Sorafenib Tosylate

Catalog No.S1040 Synonyms: Bay 43-9006

Molecular Weight(MW): 637.03

Sorafenib Tosylate 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.

Cited by 46 Publications

J Exp Clin Cancer Res, 2019, 38(1):204

PubMed: 31101057 ( click the link to review the publication )

Am J Cancer Res, 2019, 9(5):906-926

PubMed: 31218101 ( click the link to review the publication )

Clin Cancer Res, 2018, 10.1158/1078-0432.CCR-18-0693

PubMed: 30076136 ( click the link to review the publication )

J Lipid Res, 2018, 59(11):2188-2201

PubMed: 30173145 ( click the link to review the publication )

Int J Biol Sci, 2018, 14(13):1845-1858

PubMed: 30443188 ( click the link to review the publication )

Oncotarget, 2017, 8(8):13464-13475

PubMed: 28088782 ( click the link to review the publication )

Cancer Lett, 2016, 377(2):149-57

PubMed: 27132990 ( click the link to review the publication )

J Cell Physiol, 2016, 231(10):2286-302

PubMed: 27187154 ( click the link to review the publication )

Cell Death Dis, 2014, 5:e1278

PubMed: 24901049 ( click the link to review the publication )

Mol Oncol, 2014, 8(7):1339-54

PubMed: 24908424 ( click the link to review the publication )

Stem Cell Res Ther, 2014, 5(2):37

PubMed: 24635859 ( click the link to review the publication )

Mol Cancer Res, 2014, 12(10):1377-87

PubMed: 24874432 ( click the link to review the publication )

J Cell Sci, 2014, 127(Pt 7):1585-94

PubMed: 24463816 ( click the link to review the publication )

Apoptosis, 2014, 19(4):682-97

PubMed: 24337903 ( click the link to review the publication )

PLoS One, 2014, 9(6):e97739

PubMed: 24905462 ( click the link to review the publication )

PLoS One, 2014, 9(6):e100814

PubMed: 24956259 ( click the link to review the publication )

Biomed Res Int, 2014, 2014:764981

PubMed: 25057499 ( click the link to review the publication )

Biochem Biophys Res Commun, 2014, 450(1):19-24

PubMed: 24858691 ( click the link to review the publication )

FEBS Open Bio, 2014, 4:458-67

PubMed: 24918061 ( click the link to review the publication )

Blood, 2013, 122(9):1621-33

PubMed: 23863897 ( click the link to review the publication )

Hepatology, 2013, 59(4):1435-47

PubMed: 24242874 ( click the link to review the publication )

Lab Invest, 2013, 93(1):8-19

PubMed: 23108376 ( click the link to review the publication )

Drug Metab Dispos, 2013, 10.1124/dmd.113.054189

PubMed: 24335466 ( click the link to review the publication )

Mol Cell Endocrinol, 2013, 377(1-2):1-6

PubMed: 23811235 ( click the link to review the publication )
PLoS One, 2013, 8(12):e83521

PubMed: 24376712 ( click the link to review the publication )

PLoS One, 2013, 8(1):e54595

PubMed: 23355882 ( click the link to review the publication )

Mol Cell Biochem, 2013, 372(1-2):65-74

PubMed: 22941213 ( click the link to review the publication )

J Biomol Screen, 2013, 19(4):526-37

PubMed: 24361645 ( click the link to review the publication )

Blood Cells Mol Dis, 2013, 52(4):214-24

PubMed: 24314748 ( click the link to review the publication )

The Journal of Experimental Secondary Science, 2013, William Henry Bloxham

PubMed: ( click the link to review the publication )

Virginia Commonwealth University, 2013, 2013

PubMed: ( click the link to review the publication )

Blood, 2012, 120(19):4104-15

PubMed: 23007403 ( click the link to review the publication )

Haematologica, 2012, 97(11):1722-30

PubMed: 22689683 ( click the link to review the publication )

Cell Death Differ, 2012, 19(12):2029-39

PubMed: 22858545 ( click the link to review the publication )

Int J Cancer, 2012, 131(12):2961-9

PubMed: 22514082 ( click the link to review the publication )

Int J Cancer, 2012, 132(3):738-43

PubMed: 22752848 ( click the link to review the publication )

Br J Haematol, 2012, 157(4):510-4

PubMed: 22313359 ( click the link to review the publication )

Br J Haematol, 2012, 157(4):483-92

PubMed: 22409268 ( click the link to review the publication )

Mol Pharm, 2012, 9(11):3062-78

PubMed: 22971013 ( click the link to review the publication )

Biochem Pharmacol, 2012, 83(12):1674-81

PubMed: 22414727 ( click the link to review the publication )

Surgery, 2012, 152(6):1142-9

PubMed: 23158184 ( click the link to review the publication )

