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 71 Publications

12 Customer Reviews

  • (A) and (C) qPCR showing the levels of HMGA2 and SOX9 mRNA in Hep3B and Huh7 human HCC cells treated for 48 hours with 1 μM AZD6244, or 7.5 μM sorafenib relative to control-treated cells (Ctrl). (B) and (D) qPCR showing Hmga2 and Sox9 expression in p53−/−; HRAS(G12V) and p53−/−; Myc; Cas9; sgNf1 mouse liver cells. Drug treatment was the same as in (A). Error bars are s.d. of mean (n = 3). ***, P < .001.

    Gastroenterology, 2017, 152(5):1161-1173. Sorafenib purchased from Selleck.

    E-G, Shown are H&E, Ki67, and Tunel-stained representative sections from a vehicle or OTX015+panobinostat+sorafenib-treated GBM12 tumor

    Clin Cancer Res, 2018, 24(16):3941-3954. Sorafenib purchased from Selleck.

  • Western blotting of Mcl-1 in HCT116 cells treated with indicated agents for 24 hours. ABT-263, 5 μmol/L; ABT-737, 5 μmol/L; SAHA, 4 μmol/L; MS-275, 5 μmol/L; regorafenib, 40 μmol/L; sorafenib, 20 μmol/L; UCN-01, 1 μmol/L; sunitinib, 15 μmol/L.

    Cancer Res, 2018, 78(16):4704-4715. 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.

