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 NWPXVmg6T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MUfJR|UxRTBwMECwNFA{ODNizszN MXLTRW5ITVJ?
MONO-MAC-6 MmrhS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NH\0U3NKSzVyPUCuNFA1OThizszN MoPVV2FPT0WU
ALL-PO MXPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MULJR|UxRTBwMEOxPFQh|ryP M3v4[nNCVkeHUh?=
NKM-1 MU\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NVzF[HY6UUN3ME2wMlA4PDF4IN88US=> M36wSXNCVkeHUh?=
CGTH-W-1 NH\adHhIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M1roR2lEPTB;MD6yOVAzOiEQvF2= MWDTRW5ITVJ?
BB65-RCC NUnwVVFWT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M{XROGlEPTB;MD60O|A4OyEQvF2= NFTPbmJUSU6JRWK=
NOS-1 MoDnS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M{nGWmlEPTB;MD61OlM3KM7:TR?= NYX5NVdZW0GQR1XS
SH-4 Mk\xS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NYL0N41[UUN3ME2wMlY2PjF|IN88US=> MWrTRW5ITVJ?
HOP-62 NYDtc|F[T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MVXJR|UxRTBwOEWwPFgh|ryP MmfQV2FPT0WU
HCC2998 MV;Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NVvme4hRUUN3ME2wMlg5QDF6IN88US=> NVfne|RwW0GQR1XS
GDM-1 NF7BRWxIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NF71UpBKSzVyPUCuPVA3QThizszN NWT4S5pGW0GQR1XS
KM12 M2TQcGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MVzJR|UxRTFwMEKwPVgh|ryP NUPBc446W0GQR1XS
LB2518-MEL MnHkS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M1vzUWlEPTB;MT6yNFgxQSEQvF2= NX\4[WNqW0GQR1XS
NCI-H1436 M33Mbmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NGjUWZJKSzVyPUGuNlE3PzhizszN NUmzVJlYW0GQR1XS
EM-2 M3PsUGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NWjv[2I2UUN3ME2xMlM2PTd6IN88US=> NH;lPI5USU6JRWK=
LAMA-84 M1;md2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NHr2RZlKSzVyPUGuN|c3PDhizszN M1[2cHNCVkeHUh?=
KG-1 MWTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? Mn;lTWM2OD1zLkS3PVM2KM7:TR?= NFzBU2xUSU6JRWK=
A388 NX21UGIxT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NHLRWFZKSzVyPUGuOVkyPjVizszN NWrTdJF5W0GQR1XS
no-10 M{nwfWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NG[0WndKSzVyPUGuOlE4OjZizszN MWXTRW5ITVJ?
SF126 M4W0e2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M4Pse2lEPTB;MT62N|gyOiEQvF2= NXXWZoZXW0GQR1XS
MEG-01 NW[3eVdnT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NWexSpRXUUN3ME2xMlgxQThizszN M3zHUHNCVkeHUh?=
A3-KAW NUPTPZFET3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NYHlbWtWUUN3ME2xMlg5PDJizszN M1vLVnNCVkeHUh?=
D-247MG MV3Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MoiyTWM2OD1{LkG0OFgh|ryP NFjoTnRUSU6JRWK=
OVCAR-4 NH61cHJIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NF60NopKSzVyPUKuNlE{QTNizszN M3PkRXNCVkeHUh?=
NCI-SNU-1 NVnUbFV3T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M4\qemlEPTB;Mj6zNVYzKM7:TR?= MojRV2FPT0WU
NCI-H2171 NHzPc5ZIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M{O3[2lEPTB;Mj6zPVc3PCEQvF2= MmrjV2FPT0WU
SIG-M5 M4rsUGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 Ml;nTWM2OD1{LkSyNlQzKM7:TR?= MlXtV2FPT0WU
BE-13 M{TOWGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NFHQXFZKSzVyPUKuOlk3ODlizszN M3rZXnNCVkeHUh?=
K052 NH7rS4RIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M3:wXmlEPTB;Mj63OFYyPiEQvF2= MmjhV2FPT0WU
L-540 MW\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M4LoXGlEPTB;Mj63OVc5QSEQvF2= MUDTRW5ITVJ?
