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Sorafenib (Bay 43-9006) tosylate is a potent oral active multikinase inhibitor. Sorafenib blocks autophosphorylation and activity of receptor tyrosine kinases (VEGFR-2, VEGFR-3) and RAF family kinases, thereby suppressing the RAF/MEK/ERK and PI3K/Akt pathways, inhibiting STAT3 phosphorylation, and selectively inhibiting the MAPK pathway in cancer cells. Sorafenib tosylate induces cell cycle arrest, autophagy, apoptosis, and PARP cleavage, reduces Bcl-2, Bcl-XL, cyclin D1 levels, and activates Bak and Bax. Sorafenib tosylate inhibits tumor growth and metastasis in mouse and rat models. Sorafenib tosylate can be used for cancer research, such as colon, breast, non-small-cell lung cancer (NSCLC), ovarian, pancreatic, melanoma, colorectal and hepatocellular carcinoma.
For research use only. We do not sell to patients.
The cell viability of YAP-, YAP-S127A-, or YAP-R124F-overexpressed Huh-7 cells cultured in methionine-deprived medium (MD) and treated with sorafenib (1.5-3 μM) for 24 h.
Growth inhibition, IC50 and AUC values, of OCI-AML2 cells transduced with either a non-targeting control,
two PIK3CG-directed, or two PIK3R5-directed sgRNAs and treated with increasing concentrations of the FLT3
inhibitors, Gilteritinib (10-1000 nM) and Sorafenib (10-1000 nM), or KIT inhibitors, Amuvanib and Telatinib
Sorafenib tosylate (50 mg/kg; i.g.; once daily for 14 d) caused sparse trabecular bone structures in BMP-induced ossification mice, accompanied by numerous cartilage structures and amorphous matrix deposition, indicating a delay in endochondral ossification.
Sorafenib tosylate (50 mg/kg; i.g.; once daily for 14 d)caused a shorter response time to thermal stimulation and less paw withdrawal threshold to mechanical stimulation of BMP-induced ossification mice.
qPCR showing the nuclear and cytoplasmic fractions of URB1-AS1 in sorafenib-resistant HepG2 cells with β-actin and MALAT1 as cytoplasmic and nuclear controls, respectively.
PANC-1 cells were transfected with the recombinant plasmid for 24 h and treated with sorafenib (0–70 μmol/L) for another 24 h, and then total cellular extracts were subjected to Western blotting using antibodies against caspase-3, GSDME and β-tubulin.
HeLa and SiHa cells were treated with condition medium (CM) from human PBMC-derived M0 macrophages (Ctrl) and TAM. And then cells were treated with indicated dose of Sorafenib (Sora) for 48 h. Inhibition ratio of cell viability was detected by CCK-8 assay.
Hep3B, HepG2 and Huh7 cells are treated with 5 μM Sorafenib. The expressing levels of JAK1, JAK2, STAT3, SHP1, SHP2, actin and phosphorylation levels of STAT3 are determined by western blot using the antibodies, respectively.
SMMC-7721 and HepG2 cells are treated with 4 µM Sorafenib and 100 µM Berberine alone or in combination (4 µM Sorafenib+100 µM Berberine) for 72 h, and the expression levels of apoptosis-associated proteins are measured by western blot analysis.
The effect of the AKT inhibitor MK2206 (10 μM) on the expression levels of phosphor-AKT, AKT, and STMN1 in TKI-pretreated NCI-H460 cells. β-actin is used as a loading control.
The combination of sorafenib and CAI induces apoptosis in NSCLC. Effect of 10 μM CAI and/or 5 μM Sorafenib on the expression of cleaved PARP and cleaved caspase-. Protein levels of cleaved PARP and cleaved caspase-3 from treated cell lysates are normalized against GAPDH levels.
VPA potentiates anti-tumor effects of Sorafenib tosylate in vivo. The expression of cleaved caspase9, cleaved caspase3, cleaved PARP from tumor tissue homogenates are analyzed by western blot.