  • 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 MXHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? Mlv5TWM2OD1yLkCwNFAxOzB|IN88US=> M1[xZ3NCVkeHUh?=
MONO-MAC-6 M1r1Vmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NG\GTGdKSzVyPUCuNFA1OThizszN MmfIV2FPT0WU
ALL-PO M1r2[Gdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MWHJR|UxRTBwMEOxPFQh|ryP MUnTRW5ITVJ?
NKM-1 M1LSeWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NH\zOWVKSzVyPUCuNFc1OTZizszN MULTRW5ITVJ?
CGTH-W-1 NEDzSm1Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MUHJR|UxRTBwMkWwNlIh|ryP MoWxV2FPT0WU
BB65-RCC MVvHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MY\JR|UxRTBwNEewO|Mh|ryP NIjuOXRUSU6JRWK=
NOS-1 MkHTS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NF\DOodKSzVyPUCuOVY{PiEQvF2= NYPVU|ViW0GQR1XS
SH-4 MlPLS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M{m5bmlEPTB;MD62OVYyOyEQvF2= M1XWZnNCVkeHUh?=
HOP-62 M1TufWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MX;JR|UxRTBwOEWwPFgh|ryP NE\qXXRUSU6JRWK=
HCC2998 MXHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NVX6VYRMUUN3ME2wMlg5QDF6IN88US=> MYrTRW5ITVJ?
GDM-1 MoPMS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M{j4fmlEPTB;MD65NFY6QCEQvF2= NEHhVpZUSU6JRWK=
KM12 Mlz0S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MlTHTWM2OD1zLkCyNFk5KM7:TR?= NYf5NoxSW0GQR1XS
LB2518-MEL NWnWU|Z{T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MVvJR|UxRTFwMkC4NFkh|ryP MUPTRW5ITVJ?
NCI-H1436 M176Rmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NF63SWpKSzVyPUGuNlE3PzhizszN NG\C[ItUSU6JRWK=
EM-2 M2PudGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M4rZd2lEPTB;MT6zOVU4QCEQvF2= NX3ZU|VVW0GQR1XS
LAMA-84 M4rJeWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MWnJR|UxRTFwM{e2OFgh|ryP NXTtNHg1W0GQR1XS
KG-1 Mmj2S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M3zqcmlEPTB;MT60O|k{PSEQvF2= NGXHfWxUSU6JRWK=
A388 MV3Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NYf0RXd1UUN3ME2xMlU6OTZ3IN88US=> MWLTRW5ITVJ?
no-10 NVzTcnhVT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NFfj[nFKSzVyPUGuOlE4OjZizszN NIjaU|RUSU6JRWK=
SF126 Mn:3S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M33NeWlEPTB;MT62N|gyOiEQvF2= MYDTRW5ITVJ?
MEG-01 MWjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? Ml;YTWM2OD1zLkiwPVgh|ryP M{XvcXNCVkeHUh?=
A3-KAW M3X3b2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NEjzdXRKSzVyPUGuPFg1OiEQvF2= MXHTRW5ITVJ?
D-247MG M13ueGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NYS4dHdDUUN3ME2yMlE1PDhizszN NEjOcpBUSU6JRWK=
OVCAR-4 NXnYVlNET3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NXnsWYpMUUN3ME2yMlIyOzl|IN88US=> NWnyU4ZrW0GQR1XS
NCI-SNU-1 MWLHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NGjHR3dKSzVyPUKuN|E3OiEQvF2= M13hc3NCVkeHUh?=
NCI-H2171 NF\Tb|hIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MVHJR|UxRTJwM{m3OlQh|ryP NGWzT3FUSU6JRWK=
SIG-M5 MVTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MYnJR|UxRTJwNEKyOFIh|ryP MkTDV2FPT0WU
BE-13 NFnLZ2dIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M3LUT2lEPTB;Mj62PVYxQSEQvF2= MX;TRW5ITVJ?
K052 NWTSSm9DT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M1rDVWlEPTB;Mj63OFYyPiEQvF2= MmTlV2FPT0WU
L-540 NYXtPINRT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M3XENGlEPTB;Mj63OVc5QSEQvF2= NYXReYxlW0GQR1XS
KMOE-2 NXza[oFoT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M{jad2lEPTB;Mj64NVM2KM7:TR?= NG\lOXFUSU6JRWK=
MFH-ino M4TkUmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NHH5TIhKSzVyPUKuPVIyQDVizszN M{LwV3NCVkeHUh?=
HL-60 M3jXTmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MlLxTWM2OD1|LkC2Nlk6KM7:TR?= NHLidFVUSU6JRWK=
HCC2218 NUTzPI9XT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NHPYUldKSzVyPUOuNVIxODNizszN M3S0THNCVkeHUh?=
TE-5 NHm5d3NIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NFjKblBKSzVyPUOuNVMyPjJizszN MV7TRW5ITVJ?
MZ1-PC MVnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MXHJR|UxRTNwNEe1NFkh|ryP NYCxSVBSW0GQR1XS
