Sorafenib

Manufactured by Bayer

Sourced in Germany, United States, Japan, China, Italy, United Kingdom

Sorafenib is a lab equipment product manufactured by Bayer. It is a small-molecule tyrosine kinase inhibitor. Its core function is to inhibit multiple kinases involved in cellular signaling pathways.

Automatically generated - may contain errors

Lab products found in correlation

Dimethyl sulfoxide (dmso), by Merck Group (9 mentions) Regorafenib, by Bayer (7 mentions) Lenvatinib, by Eisai (6 mentions) Fetal bovine serum (fbs), by Thermo Fisher Scientific (6 mentions) Dulbecco modified eagle medium (dmem), by Thermo Fisher Scientific (5 mentions) Nexavar, by Bayer (3 mentions) Sorafenib, by Merck Group (3 mentions) Hep3b, by American Type Culture Collection (3 mentions) Sorafenib, by Thermo Fisher Scientific (3 mentions) Rpmi 1640, by Thermo Fisher Scientific (3 mentions) Apatinib, by Jiangsu Hengrui Medicine (2 mentions) Lenvatinib, by Bayer (2 mentions) Sunitinib, by Pfizer (2 mentions) Cell counting kit 8 (cck8), by Dojindo Laboratories (2 mentions) Methyl thiazolyl tetrazolium (mtt), by Merck Group (2 mentions) Plc prf 5, by American Type Culture Collection (2 mentions) Snu 387, by American Type Culture Collection (2 mentions) Sk hep1, by American Type Culture Collection (2 mentions) Gsk1838705a, by Selleck Chemicals (2 mentions) Oxaliplatin, by Merck Group (2 mentions)

Close spelling variants of this product

Sorafenib (Nexavar) (8 citations) Sorafenib tosylate (8 citations) Sorafenib tosylate (Nexavar) (2 citations)

88 protocols using sorafenib

Combination Therapy for Advanced HCC

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All patients were treated with TACE. All patients were treated with C-TACE. The treatment times of TACE were determined according to the changes of liver function and tumor volume.
Sorafenib (Bayer HealthCare AG, 200 mg/pill) was initially prescribed at 400–800 mg/day after one week after TACE, and with tumor progression, regorafenib replaced Sorafenib. regorafenib was administered orally within one week of TACE surgery at a dosage of 80–160 mg (Bayer HealthCare AG, 40 mg/pill) according to the patient’s tolerance, and during weeks 1–3 of each 4-week cycle. After tumor progression, patients were treated with TACE combined with regorafenib and PD-1 antibody (sintilimab), or with continued TACE combined with regorafenib according to the wishes of the patient. Sintilimab (Innovent Biologics, Suzhou, China) was prescribed at a fixed dose of 200 mg every 3 weeks, and adverse events (AEs) were managed by reducing the pre-specified dose and delaying the next cycle. Treatment was interrupted in patients with hepatic decompensation with Child-Pugh C, clinical progression to ECOG performance status >2, or intolerable toxicity even after the dose adjustment of Sorafenib, regorafenib, or sintilimab.

Wang H., Xiao W., Han Y., Cao S., Zhang Z., Chen G., Hu Y, & Jin L. (2022). Study on efficacy and safety of transcatheter arterial chemoembolization (TACE) combined with regorafenib and PD-1 antibody versus continued TACE combined with regorafenib in patients with hepatocellular carcinoma after failed second-line treatment with regorafenib. Journal of Gastrointestinal Oncology, 13(4), 1907-1914.

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TIPS for Advanced Hepatocellular Carcinoma with PVTT

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All patients in group A received sequential systemic therapy with molecular targeted agents after the TIPS procedure when the symptoms of portal hypertension were controlled. Patients received a daily oral dose of sorafenib (400 mg/bid, Bayer) or lenvatinib (8–12 mg/qd, Eisai Co Ltd). Patients received regorafenib (120–160 mg/qd during weeks 1–3 of each 4-week cycle, Bayer) if they were nonresponders or tolerated sorafenib or lenvatinib. The treatment strategy is shown in Fig. 3.
Fig. 3

Treatment strategy for advanced hepatocellular carcinoma (HCC) with portal vein tumour thrombus (PVTT)–related symptomatic portal hypertension to improve survival. A transjugular intrahepatic portosystemic shunt (TIPS) is used to resolve portal hypertension complications, including variceal bleeding, refractory ascites or hydrothorax, and access to antitumour treatment opportunities (molecular targeted agents)

Qiu Z., Wang G., Yan H., Qi H., Zuo M., Wang G., Jiang W., Chen Z., Xue J., Lu L., Zhang F, & Gao F. (2022). TIPS plus sequential systemic therapy of advanced HCC patients with tumour thrombus-related symptomatic portal hypertension. European Radiology, 32(10), 6777-6787.