Effect of Sorafenib on phosphorylation of ERK and AKT. Thyroid cancer cells are treated for 30 minutes with 10 μM Sorafenib, 10 μM Forskolin, and combination therapy of 10 μM Sorafenib with 10 μM Forskolin. The levels of ERK and AKT phosphorylation are examined by immunoblot analysis. β-actin is used as the control. Sorafenib suppresses phosphorylation of ERK, but not of AKT.
Effect of Sorafenib and Forskolin on expression of CDK4 and CDK regulatory proteins. Thyroid cancer cells are treated for 24 hours with 10 μM Sorafenib, 10 μM Forskolin, and combination therapy of 10 μM Sorafenib with 10 μM Forskolin. The expression of cyclin D1, CDK4, and phosphorylation of RB are examined by immunoblot analysis. β-actin is used as the control. The combination therapy suppresses expression of cyclin D1, and Forskolin monotherapy suppresses expression of cyclin D1 in TPC-1 and W
Sorafenib inhibits Pin1 biosynthesis and accumulation in Huh7 and HepG2 cells. Cells are treated with 5 or 10 μM Sorafenib for indicated times. Pin1 protein expression is determined by Western Blot.
The relationship between SOX9 and Raf/MEK/ERK signaling pathway. Co-treatment of si-SOX9-1 and Sorafenib (10uM, 15uM)/SU 11248 (2 uM, 3 uM) significantly decreases expression of MEK1 and its phosphorylated protein (p-MEK1/2, p-ERK1/2) as assayed by Western blot (with GAPDH as internal control).
The relationship between SOX9 and Raf/MEK/ERK signaling pathway. Co-treatment of si-SOX9-1 and Sorafenib (10uM, 15uM)/SU 11248 (2 uM, 3 uM) significantly decreases expression of MEK1 and its phosphorylated protein (p-MEK1/2, p-ERK1/2) as assayed by RT-PCR (with β-actin as internal control).
Sorafenib (Bay 43-9006) tosylate is a potent oral active multikinase inhibitor. Sorafenib blocks autophosphorylation and activity of receptor tyrosine kinases (VEGFR-2, VEGFR-3) and RAF family kinases, thereby suppressing the RAF/MEK/ERK and PI3K/Akt pathways, inhibiting STAT3 phosphorylation, and selectively inhibiting the MAPK pathway in cancer cells. Sorafenib tosylate induces cell cycle arrest, autophagy, apoptosis, and PARP cleavage, reduces Bcl-2, Bcl-XL, cyclin D1 levels, and activates Bak and Bax. Sorafenib tosylate inhibits tumor growth and metastasis in mouse and rat models. Sorafenib tosylate can be used for cancer research, such as colon, breast, non-small-cell lung cancer (NSCLC), ovarian, pancreatic, melanoma, colorectal and hepatocellular carcinoma[1][2][3][4][5][6].
Sorafenib (0.01-3 μM; 2 h) tosylate selectively inhibits the MAPK pathway, while has no effect on the PKB pathway in MDA-MB-231 cells[1].
Sorafenib (0.01-15 μM; 2 h) tosylate inhibits MEK 1/2 and ERK 1/2 phosphorylation in MDA-MB-231 human breast carcinoma cells (IC50s of 40 and 90 nmol/L, respectively), ERK 1/2 phosphorylation in BxPC-3, LOX, HCT 116, HT-29, Colo-205, and Mia PaCa-2 cells, but does not inhibit ERK 1/2 phosphorylation in A549 and NCI-H460 cells[1].
Sorafenib (0.01-10 μM; 72 h) tosylate inhibits proliferation of MDA-MB-231 cells with an IC50 of 2600 nmol/L)[1].