KMOE-2 MYDHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MVLJR|UxRTJwOEGzOUDPxE1? NFS4fIRUSU6JRWK=
MFH-ino M3fYSGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MmjlTWM2OD1{LkmyNVg2KM7:TR?= Ml7LV2FPT0WU
HL-60 MmTaS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NILkbmFKSzVyPUOuNFYzQTlizszN NFvWOW9USU6JRWK=
HCC2218 M{TX[mdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NVvsSYRXUUN3ME2zMlEzODB|IN88US=> NWLHNGZRW0GQR1XS
TE-5 NWLRcm8{T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= Mn;QTWM2OD1|LkGzNVYzKM7:TR?= NYnN[no3W0GQR1XS
MZ1-PC NHL5[VVIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M{XkN2lEPTB;Mz60O|UxQSEQvF2= MYTTRW5ITVJ?
MRK-nu-1 NVjibYdZT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NXvlb2J7UUN3ME2zMlYyPDZ6IN88US=> M1P5dHNCVkeHUh?=
MZ7-mel MlvCS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NFfHU4pKSzVyPUOuOlYxQTlizszN Mn3KV2FPT0WU
BC-1 MVnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NIDYclVKSzVyPUOuO|QxOiEQvF2= MXnTRW5ITVJ?
ST486 M{DGV2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NIXuNpFKSzVyPUOuPFM3PzNizszN MXHTRW5ITVJ?
KS-1 MoLKS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M{f2NmlEPTB;Mz64PFE6QCEQvF2= M3m5d3NCVkeHUh?=
SK-NEP-1 M17EdWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M2rScWlEPTB;ND6xOlgyPSEQvF2= MlSzV2FPT0WU
BC-3 MXzHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M{\KR2lEPTB;ND6yN|M6OSEQvF2= NXWwSpN4W0GQR1XS
NCI-H1581 MULHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M1HZ[WlEPTB;ND6yPFc6QCEQvF2= M4H0dHNCVkeHUh?=
MHH-PREB-1 MnXCS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NXTES3RiUUN3ME20MlQxPDh2IN88US=> M1:yWnNCVkeHUh?=
NOMO-1 NIjwdFZIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NYjFfXNiUUN3ME20MlQ5QTB3IN88US=> M1LaSXNCVkeHUh?=
QIMR-WIL MYHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MVTJR|UxRTVwMEeyPVQh|ryP MnfYV2FPT0WU
SF539 M2nQVGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NWLNSW81UUN3ME21MlE{OjJ5IN88US=> NVfaS4JyW0GQR1XS
TE-12 NWXObIRKT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NVzVW2EyUUN3ME21MlI1QTJ7IN88US=> NHfhZppUSU6JRWK=
NCI-H510A MWLHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MorSTWM2OD13LkSxOlg2KM7:TR?= MU\TRW5ITVJ?
JAR NVzSZVRvT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NYHnTHh4UUN3ME21MlUxQDJ2IN88US=> NVPFbYVbW0GQR1XS
no-11 M1;ZUmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MYLJR|UxRTVwN{O1Olgh|ryP Mn;rV2FPT0WU
BV-173 MnHNS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NVXaUZp5UUN3ME21Mlk2Pjh{IN88US=> NGrKZ5hUSU6JRWK=
SR NILqV2tIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NV7a[lduUUN3ME22MlAxPjd6IN88US=> MVPTRW5ITVJ?
MOLT-16 NID4W2lIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NWLyfmhtUUN3ME22MlI2OjZ4IN88US=> NUTESoNjW0GQR1XS
MZ2-MEL MUTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NIjnfY1KSzVyPU[uN|E5OzlizszN MX7TRW5ITVJ?