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Apoptosis and Autophagy Pathway Modulators

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The primary antibodies used in this study against cleaved caspase-7 (#9491), cleaved-PARP (#9541), phospho-Akt (Ser473) (#9275), Akt (#9272), Atg5 (#2630), Atg7 (#8558), LC3 I/II (#2775), cytochrome c (#12963), Beclin1 (#3738), p62 (#7695), were obtained from Cell Signaling Technology, p62 and GAPDH (Ab9485) from Abcam, p62 from Abnova, Bim (AAP-330) from Stressgen, Bcl-xL (610212) from BD Transduction Laboratories, β-actin (A5441) and cIAP (SAB3500268) from Sigma Aldrich, Bak, Bax (554104), Bcl-2 (554160) and RIPK1 (610459) from BD Europe; AIF (sc-9416), ULK1 (sc-33182), FADD (sc-271748), from Santa Cruz Biotechnology; Vps34 (38-2100) from Invitrogen.
Pancaspase inhibitor z-VAD-FMK (z-Val-Ala-Asp(OMe)-FMK) (FK009), Z-LEHD-FMK (Z-Leu-Glu(OMe)-His-Asp(OMe)-FMK) (FK022) from MP Biomedicals used at 10 μM, Rapamycin (R8781) used at 1 μM, Bafilomycin A1 (Sigma-Aldrich, B1793) used at 10 nM, Chloroquine (PHR1258) used at 50 μM, LY294002 (Sigma-Aldrich, L9908) used at 10 μM, Necrostatin-1 (Sigma-Aldrich, N9037) used at 50 μM, and Oligomycin A at 2.5 μg/ml (Sigma-Aldrich, 75351).
Sorafenib was provided by Bayer HealthCare Pharmaceuticals, Inc. In all the experiments, 20 μM Sorafenib was used unless stated otherwise. Control samples were treated with the equimolar concentration of the appropriate vehicle.

Kharaziha P., Chioureas D., Baltatzis G., Fonseca P., Rodriguez P., Gogvadze V., Lennartsson L., Björklund A.C., Zhivotovsky B., Grandér D., Egevad L., Nilsson S, & Panaretakis T. (2015). Sorafenib-induced defective autophagy promotes cell death by necroptosis. Oncotarget, 6(35), 37066-37082.

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Evaluating Drug Combinations and siRNA Effects on Cell Growth

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50 μl Huh7 (2000 cell/well) and Mahlavu (1000 cell/well) cells were seeded into 96-well plates in 100 μl of medium/well. The next day, cells were treated with the drugs and CI (Cell Index) values were taken every 10 min for 4 h to get the fast drug response and then every 30 min to obtain the long-term drug response. Impedance measurements displayed as CI values reflect cell growth. The SynergyFinder Zero Interaction Potency (ZIP) model is used for the evaluation of the combined effect of PIK-75, TGX-221, and their combinations with Sorafenib (Sorafenib (Nexavar) Bayer Healthcare Pharmaceuticals, Inc., NJ USA). ZIP model defines the effect of combining two compounds by comparing the change in the dose-response curves between individual drugs and their combinations [39 (link)]. For monitoring the effects of siRNA treatment for AOX1 or AGER genes, Mahlavu and Huh7 cells were seeded onto 96-well E-Plate in triplicates. After overnight incubation, siRNA treatments were done as described previously. Cell index (CI) were recorded every 30 min for total of 96 h. Data was normalized using time-zero CI values (when siRNA treatment was performed). For statistical analysis, Two-Way ANOVA was performed using GraphPad Prism 8.

Narci K., Kahraman D.C., Koyas A., Ersahin T., Tuncbag N, & Atalay R.C. (2022). Context dependent isoform specific PI3K inhibition confers drug resistance in hepatocellular carcinoma cells. BMC Cancer, 22, 320.

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Sorafenib-Resistant Hepatoblastoma Cell Line

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Full details on the development of a sorafenib-resistant cell line were previously published [18] (link). Briefly, HepG2 human hepatoblastoma cells (HB-8065-ATCC, Rockville, MD) were incubated with increasing doses of sorafenib (Bayer HealthCare, Leverkusen, Germany) over several months, resulting in a cell line resistant to sorafenib (HepG2S1).

Dekervel J., Popovic D., van Malenstein H., Windmolders P., Heylen L., Libbrecht L., Bulle A., De Moor B., Van Cutsem E., Nevens F., Verslype C, & van Pelt J. (2016). A Global Risk Score (GRS) to Simultaneously Predict Early and Late Tumor Recurrence Risk after Resection of Hepatocellular Carcinoma. Translational Oncology, 9(2), 139-146.

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Sorafenib-resistant Liver Cell Lines

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HepG2 cells, Huh-7 cells and HEK-293 T cells were obtained from the Cell Bank of Chinese Academy of Sciences (Beijing, China). Cells were cultured in a dulbecco’s modified Eagle’s medium (DMEM, Gibco) with a 1:1 ratio of penicillin and streptomycin (100 U/mL) and 10% fetal bovine serum (FBS, Gibco) [17 (link)]. Sorafenib (200 mg, tablets, Bayer Inc., Germany) was used to construct the Sorafenib-resistant HepG2 cell line (namely SR-HepG2 cells) and Huh-7 cell line (namely SR-Huh-7 cells) by continuous induction.