Sorafenib (8.9 μM) tosylate exhibits an IC50 of 8.9 μM in human colorectal carcinoma HCT8 and HT29 cell lines, and causes marked antagonism with oxaliplatin and cisplatin across all tested incubation schedules, reducing platinum-induced cytotoxicity[2].
Sorafenib (4-24 μM; 24 h) tosylate reduces expression of p21Cip1 protein and cyclin D1 expression in HCT8 and HT29 cells when incubated simultaneously with Oxaliplatin (HY-17371) or Cisplatin (HY-17394)[2].
Sorafenib (24 μM; 4 h) tosylate significantly reduces Cisplatin- and Oxaliplatin-induced DNA adduct levels in HCT8 and HT29 cells when applied simultaneously, but does not affect adduct levels or repair when applied consecutively[2].
Sorafenib (0-20 μmol/L; 24-72 h) tosylate inhibits the proliferation of HCCLM3, HepG2, and rat Morris hepatoma 3924A (MH) HCC cell lines in a time- and dose-dependent manner[3].
Sorafenib (0-20 μmol/L; 2-24 h) tosylate durably inhibits phosphorylation of STAT3Y705 and S727, ERK1/2, and Akt, and reduces cyclin D1 expression, without altering JAK2 or SHP2 phosphorylation, in HCCLM3, HepG2, and MH HCC cell lines[3].
Sorafenib (5 μM; 48 h) tosylate significantly increases clonogenicity, enhances tumoursphere formation, and upregulates cancer stem cell-associated pluripotency markers Sox2 and Oct4 in A549, NCI-H460, and NCI-H1299 NSCLC cells[5].
Sorafenib (5 μM; 48 h) tosylate increases ALDH-positive cancer stem cell populations in A549 NSCLC cells[5].
Sorafenib (5 μM; 48 h) tosylate significantly enhances migration capacity in NCI-H460 NSCLC cells[5].
Sorafenib (5 μM; 48 h) tosylate induces epithelial-to-mesenchymal transition in NCI-H460 NSCLC cells via downregulation of E-cadherin and upregulation of N-cadherin, vimentin, and MMP2, and activates the AKT pathway via increased AKT phosphorylation[5].
Sorafenib (5 μM; 48 h) tosylate upregulates STMN1, FOXM1, and E2F1 expression at the mRNA and protein levels in NCI-H460 and NCI-H1299 NSCLC cells[5].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
Dose-dependently inhibited basal MEK 1/2 phosphorylation in MDA-MB-231 cells with an IC50 of 40 nmol/L. Inhibited ERK 1/2 phosphorylation in MDA-MB-231 cells with an IC50 of 90 nmol/L. Showed no effect on PKB phosphorylation in MDA-MB-231 cells. Completely blocked activation of the MAPK pathway.
Reduced p21Cip1 protein expression induced by Oxaliplatin or Cisplatin at 4 μM when applied simultaneously. Completely inhibited platinum-induced p21Cip1 expression at 24 μM when applied simultaneously. Reduced cyclin D1 expression enhanced by Oxaliplatin when applied simultaneously. Reduced cdc2 expression enhanced by cisplatin when applied simultaneously. Showed no effect on these protein levels when applied consecutively after platinum treatment.
Inhibited HCC cell growth in a time- and dose-dependent manner across all three cell lines. Increased inhibition rates with both higher sorafenib concentrations and longer incubation periods. Exhibited the strongest inhibition at 20 μmol/L after 72 h of treatment.
Inhibited phosphorylation of STAT3 at Y705 and S727, as well as phosphorylation of ERK1/2, in a dose-dependent manner after 2 h of treatment across all three cell lines. Durably inhibited phosphorylation of STAT3 (Y705 and S727) and ERK1/2 for up to 24 h at 10 μmol/L, while total STAT3 protein levels and JAK2 phosphorylation remained unchanged. Inhibited Akt phosphorylation primarily at 2 μmol/L after 2 h and reduced cyclin D1 protein expression, while leaving SHP2 phosphorylation unchanged.
