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 Mlj2S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MVPJR|UxRTBwMECwNFA{ODNizszN NXrOUoNmW0GQR1XS
MONO-MAC-6 M3r3SWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 Mnm1TWM2OD1yLkCwOFE5KM7:TR?= MkfRV2FPT0WU
ALL-PO NFewO5BIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NEjUSYxKSzVyPUCuNFMyQDRizszN M{L2fXNCVkeHUh?=
NKM-1 MXjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NYL1XlIyUUN3ME2wMlA4PDF4IN88US=> Mnv0V2FPT0WU
CGTH-W-1 M1ewNWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MlrqTWM2OD1yLkK1NFIzKM7:TR?= MkHTV2FPT0WU
BB65-RCC NEHpPZpIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NFjoXldKSzVyPUCuOFcxPzNizszN M{XmfHNCVkeHUh?=
NOS-1 MlnUS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M{fyN2lEPTB;MD61OlM3KM7:TR?= NIDPS4NUSU6JRWK=
SH-4 NXrMRXRYT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M1TQfmlEPTB;MD62OVYyOyEQvF2= M4PtcnNCVkeHUh?=
HOP-62 M1z6[mdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MmH4TWM2OD1yLki1NFg5KM7:TR?= MkGxV2FPT0WU
HCC2998 MmnLS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M33sfmlEPTB;MD64PFgyQCEQvF2= NXvSNnExW0GQR1XS
GDM-1 NYm5U4xjT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MknMTWM2OD1yLkmwOlk5KM7:TR?= NXHDT3JHW0GQR1XS
KM12 M4fFW2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 Ml3jTWM2OD1zLkCyNFk5KM7:TR?= MYHTRW5ITVJ?
LB2518-MEL M{HWNGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NUfJ[GF2UUN3ME2xMlIxQDB7IN88US=> Mk[wV2FPT0WU
NCI-H1436 MYPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MYHJR|UxRTFwMkG2O|gh|ryP M2[1cXNCVkeHUh?=
EM-2 MlLRS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NWi1TmZ1UUN3ME2xMlM2PTd6IN88US=> NYrUN5FSW0GQR1XS
LAMA-84 MVvHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MoK4TWM2OD1zLkO3OlQ5KM7:TR?= NY\xd4RDW0GQR1XS
KG-1 MWLHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MnjBTWM2OD1zLkS3PVM2KM7:TR?= NWrWWI1kW0GQR1XS
A388 M4HrV2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M4PSPWlEPTB;MT61PVE3PSEQvF2= NXq0cpl3W0GQR1XS
no-10 NHf6U|FIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M1n0fGlEPTB;MT62NVczPiEQvF2= MWnTRW5ITVJ?
SF126 MoXkS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MVXJR|UxRTFwNkO4NVIh|ryP MYjTRW5ITVJ?
MEG-01 Mm[wS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MkLmTWM2OD1zLkiwPVgh|ryP MXvTRW5ITVJ?
A3-KAW M4LOeGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NX\OSIRXUUN3ME2xMlg5PDJizszN M1zlZnNCVkeHUh?=
D-247MG NID5d45Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M2m4dWlEPTB;Mj6xOFQ5KM7:TR?= MnLmV2FPT0WU
OVCAR-4 MlXMS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M3TaWGlEPTB;Mj6yNVM6OyEQvF2= M2HGNnNCVkeHUh?=
NCI-SNU-1 M4n1UWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M3rUWmlEPTB;Mj6zNVYzKM7:TR?= NUnTcIJoW0GQR1XS
NCI-H2171 MYHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MnjmTWM2OD1{LkO5O|Y1KM7:TR?= MVfTRW5ITVJ?
SIG-M5 NX73ZZJqT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MnTCTWM2OD1{LkSyNlQzKM7:TR?= NY\NcGU4W0GQR1XS
BE-13 NFjzZZZIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MofOTWM2OD1{Lk[5OlA6KM7:TR?= M4X3NnNCVkeHUh?=
K052 MYDHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NHvnOFRKSzVyPUKuO|Q3OTZizszN MmfLV2FPT0WU
L-540 NWLkc2U5T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MkewTWM2OD1{Lke1O|g6KM7:TR?= M{H4UXNCVkeHUh?=
KMOE-2 M1PZTGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M2jP[WlEPTB;Mj64NVM2KM7:TR?= M{XkdnNCVkeHUh?=
MFH-ino M13YZ2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NV;1N2c4UUN3ME2yMlkzOTh3IN88US=> MX3TRW5ITVJ?
HL-60 MUTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NGr0SGlKSzVyPUOuNFYzQTlizszN NFPTdXpUSU6JRWK=
HCC2218 MY\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M2fxZ2lEPTB;Mz6xNlAxOyEQvF2= NYHsVpVXW0GQR1XS
