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 MY\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NXLuWGtQUUN3ME2wMlAxODByM{CzJO69VQ>? MUTTRW5ITVJ?
MONO-MAC-6 NYnQOpV1T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MV3JR|UxRTBwMEC0NVgh|ryP NHSwdW5USU6JRWK=
ALL-PO MoHaS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MXHJR|UxRTBwMEOxPFQh|ryP MXXTRW5ITVJ?
NKM-1 MXvHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NVfONmxHUUN3ME2wMlA4PDF4IN88US=> NEPOVmJUSU6JRWK=
CGTH-W-1 M1fMOGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NUXQOJlSUUN3ME2wMlI2ODJ{IN88US=> M{Cwd3NCVkeHUh?=
BB65-RCC MXfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MWrJR|UxRTBwNEewO|Mh|ryP MVvTRW5ITVJ?
NOS-1 MUDHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M4DUU2lEPTB;MD61OlM3KM7:TR?= NGXlfY5USU6JRWK=
SH-4 NVS2OWtKT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NGjQTZFKSzVyPUCuOlU3OTNizszN M1vtUnNCVkeHUh?=
HOP-62 NUSyT|lTT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NX3iV|ROUUN3ME2wMlg2ODh6IN88US=> NUjQfllEW0GQR1XS
HCC2998 NUWxcllST3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MnLQTWM2OD1yLki4PFE5KM7:TR?= NGD3[IJUSU6JRWK=
GDM-1 MX3Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NFPIRVlKSzVyPUCuPVA3QThizszN Ml33V2FPT0WU
KM12 MYHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MWHJR|UxRTFwMEKwPVgh|ryP M2OyNHNCVkeHUh?=
LB2518-MEL MYTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M2XJeGlEPTB;MT6yNFgxQSEQvF2= NWrLeo8yW0GQR1XS
NCI-H1436 MlzmS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M4\2[2lEPTB;MT6yNVY4QCEQvF2= NF[xflVUSU6JRWK=
EM-2 NEi3bYdIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M2j4bWlEPTB;MT6zOVU4QCEQvF2= MX3TRW5ITVJ?
LAMA-84 M{XoOGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NVvZb|AxUUN3ME2xMlM4PjR6IN88US=> MmfZV2FPT0WU
KG-1 M2\1WWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MWLJR|UxRTFwNEe5N|Uh|ryP MWfTRW5ITVJ?
A388 M2XCdWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NHnzXWlKSzVyPUGuOVkyPjVizszN M1HFW3NCVkeHUh?=
no-10 NXfyVplqT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NFzxdlFKSzVyPUGuOlE4OjZizszN Ml3VV2FPT0WU
SF126 M{fzPGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M1nWWmlEPTB;MT62N|gyOiEQvF2= MlLjV2FPT0WU
MEG-01 NHXIWZVIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MlzOTWM2OD1zLkiwPVgh|ryP MoLLV2FPT0WU
A3-KAW M{O1dGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MUTJR|UxRTFwOEi0NkDPxE1? MVjTRW5ITVJ?
D-247MG MUXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NV61dXh2UUN3ME2yMlE1PDhizszN M{PVenNCVkeHUh?=
OVCAR-4 M3nrPGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M1j4S2lEPTB;Mj6yNVM6OyEQvF2= MnfzV2FPT0WU
NCI-SNU-1 NW\VN3pQT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MXfJR|UxRTJwM{G2NkDPxE1? NGLUd|hUSU6JRWK=
NCI-H2171 MW\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NYLy[oN6UUN3ME2yMlM6PzZ2IN88US=> MoXBV2FPT0WU
SIG-M5 MkO4S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MX;JR|UxRTJwNEKyOFIh|ryP MWHTRW5ITVJ?
BE-13 MofrS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NHi5Rm5KSzVyPUKuOlk3ODlizszN NVX5XVBQW0GQR1XS
K052 M2fkcmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M2fxbmlEPTB;Mj63OFYyPiEQvF2= MXPTRW5ITVJ?
L-540 NV\Qc3lKT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NVzt[W1XUUN3ME2yMlc2Pzh7IN88US=> M4XjZ3NCVkeHUh?=
KMOE-2 NXjsVoNHT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MYXJR|UxRTJwOEGzOUDPxE1? MmfkV2FPT0WU
MFH-ino M2Hjcmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NGmxdW5KSzVyPUKuPVIyQDVizszN NXG3fZZXW0GQR1XS
HL-60 NGOzXYVIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NGjz[ZpKSzVyPUOuNFYzQTlizszN MUXTRW5ITVJ?
HCC2218 MmGyS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MVnJR|UxRTNwMUKwNFMh|ryP NFjN[|hUSU6JRWK=
TE-5 MmfVS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NG\5TZZKSzVyPUOuNVMyPjJizszN MW\TRW5ITVJ?
MZ1-PC NWfOZoFQT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= Ml:wTWM2OD1|LkS3OVA6KM7:TR?= NUHoN|BtW0GQR1XS
MRK-nu-1 NW\kbnNHT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M3f4WmlEPTB;Mz62NVQ3QCEQvF2= M1ThU3NCVkeHUh?=
MZ7-mel NXnjdVRiT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M330PGlEPTB;Mz62OlA6QSEQvF2= M2X0fnNCVkeHUh?=
BC-1 MnzQS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NEHJNZFKSzVyPUOuO|QxOiEQvF2= NH64T5VUSU6JRWK=
ST486 M1S5NWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MUHJR|UxRTNwOEO2O|Mh|ryP NIPXXnZUSU6JRWK=
KS-1 M1zmfmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MY\JR|UxRTNwOEixPVgh|ryP M2PPR3NCVkeHUh?=
SK-NEP-1 MkHRS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MmPLTWM2OD12LkG2PFE2KM7:TR?= NX;TTlhJW0GQR1XS
BC-3 NWHBT5pMT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NX\SdYxkUUN3ME20MlI{OzlzIN88US=> NXPGOGtMW0GQR1XS
NCI-H1581 MXjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M2[3RmlEPTB;ND6yPFc6QCEQvF2= M3iwSXNCVkeHUh?=
MHH-PREB-1 MYLHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NHLzSZpKSzVyPUSuOFA1QDRizszN MmPwV2FPT0WU
NOMO-1 MUjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NXLIUXp2UUN3ME20MlQ5QTB3IN88US=> NEXLUGFUSU6JRWK=
QIMR-WIL NGnKTYVIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NV;NfZhlUUN3ME21MlA4Ojl2IN88US=> MVHTRW5ITVJ?
SF539 MknkS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MXvJR|UxRTVwMUOyNlch|ryP M1rkdnNCVkeHUh?=
TE-12 NHX6TpNIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MVHJR|UxRTVwMkS5Nlkh|ryP NUDmNZBEW0GQR1XS
NCI-H510A MoWyS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M1fpc2lEPTB;NT60NVY5PSEQvF2= MUPTRW5ITVJ?
JAR NXO0O|hZT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NHrNTGlKSzVyPUWuOVA5OjRizszN M3\4VnNCVkeHUh?=
no-11 NF;RTmpIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M{DxeGlEPTB;NT63N|U3QCEQvF2= MkHzV2FPT0WU
BV-173 NHmzU2RIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M2Ll[GlEPTB;NT65OVY5OiEQvF2= MWLTRW5ITVJ?
SR MV3Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NVPXNXJ2UUN3ME22MlAxPjd6IN88US=> M2PweHNCVkeHUh?=
MOLT-16 MmHGS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MV7JR|UxRTZwMkWyOlYh|ryP NHW2U2dUSU6JRWK=
MZ2-MEL MX\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M1\0RmlEPTB;Nj6zNVg{QSEQvF2= NX\KepFVW0GQR1XS
SW954 M2i1R2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NH7VToxKSzVyPU[uOFU5PjZizszN NWTqc4V3W0GQR1XS
ML-2 NHz0UpNIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MVHJR|UxRTZwNUK4OFkh|ryP NEPLcVRUSU6JRWK=
OCI-AML2 NIH5TZRIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= Ml\JTWM2OD14Lk[xNFYzKM7:TR?= NV;S[5VQW0GQR1XS
SIMA MkTLS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MnGyTWM2OD15LkCwNVAyKM7:TR?= NWTNeXI5W0GQR1XS
DOHH-2 M1jUTWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NVT1V49UUUN3ME23MlA2Pjd4IN88US=> NV3ibpAyW0GQR1XS
697 M3PMd2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MXjJR|UxRTdwMEW5PFkh|ryP MWPTRW5ITVJ?
NB1 MXjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MWTJR|UxRTdwNEC0NFch|ryP MmPjV2FPT0WU
D-392MG MX3Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NFezSopKSzVyPUeuOlI3PjNizszN MXPTRW5ITVJ?
ES8 MY\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? Ml36TWM2OD15Lke2OVA{KM7:TR?= MnnIV2FPT0WU
RPMI-8226 M3\iZmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NHXzW4NKSzVyPUeuPFQ2OTFizszN MW\TRW5ITVJ?
IST-MEL1 NUHOR4V7T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= Mn61TWM2OD16LkSwNFAzKM7:TR?= M{KyNXNCVkeHUh?=
NB14 MkOyS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M2DsUWlEPTB;OD62N|E{OyEQvF2= MlPyV2FPT0WU
HD-MY-Z NV7aSWJ4T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M1i2d2lEPTB;OD62N|c1PiEQvF2= NXmydZBRW0GQR1XS
TE-10 MX3Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M3vGcWlEPTB;OD63OlM2OyEQvF2= M3HUc3NCVkeHUh?=
LC-1F M3vTTGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MXHJR|UxRTlwMUC4N|Qh|ryP M4LlTXNCVkeHUh?=
OS-RC-2 NYftV3NqT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MYfJR|UxRTlwMUGyOFMh|ryP NInRPI5USU6JRWK=
NCI-SNU-16 MY\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M4LoXWlEPTB;OT6yNVAzPiEQvF2= NVj1eGhwW0GQR1XS
SHP-77 M4nOcWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MkHITWM2OD17LkexOlYzKM7:TR?= NWHYXpNVW0GQR1XS
A4-Fuk MoHDS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NX33NZY6UUN3ME25Mlc2PjFizszN M3mw[nNCVkeHUh?=
NB6 NV61ZW1zT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M3LET2lEPTB;OT63OlAzQSEQvF2= M2DHWnNCVkeHUh?=
JiyoyeP-2003 Mnr3S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? Mkn1TWM2OD1zMD60O|Q2KM7:TR?= NWXBZY52W0GQR1XS
DMS-114 MXjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M170d2lEPTB;MUCuOVQ1OSEQvF2= NEn5XnlUSU6JRWK=
NB7 MXvHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NFPYWZdKSzVyPUGwMlc2OjZizszN NHzpUZdUSU6JRWK=
NCI-H747 MXfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NGPwUGFKSzVyPUGxMlEzOTZizszN MUTTRW5ITVJ?
HH NE\4[GFIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NXHVZYFPUUN3ME2xNU4{QDd4IN88US=> NGPSXXpUSU6JRWK=
EW-18 NYjXZnVYT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M3fRXmlEPTB;MUGuPVA1PCEQvF2= MoP3V2FPT0WU
CHP-126 MnLuS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NYPGdZVsUUN3ME2xNU46PzN6IN88US=> NULSOnYxW0GQR1XS
NTERA-S-cl-D1 NUK5SlR{T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M33DWWlEPTB;MUKuNFI4QCEQvF2= M{Lte3NCVkeHUh?=
DEL NIX2RlNIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NG\6VmZKSzVyPUGyMlA6QDVizszN MmD2V2FPT0WU
LU-139 NYHuToxET3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M4ntNWlEPTB;MUKuOVQyOyEQvF2= NITXToZUSU6JRWK=
P30-OHK Ml3lS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M3PvXmlEPTB;MUKuOVQ4QSEQvF2= MXPTRW5ITVJ?
NCI-H1522 NUnwS5ZFT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NI\2XWFKSzVyPUGyMlc1PiEQvF2= MX;TRW5ITVJ?
NCI-H1299 NU\LWWd7T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MUTJR|UxRTF|LkK5NVEh|ryP NV64R3dqW0GQR1XS
UACC-257 NU\EW4N3T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MluyTWM2OD1zMz61NVI3KM7:TR?= M{XV[XNCVkeHUh?=
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NCI-H1882 Mnq2S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MoXFTWM2OD1zMz64OVU2KM7:TR?= NHrRO49USU6JRWK=
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HT-144 MmTjS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NYXHOmw5UUN3ME2xO{4xODZizszN MYjTRW5ITVJ?
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LU-165 MYfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MofDTWM2OD1zOT63NFA5KM7:TR?= MULTRW5ITVJ?
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A101D NX;XTnR{T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NUHTWodwUUN3ME2yNU4{PzV{IN88US=> M3Hp[XNCVkeHUh?=
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TE-9 NVzGU5c5T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MWLJR|UxRTJzLki1NVMh|ryP MX;TRW5ITVJ?
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D-542MG M1jjRmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MUnJR|UxRTJ{LkCyOVYh|ryP NUTU[JJUW0GQR1XS
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ECC12 MXLHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MXPJR|UxRTJ2LkK4NFMh|ryP M{LJcHNCVkeHUh?=
C2BBe1 MXjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M2LydWlEPTB;MkSuN|I{QSEQvF2= MWTTRW5ITVJ?
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NB13 MXPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MkLVTWM2OD1{NT6wNlY2KM7:TR?= NHvVXVJUSU6JRWK=
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COR-L88 NVT2TXRXT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NIfjZmtKSzVyPUK2MlU4QTZizszN NFfIPVZUSU6JRWK=
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TGBC1TKB NVL4bJlST3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= Mk\DTWM2OD1{Nj65PFI5KM7:TR?= NV;mXlZ3W0GQR1XS
THP-1 NVrMdHZ1T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NXHMTWFbUUN3ME2yO{4zOTRzIN88US=> NF76TZJUSU6JRWK=
ONS-76 Mm\aS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MWjJR|UxRTJ5LkOzNkDPxE1? NF\zSJlUSU6JRWK=
LC-2-ad NGfLVJBIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NF3E[YdKSzVyPUK3MlYzOzFizszN NF3iZ|VUSU6JRWK=
EW-13 NVnSS5BJT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MUjJR|UxRTJ7LkG3OFYh|ryP NGPLW4xUSU6JRWK=
MS-1 M2nMS2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NWe4N5hEUUN3ME2zNE44Ojd6IN88US=> NHrqdZJUSU6JRWK=
NCI-H2227 MX7Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MonqTWM2OD1|MD65PFA3KM7:TR?= M3;zfHNCVkeHUh?=
LXF-289 M4HaZWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MnWwTWM2OD1|MT60OFkzKM7:TR?= MojMV2FPT0WU
MC116 M3\VcWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MmC4TWM2OD1|Mj6wPFI3KM7:TR?= MnH5V2FPT0WU
EVSA-T NXHwOW5iT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NETjeoNKSzVyPUOyMlI2QDVizszN MoLIV2FPT0WU
CTB-1 MoPNS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NVfoXpRwUUN3ME2zN{4yOTBzIN88US=> M1PLXnNCVkeHUh?=
COLO-320-HSR MoqwS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NFfzN2hKSzVyPUOzMlE3ODNizszN M3TybHNCVkeHUh?=
NCI-H2196 M3j2emdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M1v5S2lEPTB;M{OuNlU2PyEQvF2= NYHWW5RxW0GQR1XS
LB2241-RCC NF;Kd3dIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NEPm[lFKSzVyPUOzMlMyOzVizszN M2OyTnNCVkeHUh?=
LS-513 NHX1OYZIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MmHMTWM2OD1|Mz64OlM5KM7:TR?= M{Pab3NCVkeHUh?=
LP-1 Mn;zS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MXfJR|UxRTN|Lkm5OVYh|ryP MVjTRW5ITVJ?
A253 M2nIN2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M3frS2lEPTB;M{SuNlI6PiEQvF2= M{nLZnNCVkeHUh?=
SK-MM-2 NGLIe2VIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M3H5ZmlEPTB;M{SuPVQ2OSEQvF2= M4PSdnNCVkeHUh?=
NCI-H1963 MmTBS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NYH2V|M5UUN3ME2zOU4{ODd{IN88US=> NUXxcYVxW0GQR1XS
MMAC-SF MYTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NWqzU|B5UUN3ME2zOU45Pzh3IN88US=> MkTYV2FPT0WU
LB831-BLC MUfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? Mk\GTWM2OD1|Nj6wOlU1KM7:TR?= NVHOSWlFW0GQR1XS
WSU-NHL MWLHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NIjpZ2NKSzVyPUO2MlE3PCEQvF2= M1:2OnNCVkeHUh?=
CESS NFjK[ZFIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MkPkTWM2OD1|Nj6yPFQ5KM7:TR?= MVPTRW5ITVJ?
NEC8 M{DSVGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MXzJR|UxRTN4LkW4N|Uh|ryP MWjTRW5ITVJ?
KNS-42 M323VWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NHPWWG1KSzVyPUO3MlEzOzdizszN M3TVdnNCVkeHUh?=
MHH-CALL-2 M3ewdGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 Mm\aTWM2OD1|Nz6xPFIyKM7:TR?= MlzqV2FPT0WU
K5 M{PQfGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 Mm\jTWM2OD1|OD60N{DPxE1? NWS5[JBVW0GQR1XS
CP66-MEL NULwUI1sT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NGjxfJZKSzVyPUO5MlA4OzNizszN NEfZUIZUSU6JRWK=
OPM-2 M{LReWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NEPneYdKSzVyPUO5Mlg1OzJizszN MVTTRW5ITVJ?
IST-MES1 Mn7QS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MWTJR|UxRTRyLkOwPVYh|ryP M1nW[HNCVkeHUh?=
EC-GI-10 MoDLS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NYHlUXZWUUN3ME20NU42QDB3IN88US=> M2m1R3NCVkeHUh?=
CTV-1 Mn2yS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NF\Gc4lKSzVyPUSyMlg1ODZizszN MlzEV2FPT0WU
DG-75 MVrHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NGjscY1KSzVyPUSzMlc2QTVizszN M3\Q[3NCVkeHUh?=
KNS-81-FD NHjRS2VIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M3LkemlEPTB;NEWuOFA2QCEQvF2= NHrYSVBUSU6JRWK=
NCI-H82 NX7ROWNZT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NX3FbGlCUUN3ME20OU42PzV6IN88US=> NFLtPW1USU6JRWK=
RPMI-8866 NYjiZ3d{T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MVTJR|UxRTR4LkG4O|Mh|ryP Mmf1V2FPT0WU
ACN NHHzSotIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MlTFTWM2OD12Nj60N|Qh|ryP NULjepQ1W0GQR1XS
NCI-H1395 MUnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NWfwdnNiUUN3ME20Ok41PzV4IN88US=> M1e3Z3NCVkeHUh?=
NCI-H209 M3vseWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NWf0NWQxUUN3ME20O{4yPDB3IN88US=> NGrXR|RUSU6JRWK=
TGW MkmyS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MW\JR|UxRTR7LkC3PVEh|ryP MVvTRW5ITVJ?
NCI-H748 Mny3S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M1zjeGlEPTB;NEmuOFc2OyEQvF2= NHrvb4pUSU6JRWK=
EKVX NXP3ZW5jT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NGTEWmdKSzVyPUS5MlY3OjhizszN MYXTRW5ITVJ?

... 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