MRK-nu-1 NIG1U2xIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NUDQTG1lUUN3ME2zMlYyPDZ6IN88US=> NXP1XI1wW0GQR1XS
MZ7-mel MW\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M33PTmlEPTB;Mz62OlA6QSEQvF2= NV3kfm51W0GQR1XS
BC-1 MYnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MmPrTWM2OD1|Lke0NFIh|ryP MYTTRW5ITVJ?
ST486 NGWwUmdIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MlnzTWM2OD1|LkizOlc{KM7:TR?= M4rwfHNCVkeHUh?=
KS-1 NYTqZ4x5T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NH6xe4ZKSzVyPUOuPFgyQThizszN NWLLNWp3W0GQR1XS
SK-NEP-1 NYr5W4xET3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MlfaTWM2OD12LkG2PFE2KM7:TR?= NVXDcGwzW0GQR1XS
BC-3 M2nGc2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MmizTWM2OD12LkKzN|kyKM7:TR?= MkfxV2FPT0WU
NCI-H1581 MnfCS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MmLETWM2OD12LkK4O|k5KM7:TR?= NWPrVVR4W0GQR1XS
MHH-PREB-1 M{j6N2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NVrZT453UUN3ME20MlQxPDh2IN88US=> NVy4ZmlOW0GQR1XS
NOMO-1 NYfFfmZNT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M3nV[mlEPTB;ND60PFkxPSEQvF2= MXLTRW5ITVJ?
QIMR-WIL NHrlWGFIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MVPJR|UxRTVwMEeyPVQh|ryP MXTTRW5ITVJ?
SF539 M2fXfmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M3f5SGlEPTB;NT6xN|IzPyEQvF2= MWfTRW5ITVJ?
TE-12 MVfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NFu3OJNKSzVyPUWuNlQ6OjlizszN MUPTRW5ITVJ?
NCI-H510A MULHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NGi4OnNKSzVyPUWuOFE3QDVizszN NGOyUnVUSU6JRWK=
JAR M3HO[2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NV3nToJSUUN3ME21MlUxQDJ2IN88US=> NHT6UZNUSU6JRWK=
no-11 NWDvZpVzT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MkC3TWM2OD13LkezOVY5KM7:TR?= NETPfoFUSU6JRWK=
BV-173 NV65VIpKT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MVnJR|UxRTVwOUW2PFIh|ryP M3e1bnNCVkeHUh?=
SR NILwWlZIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M3foUGlEPTB;Nj6wNFY4QCEQvF2= NET1XmpUSU6JRWK=
MOLT-16 NYX0WGdIT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M4LNWWlEPTB;Nj6yOVI3PiEQvF2= NVXXWGoyW0GQR1XS
MZ2-MEL M1TJOWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NXqxS5EzUUN3ME22MlMyQDN7IN88US=> MVXTRW5ITVJ?
SW954 NFfR[FdIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MmewTWM2OD14LkS1PFY3KM7:TR?= NVfKdG5PW0GQR1XS
ML-2 MUPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M2qyOGlEPTB;Nj61Nlg1QSEQvF2= MlKyV2FPT0WU
OCI-AML2 MnyyS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NF;rclRKSzVyPU[uOlExPjJizszN NULhW5FWW0GQR1XS
SIMA MmrtS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MVLJR|UxRTdwMECxNFEh|ryP NFr6e5RUSU6JRWK=
DOHH-2 NXOxR2puT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NGn5VIpKSzVyPUeuNFU3PzZizszN NUTHUHJOW0GQR1XS
697 M3zYSmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MlTiTWM2OD15LkC1PVg6KM7:TR?= NHrtNnFUSU6JRWK=
NB1 NFO0R3ZIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MlfWTWM2OD15LkSwOFA4KM7:TR?= MVTTRW5ITVJ?
D-392MG MUHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NHXJOXdKSzVyPUeuOlI3PjNizszN M{XYWHNCVkeHUh?=
ES8 MmXlS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? Mn2zTWM2OD15Lke2OVA{KM7:TR?= MUTTRW5ITVJ?
RPMI-8226 MUjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NGPlZ4lKSzVyPUeuPFQ2OTFizszN M4\DSXNCVkeHUh?=
IST-MEL1 Mn;2S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MXHJR|UxRThwNECwNFIh|ryP MkDsV2FPT0WU
NB14 NYPVWJA5T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NWHHcFdVUUN3ME24MlY{OTN|IN88US=> MmrzV2FPT0WU
HD-MY-Z NWPrcZpwT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MlfQTWM2OD16Lk[zO|Q3KM7:TR?= NGHQR4NUSU6JRWK=
TE-10 NXP2WVB4T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MlSwTWM2OD16Lke2N|U{KM7:TR?= MmG2V2FPT0WU
LC-1F NGnsUmNIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MWTJR|UxRTlwMUC4N|Qh|ryP MnPyV2FPT0WU
OS-RC-2 MYfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M4i1[WlEPTB;OT6xNVI1OyEQvF2= NWPicHhHW0GQR1XS