TE-5 MoWxS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MoTCTWM2OD1|LkGzNVYzKM7:TR?= M4THXHNCVkeHUh?=
MZ1-PC MYPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MXrJR|UxRTNwNEe1NFkh|ryP NGnmN4FUSU6JRWK=
MRK-nu-1 M4rLZ2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M33ve2lEPTB;Mz62NVQ3QCEQvF2= NGTnUHNUSU6JRWK=
MZ7-mel M3XpXmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NHfZSlJKSzVyPUOuOlYxQTlizszN MlXIV2FPT0WU
BC-1 Mk\tS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NUHGW5FHUUN3ME2zMlc1ODJizszN M3fnNHNCVkeHUh?=
ST486 MU\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NEG0co5KSzVyPUOuPFM3PzNizszN M3P4eHNCVkeHUh?=
KS-1 MUjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M4\NTWlEPTB;Mz64PFE6QCEQvF2= M37Tc3NCVkeHUh?=
SK-NEP-1 NFHrNGJIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M2\sZWlEPTB;ND6xOlgyPSEQvF2= NIfWTmpUSU6JRWK=
BC-3 MW\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? Ml;OTWM2OD12LkKzN|kyKM7:TR?= MWjTRW5ITVJ?
NCI-H1581 MYHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MlW0TWM2OD12LkK4O|k5KM7:TR?= NYrKSph[W0GQR1XS
MHH-PREB-1 NGC1ZXlIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MoHlTWM2OD12LkSwOFg1KM7:TR?= MnjkV2FPT0WU
NOMO-1 NUTPPHNYT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M2LTdGlEPTB;ND60PFkxPSEQvF2= MVrTRW5ITVJ?
QIMR-WIL NHXPXGdIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MYrJR|UxRTVwMEeyPVQh|ryP MYXTRW5ITVJ?
SF539 M3TUXWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NETTUmxKSzVyPUWuNVMzOjdizszN NXTHUm9yW0GQR1XS
TE-12 NIXvTmtIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NHXFc2ZKSzVyPUWuNlQ6OjlizszN NXvQ[5ZTW0GQR1XS
NCI-H510A MoL5S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MX\JR|UxRTVwNEG2PFUh|ryP NFe3WJdUSU6JRWK=
JAR NIWxfYtIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M{HNbWlEPTB;NT61NFgzPCEQvF2= NEntc5dUSU6JRWK=
no-11 NWHJcZF{T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MlXYTWM2OD13LkezOVY5KM7:TR?= NF7YZ4tUSU6JRWK=
BV-173 M1zzZmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NGTucpJKSzVyPUWuPVU3QDJizszN NFjGVVBUSU6JRWK=
SR MkLxS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MmXlTWM2OD14LkCwOlc5KM7:TR?= MlTIV2FPT0WU
MOLT-16 NGTV[2tIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NX7NUJJWUUN3ME22MlI2OjZ4IN88US=> Mo\1V2FPT0WU
MZ2-MEL M{nDNGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NUHsS48zUUN3ME22MlMyQDN7IN88US=> NEHBNoJUSU6JRWK=
SW954 Ml7GS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NV3KPIhWUUN3ME22MlQ2QDZ4IN88US=> MYfTRW5ITVJ?
ML-2 M1jt[Wdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MYrJR|UxRTZwNUK4OFkh|ryP M2PwNnNCVkeHUh?=
OCI-AML2 MYLHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M{nwemlEPTB;Nj62NVA3OiEQvF2= M3fzV3NCVkeHUh?=
SIMA MnrUS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NYW2N|c{UUN3ME23MlAxOTBzIN88US=> M{PIXXNCVkeHUh?=
DOHH-2 M2HJNmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NWPnZVhSUUN3ME23MlA2Pjd4IN88US=> M1;mUHNCVkeHUh?=
697 NVP5RVZzT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M1TuSmlEPTB;Nz6wOVk5QSEQvF2= Ml\CV2FPT0WU
NB1 NI\tfoFIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M2XiOWlEPTB;Nz60NFQxPyEQvF2= NF;qXoRUSU6JRWK=
D-392MG NH31NIJIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MXnJR|UxRTdwNkK2OlMh|ryP MUDTRW5ITVJ?
ES8 Mo\aS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MVzJR|UxRTdwN{[1NFMh|ryP MWPTRW5ITVJ?
RPMI-8226 MkW3S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NUnVTIt4UUN3ME23Mlg1PTFzIN88US=> M2fvN3NCVkeHUh?=
IST-MEL1 M{jJOWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NIjse2RKSzVyPUiuOFAxODJizszN NIq4SGNUSU6JRWK=
NB14 NUnZelZyT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MorYTWM2OD16Lk[zNVM{KM7:TR?= MXvTRW5ITVJ?