Upregulated expression levels of Sox2 and Oct4 in all three NSCLC cell lines compared to untreated controls. Markedly decreased the epithelial marker E-cadherin compared to untreated controls. Correspondingly increased mesenchymal markers N-cadherin, vimentin, and MMP2 compared to untreated controls. Upregulated the expression of phosphorylated AKT in NCI-H460 cells compared to untreated controls. Showed no obvious effect on phosphorylated JNK expression compared to untreated controls in NCI-H460 cells. Showed an increase in phosphorylated ERK expression compared to untreated controls in NCI-H460 cells.
Resulted in the strongest enhancement of cell migration. Showed a higher CI (the capacity for cell migration) slope indicating faster migration velocity compared to DMSO-treated controls.
Upregulated STMN1, FOXM1, and E2F1 protein expression in both cell lines compared to untreated controls.
In Vivo
Sorafenib (7.5-60 mg/kg; p.o.; daily for 5 or 9 days) tosylate inhibits tumor growth, suppresses RAF/MEK/ERK signaling, and reduces angiogenesis in mouse breast, colon, and NSCLC xenograft models, with no observed toxicity[1].
Sorafenib (30 mg/kg; i.g.; once daily; once daily from day 17 to day 38) tosylate inhibits hepatocellular carcinoma tumor growth and metastasis in an orthotopic rat Morris Hepatoma (MH) model, while inducing tumor apoptosis and suppressing STAT3, Akt, and ERK phosphorylation[3].
Sorafenib (10 mg/kg; p.o.; daily; 2 weeks) tosylate exhibits antineoplastic activity in Diethyl Nitrosamin (DENA)-induced hepatocellular carcinoma in albino rats[4].
Sorafenib (4 mg/kg; i.p.; twice a week for 4 weeks) tosylate in combined with intratumoral siTUC338 significantly reduces tumor volume in mouse HepG2/Sor xenografts via upregulation of RASAL1[6].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
Animal Model:
Female NCr-nu/nu mice subcutaneously injected with MDA-MB-231 cells [1]
Dosage:
7.5; 15; 30; 60 mg/kg
Administration:
p.o.; daily for 5 or 9 days
Result:
Produced a 42% reduction in mean tumor weight after 9 days at 30 mg/kg . Inhibited microvessel area (MVA) and microvessel density (MVD) in tumors, induced extensive tumor necrosis, reduced phosphorylated ERK 1/2 (pERK) levels, and decreased Ki-67 staining at 30 or 60 mg/kg daily for 5 days. Caused no toxicity in treated group.
Animal Model:
Female NCr-nu/nu mice subcutaneously injected with Colo-205, HT-29, and DLD-1 cells[1]
Dosage:
7.5; 15; 30; 60 mg/kg
Administration:
p.o.; daily for 5 or 9 days
Result:
Produced complete tumor stasis during treatment at 30 to 60 mg/kg daily for 9 days. Reduced MVA to ~0.4% and MVD to ~80/mm2 at 30 mg/kg daily for 5 days, and reduced MVA to ~0.2% and MVD to ~50/mm2 at 60 mg/kg daily for 5 days relative to vehicle controls. Detected no reduction in pERK levels at 30 or 60 mg/kg daily for 5 days. Caused no toxicity in any treated group. Produced complete tumor stasis during treatment at 30 to 60 mg/kg daily for 9 days. Inhibited MVA and MVD in tumors by 50 to 80%, reduced pERK levels, and inhibited MEK 1/2 phosphorylation at 30 or 60 mg/kg daily for 5 days. Caused no toxicity in any treated group..
Animal Model:
Female NCr-nu/nu mice subcutaneously injected with NCI-H460, and A549 cells[1]
Dosage:
7.5; 15; 30; 60 mg/kg
Administration:
p.o.; daily; 9 days
Result:
Produced complete tumor stasis during treatment at 30 to 60 mg/kg daily. Caused no toxicity in any treated group.