Invest New Drugs, 2012, 31(3):780-6

PubMed: 23154882 ( click the link to review the publication )

Clin Cancer Res, 2011, 17(24):7595-604

PubMed: 22038996 ( click the link to review the publication )

J Invest Dermatol, 2011, 131(9):1886-95

PubMed: 21654832 ( click the link to review the publication )

Mol Pharmacol, 2011, 80(6):1066-75

PubMed: 21896713 ( click the link to review the publication )

Int J Parasitol, 2010, 40(5):555-67

PubMed: 19887070 ( click the link to review the publication )

Purity & Quality Control

Choose Selective Raf Inhibitors

Biological Activity

Description

Sorafenib Tosylate 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)	VEGFR2/Flk1 ^[1] (Cell-free assay)	B-Raf ^[1] (Cell-free assay)	B-Raf (V599E) ^[1] (Cell-free assay)	PDGFRβ ^[1] (Cell-free assay)	View More
6 nM	15 nM	22 nM	38 nM	57 nM	View More

In vitro

Sorafenib tosylate inhibits both wild-type and V599E mutant B-Raf activity with IC50 of 22 nM and 38 nM, respectively. Sorafenib tosylate 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 tosylate 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 tosylate 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 tosylate 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 tosylate 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 tosylate significantly inhibits the phosphorylation of eIF4E and down-regulates Mcl-1 levels in hepatocellular carcinoma (HCC) cells in a MEK/ERK-independent manner. Sorafenib tosylate 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	Incubation Time	Activity Description	PMID
MDA-MB-435	NGPpNFZIem:5dHigTY5pcWKrdHnvckBCe3OjeR?=	NFjrXGo1QCCq	M{jQfWdKPTB;MjFOwG0>	MV:yNlU3ODZ{Nx?=
UACC257	M1nEXWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7	NIC2fFI1QCCq	NF\KenFIUTVyPUKg{txO	NF22S5ozOjV4ME[yOy=>
MCF7	MkD4S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?	NFHVeYw1QCCq	NFXw[ldIUTVyPUKuOUDPxE1?	MknJNlI2PjB4Mke=
EKVX	M3mycmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7	M1TRW\|Q5KGh?	NF:4[oJIUTVyPUKuOUDPxE1?	M1q3dlIzPTZyNkK3
HT-29	NYrWXpRGT3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=	NEDtbos1QCCq	MkfBS2k2OD1{LkWg{txO	M{XTdFIzPTZyNkK3
SNB19	M{GwNWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7	MWG0PEBp	NUjyWotNT0l3ME2zMlIh\|ryP	MoLDNlI2PjB4Mke=
OVCAR3	MnL3S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?	M2L3elQ5KGh?	MmnRS2k2OD1\|LkKg{txO	NET6VFkzOjV4ME[yOy=>
CAKI-1	NHL3R\|BIem:5dHigTY5pcWKrdHnvckBCe3OjeR?=	NWXkNFI4PDhiaB?=	NYrHemZpT0l3ME2zMlIh\|ryP	M4\2dFIzPTZyNkK3
SW620	MVPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?	MmPNOFghcA>?	NGj4[3JIUTVyPUOuNkDPxE1?	MYSyNlU3ODZ{Nx?=
TK10	NFTWcmlIem:5dHigTY5pcWKrdHnvckBCe3OjeR?=	MU[0PEBp	MYnHTVUxRTVizszN	M{DwdlIzPTZyNkK3

... Click to View More Cell Line Experimental Data

Assay

Methods	Test Index	PMID
Western blot	LC3-I / LC-3II / ATG5; PubMed: 23392173 Cell Death Dis 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 Cell Death Dis 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 Oncotarget 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 Oncogene 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 Oncotarget 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 Acta Pharmacol Sin 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 Proc Natl Acad Sci U S A 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
Immunofluorescence	p65; PubMed: 22286758 Oncogene 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 Cell Death Dis 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
Growth inhibition assay	Cell viability; PubMed: 26039995 Proc Natl Acad Sci U S A 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
ELISA	TGF-beta / CD206; PubMed: 26158762 Oncotarget In Macrophage, TGF-β secretion and CD206 were confirmed by ELISA. Caspase-9 / Caspase-3; PubMed: 30923462 Cancer Cell Int 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 tosylate (~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 tosylatetreatment 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 tosylate 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]

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 w Dosages: ~60 mg/kg Administration: Orally once daily (Only for Reference)

References

Solubility (25°C)

In vitro	DMSO	127 mg/mL (199.36 mM)
	Water	0.01 mg/mL (0.01 mM)
	Ethanol	Insoluble
In vivo	Add solvents to the product individually and in order(Data is from Selleck tests instead of citations): 2% Cremophor EL, 2% N,N-dimethylacetamide For best results, use promptly after mixing.	30 mg/mL (suspension)