HD-MY-Z MnrJS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M1vBfmlEPTB;OD62N|c1PiEQvF2= MXrTRW5ITVJ?
TE-10 NFThbYRIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NUHs[|VDUUN3ME24Mlc3OzV|IN88US=> M{mxUnNCVkeHUh?=
LC-1F NVvoc29iT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M1;6d2lEPTB;OT6xNFg{PCEQvF2= NXO5cGl4W0GQR1XS
OS-RC-2 MorDS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? Moi4TWM2OD17LkGxNlQ{KM7:TR?= MmrSV2FPT0WU
NCI-SNU-16 NHzu[lNIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NEnOd4hKSzVyPUmuNlExOjZizszN NF[2XW1USU6JRWK=
SHP-77 M13ieGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MlewTWM2OD17LkexOlYzKM7:TR?= MVvTRW5ITVJ?
A4-Fuk NEOyZoxIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M{j0c2lEPTB;OT63OVYyKM7:TR?= NF7DclJUSU6JRWK=
NB6 M2WxeGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MmfJTWM2OD17Lke2NFI6KM7:TR?= MWPTRW5ITVJ?
JiyoyeP-2003 Mlj5S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MkHLTWM2OD1zMD60O|Q2KM7:TR?= MX7TRW5ITVJ?
DMS-114 NUDtZlEyT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MmXjTWM2OD1zMD61OFQyKM7:TR?= NHvafnJUSU6JRWK=
NB7 M{K1XWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MX;JR|UxRTFyLke1NlYh|ryP M1XqVnNCVkeHUh?=
NCI-H747 NVLWXZJVT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NUTrb4dMUUN3ME2xNU4yOjF4IN88US=> MlzjV2FPT0WU
HH M{jHNGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MoHXTWM2OD1zMT6zPFc3KM7:TR?= M{nmXHNCVkeHUh?=
EW-18 M1nvZ2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M2q1[mlEPTB;MUGuPVA1PCEQvF2= NGfpTXlUSU6JRWK=
CHP-126 Ml20S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NWG0PVRGUUN3ME2xNU46PzN6IN88US=> NV3pe5R2W0GQR1XS
NTERA-S-cl-D1 NGHqPZRIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M4jkUmlEPTB;MUKuNFI4QCEQvF2= NW\qeI82W0GQR1XS
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TE-8 MkjiS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M13XfGlEPTB;MkGuOlM6PCEQvF2= NVrzOZZwW0GQR1XS
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C2BBe1 NG\LWGFIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NEXXZ21KSzVyPUK0MlMzOzlizszN NI[1bZRUSU6JRWK=
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DJM-1 NEXVRm1Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NEfs[YdKSzVyPUK0MlUzOjFizszN NE\jO5RUSU6JRWK=
DMS-153 MXrHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MVnJR|UxRTJ2Lki2NVQh|ryP NUfZfXZQW0GQR1XS
NB13 MkDnS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NXPuWYRTUUN3ME2yOU4xOjZ3IN88US=> NFXTdJdUSU6JRWK=
SK-N-DZ MYXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NX:xblB{UUN3ME2yOk4{PDF2IN88US=> NV;Ye49oW0GQR1XS
COR-L88 MmPjS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NXvhXoRzUUN3ME2yOk42Pzl4IN88US=> M1S3cHNCVkeHUh?=
LU-65 NGO4PJpIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NU\oWpVLUUN3ME2yOk45PTN3IN88US=> MVXTRW5ITVJ?
TGBC1TKB M1rDU2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M4PUTmlEPTB;Mk[uPVgzQCEQvF2= MVPTRW5ITVJ?
THP-1 NV;2fZE3T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NHLTSZZKSzVyPUK3MlIyPDFizszN M3fZN3NCVkeHUh?=
ONS-76 M3fPXmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M4rNcGlEPTB;MkeuN|MzKM7:TR?= MoPEV2FPT0WU
LC-2-ad MV3Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MlTiTWM2OD1{Nz62NlMyKM7:TR?= NFLKPVFUSU6JRWK=
EW-13 NEPncIpIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MUfJR|UxRTJ7LkG3OFYh|ryP NXO4[YlYW0GQR1XS
MS-1 NGjBXWxIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NHLMb4ZKSzVyPUOwMlczPzhizszN MkTuV2FPT0WU
NCI-H2227 NETJNYZIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MUnJR|UxRTNyLkm4NFYh|ryP MmjFV2FPT0WU
LXF-289 MkHjS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M3zkc2lEPTB;M{GuOFQ6OiEQvF2= MWLTRW5ITVJ?