Animal Model:
Male ACI rats (200-220 g) orthotopic implantated with Morris Hepatoma (MH) fragments[3]
Dosage:
30 mg/kg
Administration:
i.g.; once daily from day 17 to day 38
Result:
Reduced mean tumor volume to 351.26 mm3 in early treatment group and 2248.33 mm3 in late treatment group. Prevented lung, lymph node metastasis, peritoneal seeding, and ascites in 10/10 rats in early treatment group, and lymph node metastasis, peritoneal seeding, and ascites in 10/10 rats in late treatment group. Induced tumor cell apoptosis with an apoptosis index of 0.909. Reduced phosphorylation of STAT3 (Y705 and S727), Akt, and ERK in tumor tissue. Decreased cyclin D1 expression. Did not affect STAT3 mRNA levels, JAK2 phosphorylation, or SHP2 phosphorylation in tumor tissue.
Animal Model:
Male albino rats (100-120 g) with Diethyl Nitrosamin (DENA)-induced hepatocellular carcinoma)[4]
Dosage:
10 mg/kg
Administration:
p.o.; daily; 2 weeks
Result:
Improved survival rate to 83.3%. Significantly decreased liver index below normal control group level. Reduced hepatocellular foci size by 34.8% compared to the DENA-only group. Lowered total hepatic foci count to 10 compared to 18 in the DENA-only group. Decreased cyclin D1 and β-catenin gene expression. Reduced liver Bcl-2 protein and liver glutathione (GSH) levels.
Animal Model:
Male nude mice (4-6 weeks, 18-20 g) subcutaneously injected with HepG2/Sor cells[6]
Dosage:
4 mg/kg
Administration:
i.p.; twice a week; 4 weeks
Result:
Achieved statistically significantly lower mean tumor volume compared to sorafenib combined with saline or siNC. Significantly downregulated TUC338 expression in tumor tissue relative to control groups. Significantly upregulated RASAL1 mRNA and protein levels in tumor tissue relative to control groups.
DMSO : ≥ 100 mg/mL (156.98 mM; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)
*"≥" means soluble, but saturation unknown.
Preparing Stock Solutions
ConcentrationSolventMass
1 mg
5 mg
10 mg
1 mM
1.5698 mL
7.8489 mL
15.6978 mL
5 mM
0.3140 mL
1.5698 mL
3.1396 mL
10 mM
0.1570 mL
0.7849 mL
1.5698 mL
View the Complete Stock Solution Preparation Table
*Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles. Storage method and period of stock solution: -80°C, 1 year; -20°C, 6 months (sealed storage, away from moisture). When stored at -80°C, please use it within 1 year. When stored at -20°C, please use it within 6 months.
For the following dissolution methods, please ensure to first prepare a clear stock solution using an In Vitro approach and then sequentially add co-solvents:
To ensure reliable experimental results, the clarified stock solution can be appropriately stored based on storage conditions. As for the working solution for in vivo experiments, it is recommended to prepare freshly and use it on the same day. The percentages shown for the solvents indicate their volumetric ratio in the final prepared solution. If precipitation or phase separation occurs during preparation, heat and/or sonication can be used to aid dissolution.
Protocol 1
Add each solvent one by one: 10% DMSO 90% (20% SBE-β-CD in Saline)
Solubility: ≥ 2.5 mg/mL (3.92 mM); Clear solution
This protocol yields a clear solution of ≥ 2.5 mg/mL (saturation unknown).
Taking 1 mL working solution as an example, add 100 μLDMSO stock solution (25.0 mg/mL) to 900 μL 20% SBE-β-CD in Saline, and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C, storage for one week): 2 g SBE-β-CD powder is dissolved in 10 mL Saline, completely dissolve until clear.