* 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 Download Sorafenib Tosylate SDF

Molecular Weight	637.03
Formula	C₂₁H₁₆ClF₃N₄O₃.C₇H₈O₃S
CAS No.	475207-59-1
Storage	3 years -20°C powder
Storage	2 years -80°C in solvent
Synonyms	Bay 43-9006

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Clinical Trial Information (data from https://clinicaltrials.gov, updated on 2019-03-27)

NCT Number	Recruitment	Conditions	Sponsor/Collaborators	Start Date	Phases
NCT03211416	Recruiting	Advanced Adult Hepatocellular Carcinoma\|Child-Pugh Class A\|Stage III Hepatocellular Carcinoma\|Stage IIIA Hepatocellular Carcinoma\|Stage IIIB Hepatocellular Carcinoma\|Stage IIIC Hepatocellular Carcinoma\|Stage IV Hepatocellular Carcinoma\|Stage IVA Hepatocellular Carcinoma\|Stage IVB Hepatocellular Carcinoma	Roswell Park Cancer Institute\|National Cancer Institute (NCI)	September 13 2017	Phase 1\|Phase 2
NCT03211416	Recruiting	Advanced Adult Hepatocellular Carcinoma\|Child-Pugh Class A\|Stage III Hepatocellular Carcinoma\|Stage IIIA Hepatocellular Carcinoma\|Stage IIIB Hepatocellular Carcinoma\|Stage IIIC Hepatocellular Carcinoma\|Stage IV Hepatocellular Carcinoma\|Stage IVA Hepatocellular Carcinoma\|Stage IVB Hepatocellular Carcinoma	Roswell Park Cancer Institute\|National Cancer Institute (NCI)	September 13 2017	Phase 1\|Phase 2
NCT03236649	Not yet recruiting	Hepatocellular Carcinoma (HCC)	Beijing Shenogen Biomedical Co. Ltd\|Chinese Academy of Medical Sciences\|NanJing PLA 81 Hospital\|Beijing Cancer Hospital\|Chinese PLA General Hospital\|Beijing Hospital\|General Hospital of Chinese Armed Police Forces\|Guang''anmen Hospital of China Academy of Chinese Medical Sciences\|Jinan Central Hospital\|Linyi Tumour Hospital\|The First Affiliated Hospital of Anhui Medical University\|Anhui Provincial Hospital\|The First Affiliated Hospital with Nanjing Medical University\|The Affiliated Tumor Hospital of Nantong University Nantong Jiangsu Province China\|Nanfang Hospital of Southern Medical University\|First People''s Hospital of Foshan\|Affiliated Cancer Hospital & Institute of Guangzhou Medical University\|Tianjin Medical University Cancer Institute and Hospital\|Hebei Medical University Fourth Hospital\|Hunan Cancer Hospital\|First Hospital of Jilin University\|307 Hospital of PLA\|Fudan University\|Henan Cancer Hospital\|Jilin Provincial Tumor Hospital\|First Affiliated Hospital of Harbin Medical University\|First Affiliated Hospital Bengbu Medical College\|The First Affiliated Hospital of Soochow University\|Tongji Hospital\|Beijing YouAn Hospital	August 30 2017	Phase 3
NCT03236649	Not yet recruiting	Hepatocellular Carcinoma (HCC)	Beijing Shenogen Biomedical Co. Ltd\|Chinese Academy of Medical Sciences\|NanJing PLA 81 Hospital\|Beijing Cancer Hospital\|Chinese PLA General Hospital\|Beijing Hospital\|General Hospital of Chinese Armed Police Forces\|Guang''anmen Hospital of China Academy of Chinese Medical Sciences\|Jinan Central Hospital\|Linyi Tumour Hospital\|The First Affiliated Hospital of Anhui Medical University\|Anhui Provincial Hospital\|The First Affiliated Hospital with Nanjing Medical University\|The Affiliated Tumor Hospital of Nantong University Nantong Jiangsu Province China\|Nanfang Hospital of Southern Medical University\|First People''s Hospital of Foshan\|Affiliated Cancer Hospital & Institute of Guangzhou Medical University\|Tianjin Medical University Cancer Institute and Hospital\|Hebei Medical University Fourth Hospital\|Hunan Cancer Hospital\|First Hospital of Jilin University\|307 Hospital of PLA\|Fudan University\|Henan Cancer Hospital\|Jilin Provincial Tumor Hospital\|First Affiliated Hospital of Harbin Medical University\|First Affiliated Hospital Bengbu Medical College\|The First Affiliated Hospital of Soochow University\|Tongji Hospital\|Beijing YouAn Hospital	August 30 2017	Phase 3
NCT02728050	Recruiting	Acute Biphenotypic Leukemia\|Acute Myeloid Leukemia\|de Novo Myelodysplastic Syndrome\|High Risk Myelodysplastic Syndrome\|Myelodysplastic Syndrome\|Myeloproliferative Neoplasm	University of Washington\|National Cancer Institute (NCI)	December 1 2016	Phase 1\|Phase 2
NCT02728050	Recruiting	Acute Biphenotypic Leukemia\|Acute Myeloid Leukemia\|de Novo Myelodysplastic Syndrome\|High Risk Myelodysplastic Syndrome\|Myelodysplastic Syndrome\|Myeloproliferative Neoplasm	University of Washington\|National Cancer Institute (NCI)	December 1 2016	Phase 1\|Phase 2