MC116 NVzFR2lJT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NXrhNWxJUUN3ME2zNk4xQDJ4IN88US=> NFWxPJJUSU6JRWK=
EVSA-T NVfEOmxDT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NVmwemN4UUN3ME2zNk4zPTh3IN88US=> NFLzWZJUSU6JRWK=
CTB-1 NH76coRIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NXHDe4drUUN3ME2zN{4yOTBzIN88US=> MlHuV2FPT0WU
COLO-320-HSR MVvHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MVrJR|UxRTN|LkG2NFMh|ryP MlPMV2FPT0WU
NCI-H2196 M1TVUWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NX7nTVN7UUN3ME2zN{4zPTV5IN88US=> NGi4NJFUSU6JRWK=
LB2241-RCC MmrJS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M3HleWlEPTB;M{OuN|E{PSEQvF2= NHPQN2RUSU6JRWK=
LS-513 NF3nbnNIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MlWwTWM2OD1|Mz64OlM5KM7:TR?= MlLIV2FPT0WU
LP-1 NUfQdXlqT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NYHWV5VlUUN3ME2zN{46QTV4IN88US=> MmHLV2FPT0WU
A253 MojPS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NFLvb21KSzVyPUO0MlIzQTZizszN NHuyRWpUSU6JRWK=
SK-MM-2 NF7ldFlIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= Mkf0TWM2OD1|ND65OFUyKM7:TR?= MWHTRW5ITVJ?
NCI-H1963 NYHRS|ZMT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= Ml;xTWM2OD1|NT6zNFczKM7:TR?= NXTSZmJTW0GQR1XS
MMAC-SF M2TEb2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MUfJR|UxRTN3Lki3PFUh|ryP MUnTRW5ITVJ?
LB831-BLC M{LQRmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NVr6fnVKUUN3ME2zOk4xPjV2IN88US=> M3rJc3NCVkeHUh?=
WSU-NHL M4HRVGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 Ml\WTWM2OD1|Nj6xOlQh|ryP M3P0c3NCVkeHUh?=
CESS MkPCS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MYrJR|UxRTN4LkK4OFgh|ryP Mm\aV2FPT0WU
NEC8 MVTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MkXmTWM2OD1|Nj61PFM2KM7:TR?= NEnrcpNUSU6JRWK=
KNS-42 Mn7kS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MX;JR|UxRTN5LkGyN|ch|ryP NXzoTmJ4W0GQR1XS
MHH-CALL-2 M4HreWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MnLNTWM2OD1|Nz6xPFIyKM7:TR?= M33CcnNCVkeHUh?=
K5 Mo[yS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NEWyNWtKSzVyPUO4MlQ{KM7:TR?= NWS1c5BVW0GQR1XS
CP66-MEL NVnTe5c1T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NGmzU2FKSzVyPUO5MlA4OzNizszN NF;QNGhUSU6JRWK=
OPM-2 MX3Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M3P3b2lEPTB;M{muPFQ{OiEQvF2= M2O1d3NCVkeHUh?=
IST-MES1 M1K3cGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NGLRN41KSzVyPUSwMlMxQTZizszN NHrrSWNUSU6JRWK=
EC-GI-10 MVrHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MXPJR|UxRTRzLkW4NFUh|ryP MYTTRW5ITVJ?
CTV-1 NF65PVhIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MUnJR|UxRTR{Lki0NFYh|ryP NGG0b5RUSU6JRWK=
DG-75 MVLHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NYrRVYRwUUN3ME20N{44PTl3IN88US=> Mn\kV2FPT0WU
KNS-81-FD MlrWS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MmHTTWM2OD12NT60NFU5KM7:TR?= MWTTRW5ITVJ?
NCI-H82 NYf4coFYT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M1;xfmlEPTB;NEWuOVc2QCEQvF2= MmrVV2FPT0WU
RPMI-8866 MnzuS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MYjJR|UxRTR4LkG4O|Mh|ryP MXLTRW5ITVJ?
ACN NF7LRnBIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NXPIeoFjUUN3ME20Ok41OzRizszN Mn3XV2FPT0WU
NCI-H1395 MlXHS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MVTJR|UxRTR4LkS3OVYh|ryP NEPDd3lUSU6JRWK=
NCI-H209 MWXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NVH5UXdTUUN3ME20O{4yPDB3IN88US=> NXnVb5BiW0GQR1XS
TGW M{[3bGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NXz2WlJ6UUN3ME20PU4xPzlzIN88US=> NG\HT4JUSU6JRWK=
NCI-H748 Mnr4S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? Mn;hTWM2OD12OT60O|U{KM7:TR?= NETsVnZUSU6JRWK=
EKVX NVfPPWZFT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MUDJR|UxRTR7Lk[2Nlgh|ryP M{[0VnNCVkeHUh?=