Protocol 2
Add each solvent one by one: 10% DMSO 90% Corn Oil
Solubility: ≥ 2.5 mg/mL (3.92 mM); Clear solution
This protocol yields a clear solution of ≥ 2.5 mg/mL (saturation unknown). If the continuous dosing period exceeds half a month, please choose this protocol carefully.
Taking 1 mL working solution as an example, add 100 μLDMSO stock solution (25.0 mg/mL) to 900 μLCorn oil, and mix evenly.
In Vivo Dissolution Calculator
Please enter the basic information of animal experiments:
Dosage
mg/kg
Animal weight (per animal)
g
Dosing volume (per animal)
μL
Number of animals
Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.
Please enter your animal formula composition:
%
DMSO+
%
+
%
Tween-80
+
%
Saline
Recommended: Keep the proportion of DMSO in working solution below 2% if your animal is weak.
The co-solvents required include: DMSO,
. All of co-solvents are available by MedChemExpress (MCE).
, Tween 80. All of co-solvents are available by MedChemExpress (MCE).
Calculation results:
Working solution concentration:
mg/mL
Method for preparing stock solution:
mg
drug dissolved in
μL
DMSO (Stock solution concentration: mg/mL).
The concentration of the stock solution you require exceeds the measured solubility. The following solution is for reference only. If necessary, please contact MedChemExpress (MCE).
Method for preparing in vivo working solution for animal experiments: Take
μL DMSO stock solution, add
μL .
μL , mix evenly, next add
μL Tween 80, mix evenly, then add
μL Saline.
Dissolve 0.9 g sodium chloride in ddH₂O and dilute to 100 mL to obtain a clear Saline solution
If the continuous dosing period exceeds half a month, please choose this protocol carefully.
Please ensure that the stock solution in the first step is dissolved to a clear state, and add co-solvents in sequence. You can use ultrasonic heating (ultrasonic cleaner, recommended frequency 20-40 kHz), vortexing, etc. to assist dissolution.
*Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles. Storage method and period of stock solution: -80°C, 1 year; -20°C, 6 months (sealed storage, away from moisture). When stored at -80°C, please use it within 1 year. When stored at -20°C, please use it within 6 months.
Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.
Customer Validation
The cell viability of YAP-, YAP-S127A-, or YAP-R124F-overexpressed Huh-7 cells cultured in methionine-deprived medium (MD) and treated with sorafenib (1.5-3 μM) for 24 h.
Customer Validation
Growth inhibition, IC50 and AUC values, of OCI-AML2 cells transduced with either a non-targeting control,
two PIK3CG-directed, or two PIK3R5-directed sgRNAs and treated with increasing concentrations of the FLT3
inhibitors, Gilteritinib (10-1000 nM) and Sorafenib (10-1000 nM), or KIT inhibitors, Amuvanib and Telatinib
Customer Validation
Sorafenib tosylate (90-900 nM) markedly suppressed the upregulation of endothelial-like differentiation in ligament cells mediated by LOXL2.
Customer Validation
Sorafenib tosylate (50 mg/kg; i.g.; once daily for 14 d) caused sparse trabecular bone structures in BMP-induced ossification mice, accompanied by numerous cartilage structures and amorphous matrix deposition, indicating a delay in endochondral ossification.
Customer Validation
Sorafenib tosylate (50 mg/kg; i.g.; once daily for 14 d)caused a shorter response time to thermal stimulation and less paw withdrawal threshold to mechanical stimulation of BMP-induced ossification mice.
Customer Validation
Western blot to detect the ferritin H protein level by the gain or loss of URB1-AS1 in sorafenib-sensitive or sorafenib-resistant HepG2 cells.
Customer Validation
qPCR showing the nuclear and cytoplasmic fractions of URB1-AS1 in sorafenib-resistant HepG2 cells with β-actin and MALAT1 as cytoplasmic and nuclear controls, respectively.