Wang S., Liu D., Wei H., Hua Y., Shi G, & Qiao J. (2022). The hsa_circRNA_102049 mediates the sorafenib sensitivity of hepatocellular carcinoma cells by regulating Reelin gene expression. Bioengineered, 13(2), 2272-2284.

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Combination Therapy for Tumor Burden

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Animal procedures were performed in accordance with the UK Home Office guidelines and approved by the Ethical Review Group of Cardiff University. Tsc2^+/− balb/c mice were described previously [11] (link). To test whether combination of everolimus with Sorafenib could improve antitumor efficacy, we first determined the combined maximum tolerated dose in the Tsc2^+/− mice in a 2-week pilot treatment study. Tsc2^+/− littermates were randomly allocated into 4 groups of 10, balanced for gender and of the same age. Animals were treated from the age of 11 months with vehicle, everolimus (10 mg/kg), Sorafenib (42 mg/kg), or everolimus (6 mg/kg) plus Sorafenib (30 mg/kg). All mice were treated five times a week via gavage for 2 months and then sacrificed for assessment of tumor burden and analysis of protein expression and phosphorylation in the kidneys. Vehicle and everolimus were supplied by Novartis Pharma AG, Basel, Switzerland. Sorafenib was supplied by Bayer Schering Pharma AG, Leverkusen, Germany.

Yang J., Samsel P.A., Narov K., Jones A., Gallacher D., Gallacher J., Sampson J.R, & Shen M.H. (2017). Combination of Everolimus with Sorafenib for Solid Renal Tumors in Tsc2+/− Mice Is Superior to Everolimus Alone. Neoplasia (New York, N.Y.), 19(2), 112-120.

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Modulation of Cell Death Pathways

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Sorafenib was provided by Bayer Schering Pharma (Bayer Vital GmbH). PLX4720 was purchased by Symansis, U0126 was purchased from Sigma-Aldrich, Trametinib was obtained from Target molecule Corp, and Vorinostat (SAHA) was purchased from Selleck. Deferrioxamine Mesylate (DFO) and Glutathione-monoethyl-ester (GSH) were obtained from Merck., N-Acetyl-L-cysteine (NAC) was purchased from Sigma-Aldrich. Pancaspase inhibitor zVAD and cathepsin inhibitor Z-FA-fmk were purchased from R&D Systems. Etanercept (Enbrel^®) was kindly provided by Dr. Walczak, Imperial College London.

KieΔling M.K., Nicolay J.P., Schlör T., Klemke C.D., Süss D., Krammer P.H, & Gülow K. (2017). NRAS mutations in cutaneous T cell lymphoma (CTCL) sensitize tumors towards treatment with the multikinase inhibitor Sorafenib. Oncotarget, 8(28), 45687-45697.

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Liver Cancer Cell Line Characterization

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Hep-G2, HuH-7, and PLC cell lines were obtained from the Type Culture Collection Cell Bank of the Chinese Academy of Sciences, Shanghai, China, and HCC-LM3 and L-02 cell lines were acquired from the Liver Cancer Institute, Fudan University, Shanghai, China. These cells are commonly used in liver cancer research. L-02 is a normal liver cell, and the four other types are hepatocellular carcinoma cells. HCC-LM3 is an HCC cell line with highly invasive lung metastasis. Sorafenib (Bayer Ag) and recombinant human IL‑6 (R&D Systems, Inc.) were administered as in the previous study20 (link).

Zhuang P., Wang D., Zhang K., Wang J, & Shen J. (2023). Sorafenib promotes hepatocellular carcinoma invasion via interleukin-6/HIF-1α/PFKFB3. Journal of Cancer, 14(10), 1859-1874.

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Combinatorial Therapy for Orthotopic HCC

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For the established orthotopic HCC model, we confirmed tumor growth by MRI fourteen days after tissue implantation and then randomly divided the mice into different groups (Sorafenib, DC-TEX, PD-1 Ab, Sorafenib plus DC-TEX, Sorafenib plus PD-1 Ab, DC-TEX plus PD-1 Ab, Triple combination of Sorafenib, PD-1 Ab, and DC-TEX, Phosphate buffered saline, n = 6 mice/group). The tumor volume in each group was not significantly different. Sorafenib (Nexavar, Bayer Healthcare, Leverkusen, Germany) was dissolved in phosphate buffered saline (PBS) containing 1% Tween 80 and the final dose of 50 mg/kg was administered by gavage daily for three weeks. DCs were pulsed with exosomes (4×10⁶, injected intravenously) three times, at 5-day intervals. PD-1 Ab (200 μg) was injected intraperitoneally three times at 5-day intervals (clone J43; BioXCell, West Lebanon, USA). After one week of treatment, the established orthotopic HCC model were to sacrifice and to analyze the variation. For survival analysis, the treatment was conducted as above described (n = 10 mice/group).

Shi S., Rao Q., Zhang C., Zhang X., Qin Y, & Niu Z. (2018). Dendritic Cells Pulsed with Exosomes in Combination with PD-1 Antibody Increase the Efficacy of Sorafenib in Hepatocellular Carcinoma Model. Translational Oncology, 11(2), 250-258.

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