NCI-SNU-16 NYnROXRQT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NXPhNZdTUUN3ME25MlIyODJ4IN88US=> M1TvWnNCVkeHUh?=
SHP-77 NVPVbZVCT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NEj3c|ZKSzVyPUmuO|E3PjJizszN MoDBV2FPT0WU
A4-Fuk M3vufWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NH;kW|JKSzVyPUmuO|U3OSEQvF2= NFzJe49USU6JRWK=
NB6 NEDqOoRIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NHO5dnFKSzVyPUmuO|YxOjlizszN NWXDPVVPW0GQR1XS
JiyoyeP-2003 Mn65S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MoTTTWM2OD1zMD60O|Q2KM7:TR?= MYfTRW5ITVJ?
DMS-114 MVPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MnPJTWM2OD1zMD61OFQyKM7:TR?= MlK3V2FPT0WU
NB7 M3\rZWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M{nZWGlEPTB;MUCuO|UzPiEQvF2= NVzKbpd5W0GQR1XS
NCI-H747 Mm\PS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M1HIOWlEPTB;MUGuNVIyPiEQvF2= NG\r[pRUSU6JRWK=
HH MULHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NH\jU|FKSzVyPUGxMlM5PzZizszN NEXU[YpUSU6JRWK=
EW-18 MXjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MVzJR|UxRTFzLkmwOFQh|ryP M1fkNXNCVkeHUh?=
CHP-126 M2fFZWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NFnzenRKSzVyPUGxMlk4OzhizszN NHf6TJFUSU6JRWK=
NTERA-S-cl-D1 M{PodGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MYHJR|UxRTF{LkCyO|gh|ryP NVLzXlF{W0GQR1XS
DEL M2XjSmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NU[4e5FnUUN3ME2xNk4xQTh3IN88US=> M2HCdHNCVkeHUh?=
LU-139 MoDES5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M3nSVmlEPTB;MUKuOVQyOyEQvF2= M4fKNXNCVkeHUh?=
P30-OHK NXLSflRnT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= Mlm4TWM2OD1zMj61OFc6KM7:TR?= NEOxUFVUSU6JRWK=
NCI-H1522 MnLQS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MoDrTWM2OD1zMj63OFYh|ryP NXiwbHdpW0GQR1XS
NCI-H1299 NIG0TWhIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MmP3TWM2OD1zMz6yPVEyKM7:TR?= NYflXJhiW0GQR1XS
UACC-257 NUHEU3g5T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MYfJR|UxRTF|LkWxNlYh|ryP M3G0T3NCVkeHUh?=
Calu-6 NUjTR3NzT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MoXvTWM2OD1zMz62NFQ3KM7:TR?= NUTGPHRZW0GQR1XS
NCI-H1882 MlvvS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MoD6TWM2OD1zMz64OVU2KM7:TR?= NInGOYdUSU6JRWK=
BB30-HNC M37FVWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NGj3V|JKSzVyPUG0MlA3ODlizszN Mn:3V2FPT0WU
ES1 MXnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MUTJR|UxRTF2LkG1OVEh|ryP NFq2XY5USU6JRWK=
NCI-H1694 M{HZfmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NUPJO2p4UUN3ME2xOE41QDFzIN88US=> NV[3[YZ[W0GQR1XS
IST-SL1 M2DQSmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MVnJR|UxRTF2Lkm2NVYh|ryP MUDTRW5ITVJ?
ECC4 NX[xSW53T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NUX6TItXUUN3ME2xOU4xPTV6IN88US=> MWHTRW5ITVJ?
MDA-MB-134-VI NWe0NGhHT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MmTyTWM2OD1zNT60NVMyKM7:TR?= MXfTRW5ITVJ?
SCH M4nCV2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MljXTWM2OD1zNT60O|I5KM7:TR?= NHP4NG5USU6JRWK=
SK-N-FI MVPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NFr6SoFKSzVyPUG1MlY2OzRizszN MlzhV2FPT0WU
HDLM-2 MWXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M13HbGlEPTB;MU[uNFcyPCEQvF2= MV3TRW5ITVJ?
Ramos-2G6-4C10 NXf2[HBPT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NXHJUXplUUN3ME2xOk4yOjl5IN88US=> NFHiTWVUSU6JRWK=
EW-24 MmDLS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NG\yW4JKSzVyPUG2MlE3PjFizszN MmTyV2FPT0WU
NCI-H2141 M3XuRmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M{nWSmlEPTB;MU[uNVg6KM7:TR?= M1\rPXNCVkeHUh?=
LC4-1 Mnm4S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M37HemlEPTB;MU[uOlEyQSEQvF2= MkPUV2FPT0WU
HT-144 NFvHUWFIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M1jHSGlEPTB;MUeuNFA3KM7:TR?= MoPFV2FPT0WU
SK-MEL-1 NFHwZ5NIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MUDJR|UxRTF5LkCwO|Ih|ryP NYO2SWpnW0GQR1XS
SCC-15 NY\1dZFST3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MkPMTWM2OD1zNz6xOlM5KM7:TR?= MUjTRW5ITVJ?