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Raf Signaling Pathway Map

Raf Inhibitors with Unique Features

Selective Raf Inhibitor

GDC-0879 : B-Raf-selective, IC50=0.13 nM.
FDA-approved Raf Inhibitor

Vemurafenib (PLX4032, RG7204) : Approved by FDA for late-stage melanoma.
Newest Raf Inhibitor

TAK-632 ^New : Potent pan-Raf inhibitor with IC50 of 8.3 nM and 1.4 nM for B-Raf(wt) and C-Raf, respectively, showing less or no inhibition against other tested kinases.

Related Raf Products3

LY3009120 ^New

LY03009120 is a potent pan-Raf inhibitor with IC50 of 44 nM, 31-47 nM, and 42 nM for A-raf, B-Raf, and C-Raf in A375 cells, respectively. Phase 1.
Ravoxertinib (GDC-0994) ^New

GDC-0994 is a potent, orally available and highly selective ERK1/2 inhibitor with IC50 of 1.1 nM and 0.3 nM, respectively. Phase 1.
Ulixertinib (BVD-523, VRT752271) ^New

Ulixertinib (BVD-523, VRT752271) is a potent and reversible ERK1/ERK2 inhibitor with IC50 of <0.3 nM for ERK2. Phase 1.
Vemurafenib (PLX4032, RG7204)

Vemurafenib (PLX4032, RG7204) is a novel and potent inhibitor of B-Raf^V600E with IC50 of 31 nM in cell-free assay. 10-fold selective for B-Raf^V600E over wild-type B-Raf in enzymatic assays and the cellular selectivity can exceed 100-fold.

Features:A novel and potent inhibitor of the B-RAF^V600E oncoprotein.
Dabrafenib (GSK2118436)

Dabrafenib (GSK2118436) is a mutant BRAFV600 specific inhibitor with IC50 of 0.7 nM in cell-free assays, with 7- and 9-fold less potency against B-Raf(wt) and c-Raf, respectively.
Sorafenib

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.
PLX-4720

PLX4720 is a potent and selective inhibitor of B-Raf^V600E with IC50 of 13 nM in a cell-free assay, equally potent to c-Raf-1(Y340D and Y341D mutations), 10-fold selectivity for B-RafV600E than wild-type B-Raf.
TAK-632

TAK-632 is a potent pan-Raf inhibitor with IC50 of 8.3 nM and 1.4 nM for B-Raf(wt) and C-Raf in cell-free assays, respectively, showing less or no inhibition against other tested kinases.
GDC-0879

GDC-0879 is a novel, potent, and selective B-Raf inhibitor with IC50 of 0.13 nM in A375 and Colo205 cells with activity against c-Raf as well; no inhibition known to other protein kinases.
GW5074

GW5074 is a potent and selective c-Raf inhibitor with IC50 of 9 nM, no effect on the activities of JNK1/2/3, MEK1, MKK6/7, CDK1/2, c-Src, p38 MAP, VEGFR2 or c-Fms is noted.

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Sorafenib Tosylate

Cited by 46 Publications

Purity & Quality Control

Choose Selective Raf Inhibitors

Biological Activity

Protocol

References

Solubility (25°C)

Chemical Information Download Sorafenib Tosylate SDF

Bio Calculators

Molarity Calculator

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

Dilution Calculator

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

The Serial Dilution Calculator Equation

Serial Dilutions

Computed Result

Molecular Weight Calculator

Total Molecular Weight: g/mol

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

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

Molarity Calculator

Clinical Trial Information (data from https://clinicaltrials.gov, updated on 2019-03-27)

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Sorafenib Tosylate

Cited by 46 Publications

Purity & Quality Control

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Biological Activity

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Solubility (25°C)

Chemical Information Download Sorafenib Tosylate SDF

Bio Calculators

Molarity Calculator

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

Dilution Calculator

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

The Serial Dilution Calculator Equation

Serial Dilutions

Computed Result

Molecular Weight Calculator

Total Molecular Weight: g/mol

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

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

Molarity Calculator

Clinical Trial Information (data from https://clinicaltrials.gov, updated on 2019-03-27)

Tech Support

Raf Signaling Pathway Map

Raf Inhibitors with Unique Features

Related Raf Products3

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