SW954 NVzIUolzT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MVfJR|UxRTZwNEW4OlYh|ryP NGf1OGVUSU6JRWK=
ML-2 NF3pR|hIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MXTJR|UxRTZwNUK4OFkh|ryP NGfYeGRUSU6JRWK=
OCI-AML2 MmOzS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MYrJR|UxRTZwNkGwOlIh|ryP MnrvV2FPT0WU
SIMA NUnwR3FsT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MVfJR|UxRTdwMECxNFEh|ryP Mn;CV2FPT0WU
DOHH-2 NEnaVG5Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NFjkNWJKSzVyPUeuNFU3PzZizszN Mo\1V2FPT0WU
697 NGPGZmJIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M3nQc2lEPTB;Nz6wOVk5QSEQvF2= NUnPSVJ{W0GQR1XS
NB1 MorQS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M1y5eGlEPTB;Nz60NFQxPyEQvF2= Mn73V2FPT0WU
D-392MG M4LzO2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NXPKO3o5UUN3ME23MlYzPjZ|IN88US=> MV3TRW5ITVJ?
ES8 MUjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NFTpeYhKSzVyPUeuO|Y2ODNizszN NEX0OlJUSU6JRWK=
RPMI-8226 NV3hWmx2T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M1fBbWlEPTB;Nz64OFUyOSEQvF2= MWPTRW5ITVJ?
IST-MEL1 NHvlXoxIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NF7F[ohKSzVyPUiuOFAxODJizszN NGiyWXJUSU6JRWK=
NB14 Mk[yS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NGn3SoRKSzVyPUiuOlMyOzNizszN MnzzV2FPT0WU
HD-MY-Z NV32W5lCT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NFnhUlNKSzVyPUiuOlM4PDZizszN NVvSRXlrW0GQR1XS
TE-10 NEL3[oxIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NIizb5ZKSzVyPUiuO|Y{PTNizszN NXzuV4plW0GQR1XS
LC-1F M17rNmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MknSTWM2OD17LkGwPFM1KM7:TR?= MYnTRW5ITVJ?
OS-RC-2 Mnr6S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NW\Vcmh[UUN3ME25MlEyOjR|IN88US=> NEHJOXpUSU6JRWK=
NCI-SNU-16 MnjYS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MnLVTWM2OD17LkKxNFI3KM7:TR?= M{TmOnNCVkeHUh?=
SHP-77 MV\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NV7iVI16UUN3ME25MlcyPjZ{IN88US=> MnH5V2FPT0WU
A4-Fuk NIjhSGRIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NUW2c3JuUUN3ME25Mlc2PjFizszN NHP2Ro9USU6JRWK=
NB6 M4Pabmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MnLLTWM2OD17Lke2NFI6KM7:TR?= MYTTRW5ITVJ?
JiyoyeP-2003 MkLqS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M1O2SmlEPTB;MUCuOFc1PSEQvF2= MUfTRW5ITVJ?
DMS-114 M1ez[mdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M3LWcmlEPTB;MUCuOVQ1OSEQvF2= MoD6V2FPT0WU
NB7 M3X3ZWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NXXue3hjUUN3ME2xNE44PTJ4IN88US=> MoHMV2FPT0WU
NCI-H747 MWLHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NXriRnBWUUN3ME2xNU4yOjF4IN88US=> M2rtWXNCVkeHUh?=
HH M{PMOmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NHuyNZdKSzVyPUGxMlM5PzZizszN MY\TRW5ITVJ?
EW-18 M3LLO2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MU\JR|UxRTFzLkmwOFQh|ryP MXPTRW5ITVJ?