C8166 M3PzR2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 Mo\xTWM2OD1zNz62PFM{KM7:TR?= M320[3NCVkeHUh?=
GOTO M3rqOGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MXvJR|UxRTF5LkizOFQh|ryP M2DuZnNCVkeHUh?=
COR-L279 NYLDcYczT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NV7xRlBsUUN3ME2xPE4yOzZ{IN88US=> MoTpV2FPT0WU
K-562 M2rEZ2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NECxfoRKSzVyPUG4MlcyPDNizszN NUfhN4FIW0GQR1XS
ES3 NHHCdZFIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NYDWcoxMUUN3ME2xPE45ODRzIN88US=> M{TpR3NCVkeHUh?=
LU-165 M3n5NGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MlG3TWM2OD1zOT63NFA5KM7:TR?= MWjTRW5ITVJ?
KM-H2 NITmTZVIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NYHmflV4UUN3ME2yNE4{OTh2IN88US=> M3e2dnNCVkeHUh?=
RL M3TvXmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NXjKVI9TUUN3ME2yNE46Pjl{IN88US=> NV7k[m9PW0GQR1XS
EW-3 M{O5PWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NVq0OXdYUUN3ME2yNU4yQDh7IN88US=> NYHMUpBWW0GQR1XS
A101D M{\rOWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MYfJR|UxRTJzLkO3OVIh|ryP MnfXV2FPT0WU
HUTU-80 MnHQS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NULxT2cxUUN3ME2yNU4{QTR4IN88US=> NVvqb2FqW0GQR1XS
NCI-H23 MVjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MWLJR|UxRTJzLkO5PVIh|ryP NVq2S2ZMW0GQR1XS
PF-382 NFHxfphIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MXrJR|UxRTJzLkS0NFMh|ryP NH3JNmlUSU6JRWK=
LB373-MEL-D M3njXWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MkHrTWM2OD1{MT61OlE2KM7:TR?= NGnQepNUSU6JRWK=
TE-8 MYrHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M1L3eGlEPTB;MkGuOlM6PCEQvF2= MoXmV2FPT0WU
TE-9 MnLMS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MXXJR|UxRTJzLki1NVMh|ryP M4\CTXNCVkeHUh?=
Daudi MVPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MlLpTWM2OD1{MT65N|A1KM7:TR?= NEH1RnZUSU6JRWK=
D-542MG M1X5Tmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 Mlz2TWM2OD1{Mj6wNlU3KM7:TR?= NF;DNlJUSU6JRWK=
U-698-M NGHFcWNIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MljnTWM2OD1{Mj60OlA{KM7:TR?= MU\TRW5ITVJ?
ES6 NFPPXXlIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NHvTO25KSzVyPUKyMlc{PjZizszN NWSzTFg4W0GQR1XS
DU-4475 MXfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? Ml[zTWM2OD1{Mz64PFk4KM7:TR?= MV;TRW5ITVJ?
ECC12 M1TYTGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NWPiXVJYUUN3ME2yOE4zQDB|IN88US=> MmLFV2FPT0WU
C2BBe1 M2nBe2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M1W3TGlEPTB;MkSuN|I{QSEQvF2= MlTTV2FPT0WU
IST-SL2 M3n5Vmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M4nLUWlEPTB;MkSuOFM3OiEQvF2= NUjTc2xbW0GQR1XS
DJM-1 NIjleIhIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NVrxfVZmUUN3ME2yOE42OjJzIN88US=> M3rBeHNCVkeHUh?=
DMS-153 M13JSWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MkH5TWM2OD1{ND64OlE1KM7:TR?= NXjnXlh5W0GQR1XS
NB13 NFXBTY5Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MlvZTWM2OD1{NT6wNlY2KM7:TR?= NEj3d5lUSU6JRWK=
SK-N-DZ NFP3W|FIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MXPJR|UxRTJ4LkO0NVQh|ryP NFW1NWdUSU6JRWK=
COR-L88 NFv5e5NIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NHnJbZJKSzVyPUK2MlU4QTZizszN MkDHV2FPT0WU
LU-65 MnTqS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MoLPTWM2OD1{Nj64OVM2KM7:TR?= M3vZOnNCVkeHUh?=
TGBC1TKB NWW0bnYxT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M1j1d2lEPTB;Mk[uPVgzQCEQvF2= NGjDfVVUSU6JRWK=
THP-1 M1PaZmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NUDYbHVlUUN3ME2yO{4zOTRzIN88US=> NUHSUFFpW0GQR1XS
ONS-76 NH3z[|ZIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NFW2TIVKSzVyPUK3MlM{OiEQvF2= M3nvNXNCVkeHUh?=
LC-2-ad Ml3HS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NFnrXYlKSzVyPUK3MlYzOzFizszN NHjiNWxUSU6JRWK=
EW-13 Mn\TS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NFXYTFRKSzVyPUK5MlE4PDZizszN MkTXV2FPT0WU
MS-1 Mn;XS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NYjLfld3UUN3ME2zNE44Ojd6IN88US=> M4LVfnNCVkeHUh?=