Customer Validation
PANC-1 cells were transfected with the recombinant plasmid for 24 h and treated with sorafenib (0–70 μmol/L) for another 24 h, and then total cellular extracts were subjected to Western blotting using antibodies against caspase-3, GSDME and β-tubulin.
Customer Validation
HeLa and SiHa cells were treated with condition medium (CM) from human PBMC-derived M0 macrophages (Ctrl) and TAM. And then cells were treated with indicated dose of Sorafenib (Sora) for 48 h. Inhibition ratio of cell viability was detected by CCK-8 assay.
Customer Validation
Hep3B, HepG2 and Huh7 cells are treated with 5 μM Sorafenib. The expressing levels of JAK1, JAK2, STAT3, SHP1, SHP2, actin and phosphorylation levels of STAT3 are determined by western blot using the antibodies, respectively.
Customer Validation
SMMC-7721 and HepG2 cells are treated with 4 µM Sorafenib and 100 µM Berberine alone or in combination (4 µM Sorafenib+100 µM Berberine) for 72 h, and the expression levels of apoptosis-associated proteins are measured by western blot analysis.
Customer Validation
The effect of the AKT inhibitor MK2206 (10 μM) on the expression levels of phosphor-AKT, AKT, and STMN1 in TKI-pretreated NCI-H460 cells. β-actin is used as a loading control.
Customer Validation
The combination of sorafenib and CAI induces apoptosis in NSCLC. Effect of 10 μM CAI and/or 5 μM Sorafenib on the expression of cleaved PARP and cleaved caspase-. Protein levels of cleaved PARP and cleaved caspase-3 from treated cell lysates are normalized against GAPDH levels.
Customer Validation
VPA potentiates anti-tumor effects of Sorafenib tosylate in vivo. The expression of cleaved caspase9, cleaved caspase3, cleaved PARP from tumor tissue homogenates are analyzed by western blot.
Customer Validation
Effect of Sorafenib on phosphorylation of ERK and AKT. Thyroid cancer cells are treated for 30 minutes with 10 μM Sorafenib, 10 μM Forskolin, and combination therapy of 10 μM Sorafenib with 10 μM Forskolin. The levels of ERK and AKT phosphorylation are examined by immunoblot analysis. β-actin is used as the control. Sorafenib suppresses phosphorylation of ERK, but not of AKT.
Customer Validation
Effect of Sorafenib and Forskolin on expression of CDK4 and CDK regulatory proteins. Thyroid cancer cells are treated for 24 hours with 10 μM Sorafenib, 10 μM Forskolin, and combination therapy of 10 μM Sorafenib with 10 μM Forskolin. The expression of cyclin D1, CDK4, and phosphorylation of RB are examined by immunoblot analysis. β-actin is used as the control. The combination therapy suppresses expression of cyclin D1, and Forskolin monotherapy suppresses expression of cyclin D1 in TPC-1 and W
Customer Validation
Sorafenib inhibits Pin1 biosynthesis and accumulation in Huh7 and HepG2 cells. Cells are treated with 5 or 10 μM Sorafenib for indicated times. Pin1 protein expression is determined by Western Blot.
Customer Validation
The relationship between SOX9 and Raf/MEK/ERK signaling pathway. Co-treatment of si-SOX9-1 and Sorafenib (10uM, 15uM)/SU 11248 (2 uM, 3 uM) significantly decreases expression of MEK1 and its phosphorylated protein (p-MEK1/2, p-ERK1/2) as assayed by Western blot (with GAPDH as internal control).
Customer Validation
The relationship between SOX9 and Raf/MEK/ERK signaling pathway. Co-treatment of si-SOX9-1 and Sorafenib (10uM, 15uM)/SU 11248 (2 uM, 3 uM) significantly decreases expression of MEK1 and its phosphorylated protein (p-MEK1/2, p-ERK1/2) as assayed by RT-PCR (with β-actin as internal control).
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