... Click to View More Cell Line Experimental Data

In vivo Oral administration of Sorafenib (~60 mg/kg) demonstrates broad spectrum, dose-dependent anti-tumor activity against a variety of human tumor xenograft models including MDA-MB-231, Colo-205, HT-29, DLD-1, NCI-H460, and A549, with no evidence of toxicity. In association with the anti-tumor efficacy, Sorafenib treatment potently inhibits MEK 1/2 phosphorylation and pERK 1/2 levels in HT-29 and MDA-MB-231 xenografts but not in Colo-205 xenografts, and significantly suppresses tumor microvessel area (MVA) and microvessel density (MVD) in MDA MB-231, HT-29 and Colo-205 tumor xenografts. [1] Sorafenib treatment produces dose-dependent growth inhibition of PLC/PRF/5 tumor xenografts in SCID mice with TGIs of 49% and 78% at 10 mg/kg and 30 mg/kg, respectively, consistent with the inhibition of ERK and eIF4E phosphorylation, reduction of the microvessel area, and induction of tumor cell apoptosis. [2] Sorafenib sensitizes bax-/- cells to TRAIL in a dose-dependent manner, through a mechanism involving down-regulating NF-κB mediated Mcl-1 and cIAP2 expression. Combining Sorafenib (30-60 mg/kg) with TRAIL (5 mg/kg) show dramatic efficacy in TRAIL-resistant HCT116 bax-/- and HT29 tumor xenografts. [3]

Protocol

Kinase Assay:

[1]

+ Expand

Biochemical assays:

Recombinant baculoviruses expressing Raf-1 (residues 305–648) and B-Raf (residues 409–765) are purified as fusion proteins. Full-length human MEK-1 is generated by PCR and purified as a fusion protein from Escherichia coli lysates. Sorafenib tosylate is added to a mixture of Raf-1 (80 ng), or B-Raf (80 ng) with MEK-1 (1 μg) in assay buffer [20 mM Tris (pH 8.2), 100 mM NaCl, 5 mM MgCl2, and 0.15% β-mercaptoethanol] at a final concentration of 1% DMSO. The Raf kinase assay (final volume of 50 μL) is initiated by adding 25 μL of 10 μM γ[33P]ATP (400 Ci/mol) and incubated at 32 °C for 25 minutes. Phosphorylated MEK-1 is harvested by filtration onto a phosphocellulose mat, and 1% phosphoric acid is used to wash away unbound radioactivity. After drying by microwave heating, a β-plate counter is used to quantify filter-bound radioactivity. Human VEGFR2 (KDR) kinase domain is expressed and purified from Sf9 lysates. Time-resolved fluorescence energy transfer assays for VEGFR2 are performed in 96-well opaque plates in the time-resolved fluorescence energy transfer format. Final reaction conditions are as follows: 1 to 10 μM ATP, 25 nM poly GT-biotin, 2 nM Europium-labeled phospho (p)-Tyr antibody (PY20), 10 nM APC, 1 to 7 nM cytoplasmic kinase domain in final concentrations of 1% DMSO, 50 mM HEPES (pH 7.5), 10 mM MgCl2, 0.1 mM EDTA, 0.015% Brij-35, 0.1 mg/mL BSA, and 0.1% β-mercaptoethanol. Reaction volumes are 100 μL and are initiated by addition of enzyme. Plates are read at both 615 and 665 nM on a Perkin-Elmer VictorV Multilabel counter at ~1.5 to 2.0 hours after reaction initiation. Signal is calculated as a ratio: (665 nm/615 nM) × 10,000 for each well. For IC50 generation, Sorafenib tosylate is added before the enzyme initiation. A 50-fold stock plate is made with Sorafenib tosylate serially diluted 1:3 in a 50% DMSO/50% distilled water solution. Final Sorafenib tosylate concentrations range from 10 μM to 4.56 nM in 1% DMSO.
Cell Research:

[1]

+ Expand
  • Cell lines: MDA-MB-231, and HAoSMC
  • Concentrations: Dissolved in DMSO, final concentrations ~10 μM
  • Incubation Time: 72 hours
  • Method:

    Cells are exposed to increasing concentrations of Sorafenib tosylate for 72 hours. Cell number is quantitated using the Cell TiterGlo ATP Luminescent assay kit. This assay measures the number of viable cells per well by measurement of luminescent signal based on amount of cellular ATP.


    (Only for Reference)
Animal Research:

[1]

+ Expand
  • Animal Models: Female NCr-nu/nu mice implanted s.c. with MDA-MB-231, Colo-205, HT-29, H460, or A549 cells
  • Formulation: Dissolved in Cremophor EL/ethanol (50:50) as 4-fold (4 × stock solution, and diluted to 1 × with water
  • Dosages: ~60 mg/kg
  • Administration: Orally once daily
    (Only for Reference)

Solubility (25°C)

In vitro DMSO 63 mg/mL warmed (135.53 mM)
Water Insoluble
Ethanol Insoluble
In vivo Add solvents to the product individually and in order(Data is from Selleck tests instead of citations):
5% DMSO+45% PEG 400+ddH2O
For best results, use promptly after mixing.
3mg/mL

* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.

Chemical Information

Molecular Weight 464.82
Formula

C21H16ClF3N4O3

CAS No. 284461-73-0
Storage powder
in solvent
Synonyms BAY 43-9006

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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* 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

If you have any other enquiries, please leave a message.

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID