\TRW5ITVJ?
KM12 NGDB[HRIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M3PPN2lEPTB;MT6wNlA6QCEQvF2= MYXTRW5ITVJ?
LB2518-MEL MYrHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? Mm\sTWM2OD1zLkKwPFA6KM7:TR?= NUnUUZJSW0GQR1XS
NCI-H1436 MnvmS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NXHVVmRyUUN3ME2xMlIyPjd6IN88US=> MknkV2FPT0WU
EM-2 Mn\LS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MVvJR|UxRTFwM{W1O|gh|ryP M4rBTXNCVkeHUh?=
LAMA-84 MUTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NX7hO3c3UUN3ME2xMlM4PjR6IN88US=> MUfTRW5ITVJ?
KG-1 NHPSWWdIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MnSyTWM2OD1zLkS3PVM2KM7:TR?= NIT5VIJUSU6JRWK=
A388 NYDLOnJYT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M{O4dmlEPTB;MT61PVE3PSEQvF2= MlTvV2FPT0WU
no-10 M17URmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NGPhe3BKSzVyPUGuOlE4OjZizszN NHPKS3pUSU6JRWK=
SF126 MVjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M1vXNWlEPTB;MT62N|gyOiEQvF2= M3u0[3NCVkeHUh?=
MEG-01 NGrRXFdIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NV\UT2d1UUN3ME2xMlgxQThizszN MlziV2FPT0WU
A3-KAW MU\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MofjTWM2OD1zLki4OFIh|ryP NVraVY97W0GQR1XS
D-247MG M{jBcmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NFLtTFVKSzVyPUKuNVQ1QCEQvF2= MnH4V2FPT0WU
OVCAR-4 MU\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MlrYTWM2OD1{LkKxN|k{KM7:TR?= MVTTRW5ITVJ?
NCI-SNU-1 MmezS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M{\iWGlEPTB;Mj6zNVYzKM7:TR?= NVTRUmUzW0GQR1XS
NCI-H2171 M3\Ic2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M1nlRWlEPTB;Mj6zPVc3PCEQvF2= MkXDV2FPT0WU
SIG-M5 MXHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MmCwTWM2OD1{LkSyNlQzKM7:TR?= MmnQV2FPT0WU
BE-13 NF\ZT3hIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NHv1eVRKSzVyPUKuOlk3ODlizszN NFrke2ZUSU6JRWK=
K052 MmrSS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NXSzXGpQUUN3ME2yMlc1PjF4IN88US=> MV\TRW5ITVJ?
L-540 MmDSS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MlvKTWM2OD1{Lke1O|g6KM7:TR?= MnHrV2FPT0WU
KMOE-2 MmLrS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NFvBRotKSzVyPUKuPFE{PSEQvF2= NH3FfHdUSU6JRWK=
MFH-ino NV7sNXhVT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NIKyfG5KSzVyPUKuPVIyQDVizszN MkjYV2FPT0WU
HL-60 M1\Zbmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MWjJR|UxRTNwME[yPVkh|ryP MVLTRW5ITVJ?
HCC2218 NIHUd5dIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NHu4OItKSzVyPUOuNVIxODNizszN NULOeo9oW0GQR1XS
TE-5 NVPl[GI3T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NFjC[2RKSzVyPUOuNVMyPjJizszN MlzHV2FPT0WU
MZ1-PC M{DFOGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MoeyTWM2OD1|LkS3OVA6KM7:TR?= MkXjV2FPT0WU
MRK-nu-1 NXnIdodjT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NHLKUlJKSzVyPUOuOlE1PjhizszN NYTXRmpGW0GQR1XS
MZ7-mel MX\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NFXidHJKSzVyPUOuOlYxQTlizszN MkHHV2FPT0WU
BC-1 NHjVXWRIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M3;TcWlEPTB;Mz63OFAzKM7:TR?= M{foNHNCVkeHUh?=
ST486 NIPRSotIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NULURW9qUUN3ME2zMlg{Pjd|IN88US=> MYDTRW5ITVJ?
KS-1 MWTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NUPJbo43UUN3ME2zMlg5OTl6IN88US=> NYnucldSW0GQR1XS
SK-NEP-1 MUPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NVjyTYYzUUN3ME20MlE3QDF3IN88US=> NYHFRWV[W0GQR1XS
BC-3 MX\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NEnDdFVKSzVyPUSuNlM{QTFizszN Mlj0V2FPT0WU
NCI-H1581 MXPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MoXqTWM2OD12LkK4O|k5KM7:TR?= MlnzV2FPT0WU
MHH-PREB-1 NVGwVVl5T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NGmzeINKSzVyPUSuOFA1QDRizszN MYrTRW5ITVJ?
NOMO-1 M1vPZWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MVLJR|UxRTRwNEi5NFUh|ryP MnfBV2FPT0WU
QIMR-WIL MVTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MnLTTWM2OD13LkC3Nlk1KM7:TR?= NU\w[2JMW0GQR1XS
SF539 MnnDS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MkfiTWM2OD13LkGzNlI4KM7:TR?= NFfuW3BUSU6JRWK=
TE-12 M32wUWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M2XEN2lEPTB;NT6yOFkzQSEQvF2= MVXTRW5ITVJ?
NCI-H510A NEP6XnJIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MUjJR|UxRTVwNEG2PFUh|ryP Mnq5V2FPT0WU
JAR M4LFemdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NFrlXYFKSzVyPUWuOVA5OjRizszN MX;TRW5ITVJ?
no-11 NHzwbXJIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MmXJTWM2OD13LkezOVY5KM7:TR?= MkSxV2FPT0WU
BV-173 MUPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MWjJR|UxRTVwOUW2PFIh|ryP MYrTRW5ITVJ?
SR NFnpNZpIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MYfJR|UxRTZwMEC2O|gh|ryP NV7nSnl5W0GQR1XS
MOLT-16 M1;wTGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NIKwbVlKSzVyPU[uNlUzPjZizszN MkLpV2FPT0WU
MZ2-MEL M2TSRWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M3P2U2lEPTB;Nj6zNVg{QSEQvF2= Mkf2V2FPT0WU
SW954 NHLnfm1Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= Mk\kTWM2OD14LkS1PFY3KM7:TR?= NF\sblFUSU6JRWK=
ML-2 M3O0S2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 Mnj0TWM2OD14LkWyPFQ6KM7:TR?= M2PEU3NCVkeHUh?=
OCI-AML2 NFnIcJVIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NHfPblBKSzVyPU[uOlExPjJizszN MVvTRW5ITVJ?
SIMA NYfsXZBzT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MYPJR|UxRTdwMECxNFEh|ryP MnTkV2FPT0WU
DOHH-2 NVP0S2dRT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MXXJR|UxRTdwMEW2O|Yh|ryP M1HCOnNCVkeHUh?=
697 MXfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M3X1fWlEPTB;Nz6wOVk5QSEQvF2= MV;TRW5ITVJ?
NB1 NHfHOINIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NX\rfmpJUUN3ME23MlQxPDB5IN88US=> NI\yUZlUSU6JRWK=
D-392MG MmToS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NW\6UYN4UUN3ME23MlYzPjZ|IN88US=> M1[xVnNCVkeHUh?=
ES8 MlrpS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NYLiVINMUUN3ME23Mlc3PTB|IN88US=> MoHSV2FPT0WU
RPMI-8226 NH;VeWVIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NVPTdJlqUUN3ME23Mlg1PTFzIN88US=> NGjtbY1USU6JRWK=
IST-MEL1 NEGzTXRIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NXPVZlJkUUN3ME24MlQxODB{IN88US=> MXLTRW5ITVJ?
NB14 NUDnWHQxT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NG\1b4pKSzVyPUiuOlMyOzNizszN MVvTRW5ITVJ?
HD-MY-Z NWLaUJVlT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M4XxfmlEPTB;OD62N|c1PiEQvF2= NEDndYhUSU6JRWK=
TE-10 M3e2emdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 Mn3aTWM2OD16Lke2N|U{KM7:TR?= NVvsU4xLW0GQR1XS
LC-1F NG\HeXVIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M2PrZ2lEPTB;OT6xNFg{PCEQvF2= NUDhSmhQW0GQR1XS
OS-RC-2 NInRdppIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NUPlRlZPUUN3ME25MlEyOjR|IN88US=> MXjTRW5ITVJ?
NCI-SNU-16 M1\CNGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MX7JR|UxRTlwMkGwNlYh|ryP NYqyN3FCW0GQR1XS
SHP-77 NX\0S|lCT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NUTQVYd3UUN3ME25MlcyPjZ{IN88US=> M1HIUHNCVkeHUh?=
A4-Fuk NEnMcXpIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MlHnTWM2OD17Lke1OlEh|ryP Mn\NV2FPT0WU
NB6 MoDBS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MnTpTWM2OD17Lke2NFI6KM7:TR?= M3m5eXNCVkeHUh?=
JiyoyeP-2003 MmPvS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MlrMTWM2OD1zMD60O|Q2KM7:TR?= NGSybYtUSU6JRWK=
DMS-114 NVjCbI9OT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NVi1dFdSUUN3ME2xNE42PDRzIN88US=> M3jTPXNCVkeHUh?=
NB7 M2fPcmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MlTiTWM2OD1zMD63OVI3KM7:TR?= MlvSV2FPT0WU
NCI-H747 NF\6dXJIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MXjJR|UxRTFzLkGyNVYh|ryP M2jlOnNCVkeHUh?=
HH NXfISmhzT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MoLtTWM2OD1zMT6zPFc3KM7:TR?= MWjTRW5ITVJ?