NCI-H2227 MULHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MUTJR|UxRTNyLkm4NFYh|ryP NESyTopUSU6JRWK=
LXF-289 NHfMPVRIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MVTJR|UxRTNzLkS0PVIh|ryP M{jRTXNCVkeHUh?=
MC116 M2HkSWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NVfCSHFTUUN3ME2zNk4xQDJ4IN88US=> MY\TRW5ITVJ?
EVSA-T Mli3S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NX63UVBZUUN3ME2zNk4zPTh3IN88US=> MWrTRW5ITVJ?
CTB-1 MWnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NXjEXm9HUUN3ME2zN{4yOTBzIN88US=> MXfTRW5ITVJ?
COLO-320-HSR MWfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M2HZb2lEPTB;M{OuNVYxOyEQvF2= M4PQcXNCVkeHUh?=
NCI-H2196 NGn2eYVIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MkDZTWM2OD1|Mz6yOVU4KM7:TR?= M4exRnNCVkeHUh?=
LB2241-RCC M{P1eGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MXLJR|UxRTN|LkOxN|Uh|ryP MonpV2FPT0WU
LS-513 MkXhS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NXn2XGhEUUN3ME2zN{45PjN6IN88US=> MYrTRW5ITVJ?
LP-1 NVrHVIt5T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NXHyWXlwUUN3ME2zN{46QTV4IN88US=> NGXhRW1USU6JRWK=
A253 NFf0VlFIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NGn3dmhKSzVyPUO0MlIzQTZizszN NYG2fmYyW0GQR1XS
SK-MM-2 NHnI[GxIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MnnHTWM2OD1|ND65OFUyKM7:TR?= NX7xeFU{W0GQR1XS
NCI-H1963 M3fYXmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M1LLcGlEPTB;M{WuN|A4OiEQvF2= MnfQV2FPT0WU
MMAC-SF M1PXSmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NIn3W3BKSzVyPUO1Mlg4QDVizszN MXPTRW5ITVJ?
LB831-BLC MVTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MmLwTWM2OD1|Nj6wOlU1KM7:TR?= NUL1O2V{W0GQR1XS
WSU-NHL MmTpS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MUTJR|UxRTN4LkG2OEDPxE1? M1TKSnNCVkeHUh?=
CESS M{XWOGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MmHhTWM2OD1|Nj6yPFQ5KM7:TR?= NWjreZA3W0GQR1XS
NEC8 NVLCTJFrT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NGTOOm9KSzVyPUO2MlU5OzVizszN NUTKRld[W0GQR1XS
KNS-42 MUPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NIG5dJFKSzVyPUO3MlEzOzdizszN NYfXU49GW0GQR1XS
MHH-CALL-2 MXvHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M1uxeWlEPTB;M{euNVgzOSEQvF2= NXi1VHV5W0GQR1XS
K5 MXfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NE\tUHpKSzVyPUO4MlQ{KM7:TR?= NVXaNploW0GQR1XS
CP66-MEL NXi3WIxqT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M4TzOmlEPTB;M{muNFc{OyEQvF2= NYDnTGlwW0GQR1XS
OPM-2 NEW3T3dIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MWLJR|UxRTN7Lki0N|Ih|ryP MmTmV2FPT0WU
IST-MES1 NEHNU2pIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MoXRTWM2OD12MD6zNFk3KM7:TR?= M3nxO3NCVkeHUh?=
EC-GI-10 NWrvO5dbT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NID5S5RKSzVyPUSxMlU5ODVizszN NGrvfotUSU6JRWK=
CTV-1 MULHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MXLJR|UxRTR{Lki0NFYh|ryP MoLOV2FPT0WU
DG-75 NUC4bZdNT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= Ml;nTWM2OD12Mz63OVk2KM7:TR?= MlTOV2FPT0WU
KNS-81-FD MYTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MUTJR|UxRTR3LkSwOVgh|ryP M1flWXNCVkeHUh?=
NCI-H82 NH;IcWdIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MnK5TWM2OD12NT61O|U5KM7:TR?= Ml3tV2FPT0WU
RPMI-8866 MWDHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M2T1d2lEPTB;NE[uNVg4OyEQvF2= MlntV2FPT0WU
ACN MXjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MYPJR|UxRTR4LkSzOEDPxE1? NWiyTolXW0GQR1XS
NCI-H1395 MmfpS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M2HOZ2lEPTB;NE[uOFc2PiEQvF2= NYrrXZhHW0GQR1XS
NCI-H209 NXLMXGtST3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NXzEeFl{UUN3ME20O{4yPDB3IN88US=> MmPlV2FPT0WU
TGW MYrHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MVvJR|UxRTR7LkC3PVEh|ryP NH[xWJRUSU6JRWK=
NCI-H748 MoXHS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NV\JZmJXUUN3ME20PU41PzV|IN88US=> MVvTRW5ITVJ?
EKVX M2HVb2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M4XDWWlEPTB;NEmuOlYzQCEQvF2= MnXyV2FPT0WU