CHP-126 MVvHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NWfvOYF[UUN3ME2xNU46PzN6IN88US=> M3LwfnNCVkeHUh?=
NTERA-S-cl-D1 MoH5S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MojDTWM2OD1zMj6wNlc5KM7:TR?= M1jhcnNCVkeHUh?=
DEL NV7LbIs3T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NIPrWJBKSzVyPUGyMlA6QDVizszN NFvS[VhUSU6JRWK=
LU-139 NHHE[HpIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MoLVTWM2OD1zMj61OFE{KM7:TR?= NXj2clB2W0GQR1XS
P30-OHK MoO4S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MlLlTWM2OD1zMj61OFc6KM7:TR?= MlruV2FPT0WU
NCI-H1522 NGTOZ4tIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NXrMR5hUUUN3ME2xNk44PDZizszN M2riWHNCVkeHUh?=
NCI-H1299 NE[yWmRIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MorsTWM2OD1zMz6yPVEyKM7:TR?= MmLzV2FPT0WU
UACC-257 NXLyOllXT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MnTWTWM2OD1zMz61NVI3KM7:TR?= NWm3Z2VbW0GQR1XS
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K-562 NYfaeppPT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MVvJR|UxRTF6LkexOFMh|ryP NGHmRlBUSU6JRWK=
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ECC12 MoDES5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M3q3XmlEPTB;MkSuNlgxOyEQvF2= M1K5PXNCVkeHUh?=
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DJM-1 M3rRUmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NWLrNVlNUUN3ME2yOE42OjJzIN88US=> MYDTRW5ITVJ?
DMS-153 MYPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MXPJR|UxRTJ2Lki2NVQh|ryP NF\SfGVUSU6JRWK=
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SK-N-DZ NXLuW4Y4T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NVKxOoFLUUN3ME2yOk4{PDF2IN88US=> MkDXV2FPT0WU
COR-L88 NEf1XWhIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NVzjN5FyUUN3ME2yOk42Pzl4IN88US=> NWTqXm96W0GQR1XS
LU-65 NH24Z4NIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MV;JR|UxRTJ4Lki1N|Uh|ryP NWH6W4JmW0GQR1XS
TGBC1TKB NIfVbXhIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MWrJR|UxRTJ4Lkm4Nlgh|ryP M4fGVnNCVkeHUh?=
THP-1 NGrBUXlIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NFu4N3lKSzVyPUK3MlIyPDFizszN NYTqXndIW0GQR1XS
ONS-76 M1fPOWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NGLYdYNKSzVyPUK3MlM{OiEQvF2= M1jORnNCVkeHUh?=
LC-2-ad NF:wbHZIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MVvJR|UxRTJ5Lk[yN|Eh|ryP MmD5V2FPT0WU
EW-13 NG[yNmVIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NV\ZXIUxUUN3ME2yPU4yPzR4IN88US=> M4fsU3NCVkeHUh?=
MS-1 MlrPS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M2G4b2lEPTB;M{CuO|I4QCEQvF2= MmflV2FPT0WU
NCI-H2227 M1f4emdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MnP2TWM2OD1|MD65PFA3KM7:TR?= NF:1d5pUSU6JRWK=
LXF-289 NHiyZlBIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MUPJR|UxRTNzLkS0PVIh|ryP M3mxbXNCVkeHUh?=
MC116 MlLQS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NEPEUnFKSzVyPUOyMlA5OjZizszN M1XWenNCVkeHUh?=
EVSA-T MkTpS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M3PuV2lEPTB;M{KuNlU5PSEQvF2= MlrMV2FPT0WU
CTB-1 Ml3iS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NGnkVY1KSzVyPUOzMlEyODFizszN MX7TRW5ITVJ?
COLO-320-HSR MmjsS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MV;JR|UxRTN|LkG2NFMh|ryP M2\ZUnNCVkeHUh?=
NCI-H2196 MlPlS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MX7JR|UxRTN|LkK1OVch|ryP NEixflNUSU6JRWK=
LB2241-RCC NGrQboNIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= Mn24TWM2OD1|Mz6zNVM2KM7:TR?= MnX5V2FPT0WU
LS-513 NFjPdVZIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MlTKTWM2OD1|Mz64OlM5KM7:TR?= M3zQOHNCVkeHUh?=
LP-1 Ml;3S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MULJR|UxRTN|Lkm5OVYh|ryP MXfTRW5ITVJ?
A253 MXfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M33zSWlEPTB;M{SuNlI6PiEQvF2= NWi4fGxMW0GQR1XS
SK-MM-2 NUTDRXJtT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NVPKNI1CUUN3ME2zOE46PDVzIN88US=> NIPOZ3hUSU6JRWK=
NCI-H1963 MoHmS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MnTaTWM2OD1|NT6zNFczKM7:TR?= NU\YZ4E4W0GQR1XS
MMAC-SF MkW4S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NXrVcIprUUN3ME2zOU45Pzh3IN88US=> MofnV2FPT0WU
LB831-BLC NIjYdoNIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M4PEbWlEPTB;M{[uNFY2PCEQvF2= NIDnSIlUSU6JRWK=
WSU-NHL NUHKboU1T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M3jZd2lEPTB;M{[uNVY1KM7:TR?= M4TxdXNCVkeHUh?=
CESS NGrjW4JIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M3LuVWlEPTB;M{[uNlg1QCEQvF2= MlmxV2FPT0WU
NEC8 MVXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MlztTWM2OD1|Nj61PFM2KM7:TR?= MXTTRW5ITVJ?
KNS-42 M4LQR2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NVnaVGw3UUN3ME2zO{4yOjN5IN88US=> NXPUT|MzW0GQR1XS
MHH-CALL-2 NGGxfXpIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NX7BNXhMUUN3ME2zO{4yQDJzIN88US=> NH7y[nhUSU6JRWK=
K5 NFnWOZVIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= Mof0TWM2OD1|OD60N{DPxE1? M3TYO3NCVkeHUh?=
CP66-MEL MkL0S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MWfJR|UxRTN7LkC3N|Mh|ryP M1ryeHNCVkeHUh?=
OPM-2 MmDvS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M4faZWlEPTB;M{muPFQ{OiEQvF2= NYfVTmhKW0GQR1XS
IST-MES1 NEPncW1Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NF;yNlJKSzVyPUSwMlMxQTZizszN MUTTRW5ITVJ?
EC-GI-10 MnW1S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MVzJR|UxRTRzLkW4NFUh|ryP NE\4bFNUSU6JRWK=
CTV-1 M4rweGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NIraT4tKSzVyPUSyMlg1ODZizszN NGTzR2VUSU6JRWK=
DG-75 NUK5T3lXT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MkLvTWM2OD12Mz63OVk2KM7:TR?= NWLDTpJRW0GQR1XS
KNS-81-FD MkewS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NX3ufJp[UUN3ME20OU41ODV6IN88US=> MWrTRW5ITVJ?
NCI-H82 NYXpbZRkT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M3vDT2lEPTB;NEWuOVc2QCEQvF2= NGLPcXRUSU6JRWK=
RPMI-8866 MX;Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NY\VV4hvUUN3ME20Ok4yQDd|IN88US=> MmLtV2FPT0WU
ACN NIryNYpIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NHLwd5ZKSzVyPUS2MlQ{PCEQvF2= MWjTRW5ITVJ?
NCI-H1395 NGDiO4ZIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MlT5TWM2OD12Nj60O|U3KM7:TR?= NFnhO5FUSU6JRWK=
NCI-H209 M2DKc2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NYP3OWROUUN3ME20O{4yPDB3IN88US=> MmjyV2FPT0WU
TGW NHr1OHBIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MkjTTWM2OD12OT6wO|kyKM7:TR?= NHnrfVdUSU6JRWK=
NCI-H748 Mm\DS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? Ml7oTWM2OD12OT60O|U{KM7:TR?= NGjGNpFUSU6JRWK=
EKVX Mlm2S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NIrnTplKSzVyPUS5MlY3OjhizszN MUnTRW5ITVJ?

... 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 <1 mg/mL
Ethanol <1 mg/mL
In vivo 5% DMSO+45% PEG 400+ddH2O 3mg/mL

* 1 mg/ml means slightly soluble or insoluble.
* 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