EW-18 NVXQTllTT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NGPTcG1KSzVyPUGxMlkxPDRizszN M3vxOHNCVkeHUh?=
CHP-126 NUnxTI9qT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MUXJR|UxRTFzLkm3N|gh|ryP MXrTRW5ITVJ?
NTERA-S-cl-D1 NIn5UndIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NVHBNnp2UUN3ME2xNk4xOjd6IN88US=> M3fQUXNCVkeHUh?=
DEL MVzHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NHH4e|dKSzVyPUGyMlA6QDVizszN M33SbnNCVkeHUh?=
LU-139 NHnYTYxIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NXSwcVVTUUN3ME2xNk42PDF|IN88US=> M1TpdnNCVkeHUh?=
P30-OHK NW\UZoNHT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MmTSTWM2OD1zMj61OFc6KM7:TR?= NYnzSpRZW0GQR1XS
NCI-H1522 MWjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MoThTWM2OD1zMj63OFYh|ryP MULTRW5ITVJ?
NCI-H1299 M4L0PWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MYfJR|UxRTF|LkK5NVEh|ryP NILic|dUSU6JRWK=
UACC-257 Ml74S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NWnGVnJXUUN3ME2xN{42OTJ4IN88US=> NWTWRm1NW0GQR1XS
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A253 NF3KZ3lIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M2OzNWlEPTB;M{SuNlI6PiEQvF2= M{jrfHNCVkeHUh?=
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NCI-H1963 MVHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MmDUTWM2OD1|NT6zNFczKM7:TR?= NEH2SmZUSU6JRWK=
MMAC-SF MoTuS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NUntXpRTUUN3ME2zOU45Pzh3IN88US=> MnX2V2FPT0WU
LB831-BLC NHWwbodIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NVzzV5VoUUN3ME2zOk4xPjV2IN88US=> MoO0V2FPT0WU
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CESS NInseZVIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= Ml\6TWM2OD1|Nj6yPFQ5KM7:TR?= MlXTV2FPT0WU
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K5 MlvSS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MVnJR|UxRTN6LkSzJO69VQ>? NFj0[Y1USU6JRWK=
CP66-MEL NGXmbGZIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NX7kd45NUUN3ME2zPU4xPzN|IN88US=> NVvsRod1W0GQR1XS
OPM-2 MoS0S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NEnrdWRKSzVyPUO5Mlg1OzJizszN MXnTRW5ITVJ?
IST-MES1 M4fuRmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MUnJR|UxRTRyLkOwPVYh|ryP Mn;SV2FPT0WU
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CTV-1 MkLSS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MUPJR|UxRTR{Lki0NFYh|ryP NVHoUlR2W0GQR1XS
DG-75 MmnXS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MnzqTWM2OD12Mz63OVk2KM7:TR?= M{i4eXNCVkeHUh?=
KNS-81-FD M13xXWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MmPETWM2OD12NT60NFU5KM7:TR?= Mnf6V2FPT0WU
NCI-H82 MnPMS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? Moj2TWM2OD12NT61O|U5KM7:TR?= NHz2ZmJUSU6JRWK=
RPMI-8866 MnjBS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MkPRTWM2OD12Nj6xPFc{KM7:TR?= MYLTRW5ITVJ?
ACN NVz4WYdVT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M{D2SGlEPTB;NE[uOFM1KM7:TR?= NVP5[XhpW0GQR1XS
NCI-H1395 M4HKcmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NHPMVGFKSzVyPUS2MlQ4PTZizszN MnLMV2FPT0WU
NCI-H209 NXf5fGZNT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M1rjWGlEPTB;NEeuNVQxPSEQvF2= MnPJV2FPT0WU
TGW MUDHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MWjJR|UxRTR7LkC3PVEh|ryP MlvOV2FPT0WU
NCI-H748 Mon1S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? Mne1TWM2OD12OT60O|U{KM7:TR?= MkDhV2FPT0WU
EKVX Mo\rS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M3voO2lEPTB;NEmuOlYzQCEQvF2= NEHtd2FUSU6JRWK=

... 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 individually and in order:
5% DMSO+45% PEG 400+ddH2O
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