... Click to View More Cell Line Experimental Data

Assay
Methods Test Index PMID
Western blot
LC3-I / LC-3II / ATG5; 

PubMed: 23392173     


Sorafenib induces the conversion of LC3 in a dose-dependent manner. PLC5, Hep3B, SK-Hep1 and HepG2 were exposed to sorafenib at the indicated doses for 16 h and the expression levels of LC3-II were analyzed by western blot.

p-STAT3 / STAT3 / Mcl-1; 

PubMed: 23392173     


Effects of sorafenib on STAT3-related proteins in HCC cells. The cells were treated with sorafenib at the indicated dose for 16 h. 

β-catenin / Survivin / Mcl-1 / PTMA; 

PubMed: 26517516     


Co-inhibition of β-catenin and PTMA by sorafenib in HCC cells. Cell lines indicated on top were treated or not with 10 μM sorafenib for 24 hrs and processed for immuno-blotting. IC50 values (the concentration of sorafenib that inhibits 50% of cell growth) for each cell line are indicated below the panels.

pERK / ERK; 

PubMed: 22286758     


Western blot analysis of p-ERK (T202/Y204) and ERK at indicated time points in HCT116 cells treated with 20 μmol/L sorafenib.

p-PKM2(y105) / PMK2 / Caspase-9; 

PubMed: 26959741     


Sorafenib downregulates the p-PKM2 (Y105) at the indicated doses after treatment for 24 h.

RET(pY1016) / VEGFR2(pY1214) / MEK1(pT292) / ERK(pY204); 

PubMed: 22941289     


Sorafenib affected the phosphorylation of receptor tyrosine kinase RET and VEGFR2, as well as MEK/ERK kinases signaling cascades in three cell lines. Three cell lines were treated by sorafenib with two concentration gradients, 1 and 5 μmol/L/L, and then collected after 2, 4, and 8 h, cells without sorafenib treatment were as the controls (0 h). Total proteins were extracted and quantified to be used in Western blot assays. (A) Sorafenib inhibited RET and VEGFR2 phosphorylation dose-dependently while activated MEK and ERK phosphorylation in A549 cells. (B) Sorafenib also inhibited RET and VEGFR2 phosphorylation, and slightly activated MEK and ERK phosphorylation in HeLa cells. (C) Sorafenib activated the phosphorylation of RET, VEGFR2, and MEK, but inhibited ERK phosphorylation in HepG2 cells.

Cyclin D1; 

PubMed: 26039995     


Dose-escalation effects of sorafenib or SC-1 for 24 h on STAT3-related proteins in HSC-T6 and LX2 cells.

23392173 26517516 22286758 26959741 22941289 26039995
Growth inhibition assay
Cell viability; 

PubMed: 26039995     


Dose-escalation and time-dependent effects of sorafenib for 24 or 48 h on cell viability in HSC-T6, LX2, and mouse primary HSCs. Circles, mean; bars, SE (n = 3).

26039995
Immunofluorescence
p65; 

PubMed: 22286758     


HCT116 cells were treated with 20 μmol/L sorafenib or 10 ng/mL TNF-α for 3 hours then fixed. Immunofluorescence was carried out as described in the Materials and Methods for p65 (green) and DAPI (blue). Representative pictures (400×) are shown.

cytochrome c; 

PubMed: 22278289     


Immunoflourescent staining and quantification of mitochondrial membrane potential (appearing in red, mitotracker) and cytochrome c (appearing in green, FITC) in 22Rv1 and PC3 treated with 20 μM sorafenib for 24 h.

22286758 22278289
ELISA
TGF-beta / CD206; 

PubMed: 26158762     


In Macrophage, TGF-β secretion and CD206 were confirmed by ELISA.

Caspase-9 / Caspase-3; 

PubMed: 30923462     


Caspase-9 and caspase-3 activities were measured via ELISA assay. FCCP, an activator of mitophagy, was added into the medium of sorafenib-treated cells to activate mitophagy. Adenovirus-loaded LATS2 (Ad-LATS2) was transfected into HepG2 cells in the presence of sorafenib. *p < 0.05 vs. control group; #p < 0.05 vs. Sorafenib + Ad-cont group; #p < 0.05 vs. Sorafenib + Ad-LATS2 group.

26158762 30923462
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]

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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:

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  • 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:

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  • 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

Bio Calculators

Molarity Calculator

Molarity Calculator

Calculate the mass, volume or concentration required for a solution. The Selleck molarity calculator is based on the following equation:

Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)

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*When preparing stock solutions, please always use the batch-specific molecular weight of the product found on the via label and MSDS / COA (available on product pages).

Dilution Calculator

Dilution Calculator

Calculate the dilution required to prepare a stock solution. The Selleck dilution calculator is based on the following equation:

Concentration (start) x Volume (start) = Concentration (final) x Volume (final)

This equation is commonly abbreviated as: C1V1 = C2V2 ( Input Output )

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    C2
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* When preparing stock solutions always use the batch-specific molecular weight of the product found on the vial label and MSDS / COA (available online).

The Serial Dilution Calculator Equation

  • Serial Dilutions

  • Computed Result

  • C1=C0/X C1: LOG(C1):
    C2=C1/X C2: LOG(C2):
    C3=C2/X C3: LOG(C3):
    C4=C3/X C4: LOG(C4):
    C5=C4/X C5: LOG(C5):
    C6=C5/X C6: LOG(C6):
    C7=C6/X C7: LOG(C7):
    C8=C7/X C8: LOG(C8):
Molecular Weight Calculator

Molecular Weight Calculator

Enter the chemical formula of a compound to calculate its molar mass and elemental composition:

Total Molecular Weight: g/mol

Tip: Chemical formula is case sensitive. C10H16N2O2 c10h16n2o2

Instructions to calculate molar mass (molecular weight) of a chemical compound:

To calculate molar mass of a chemical compound, please enter its chemical formula and click 'Calculate'.

Definitions of molecular mass, molecular weight, molar mass and molar weight:

Molecular mass (molecular weight) is the mass of one molecule of a substance and is expressed in the unified atomic mass units (u). (1 u is equal to 1/12 the mass of one atom of carbon-12)
Molar mass (molar weight) is the mass of one mole of a substance and is expressed in g/mol.

Molarity Calculator

Mass Concentration Volume Molecular Weight

Clinical Trial Information

NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT03780634 Not yet recruiting Hepatocellular Carcinoma Sun Yat-sen University|Kaiping Central Hospital|Guangzhou No.12 People''s Hospital April 1 2019 Phase 2
NCT03780634 Not yet recruiting Hepatocellular Carcinoma Sun Yat-sen University|Kaiping Central Hospital|Guangzhou No.12 People''s Hospital April 1 2019 Phase 2
NCT03878524 Not yet recruiting Breast Cancer|Prostate Cancer|Pancreatic Cancer|Acute Myelogenous Leukemia OHSU Knight Cancer Institute|Oregon Health and Science University|Prospect Creek Foundation March 14 2019 Phase 1
NCT03878524 Not yet recruiting Breast Cancer|Prostate Cancer|Pancreatic Cancer|Acute Myelogenous Leukemia OHSU Knight Cancer Institute|Oregon Health and Science University|Prospect Creek Foundation March 14 2019 Phase 1
NCT03644511 Recruiting Hepatocellular Carcinoma Bayer February 28 2019 --
NCT03606590 Recruiting Hepatocellular Carcinoma NovoCure GmbH|NovoCure Ltd. February 15 2019 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

Tel: +1-832-582-8158 Ext:3

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Raf Signaling Pathway Map

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID