Vemurafenib

Manufactured by Apexbio

Sourced in United States

Vemurafenib is a laboratory reagent used for research purposes. It is a small-molecule inhibitor that targets the BRAF V600E mutation. Vemurafenib is commonly used in cancer research studies.

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Lab products found in correlation

Trametinib, by Apexbio (2 mentions) Dabrafenib, by Apexbio (1 mentions) Doxorubicin, by Apexbio (1 mentions) Fr180204, by Bio-Techne (1 mentions) Fisetin, by Merck Group (1 mentions) Selumetinib, by Selleck Chemicals (1 mentions) Cetuximab, by Merck Group (1 mentions) Anti erk, by Cell Signaling Technology (1 mentions) Recombinant human il 36γ, by R&D Systems (1 mentions) Anti t7 antibody, by Abcam (1 mentions) Anti phospho erk, by Cell Signaling Technology (1 mentions) Anti myc, by Merck Group (1 mentions) Anti ha antibody, by Santa Cruz Biotechnology (1 mentions) Anti flag, by Merck Group (1 mentions) Mg132, by Selleck Chemicals (1 mentions) Anti β actin, by Merck Group (1 mentions) Pam3csk4, by InvivoGen (1 mentions) Erlotinib, by MedChemExpress (1 mentions) Niclosamide, by Merck Group (1 mentions) Phospho erk thr202 tyr204, by Cell Signaling Technology (1 mentions)

4 protocols using vemurafenib

Cell Viability Assay for Drug Screening

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Cells were seeded in triplicate in 96-well culture plates at 2000 cells per well and grown overnight in the absence of any drug treatment. The following day, the indicated concentration of drug or an equivalent volume of DMSO vehicle control was added and the cells were grown for an additional three days. After three days of treatment, cell viability was assessed using CellTiter-Glo luminescent cell viability agent (Promega) according to manufacturer instructions. Luminescence was measured with a SpectraMax i3x multi-mode plate reader. The cell survival rate of drugged cells was normalized to the DMSO control group. The dose-response curves and IC50 values were generated using Prism (GraphPad). The BRAF inhibitors dabrafenib and vemurafenib, the MEK inhibitors trametinib and binimetinib, and the non-specific chemotherapeutic doxorubicin were obtained from ApexBio and Selleckchem.

Turner E., Chen L., Foulke J.G., Gu Z, & Tian F. (2022). CRISPR/Cas9 Edited RAS & MEK Mutant Cells Acquire BRAF and MEK Inhibitor Resistance with MEK1 Q56P Restoring Sensitivity to MEK/BRAF Inhibitor Combo and KRAS G13D Gaining Sensitivity to Immunotherapy. Cancers, 14(21), 5449.

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Fisetin and Small Molecule Inhibitors

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Fisetin was purchased from Sigma Chemical Co. (St. Louis, MO). FR180204 was obtained from Tocris Biosciences (Minneapolis, MN). BI-D1870 and vemurafenib were purchased from ApexBio (Houston, TX). Antibodies were obtained from Cell Signaling Technology (Danvers, MA).

Sechi M., Lall R.K., Afolabi S.O., Singh A., Joshi D.C., Chiu S.Y., Mukhtar H, & Syed D.N. (2018). Fisetin targets YB-1/RSK axis independent of its effect on ERK signaling: insights from in vitro and in vivo melanoma models. Scientific Reports, 8, 15726.

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Elucidating Inflammatory Signaling Pathways

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Erlotinib was purchased from MedChem Express. Cetuximab was from MERCK Serono. Trametinib and vemurafenib were from ApexBio. Selumetinib and MG132 were from Selleckchem. Recombinant human IL-36γ (catalog 6835), mouse IL-36γ (catalog 6996), and human IL-36Ra (catalog 1275) were from R&D Systems. Pam3CSK4 was from InvivoGen. The goat anti–IL-36γ (catalog AF2320) and anti-mouse KLF4 (catalog AF3158) antibodies were from R&D Systems. The rabbit anti–IL-36γ (catalog LS‑C201142) and its blocking peptide (catalog LS-E45854) were from LifeSpan BioSciences. The anti–human KLF4 antibody (catalog AM09057PU-N) was from Acris. The anti–β-actin (catalog A5441), anti-FLAG (catalog F1804), and anti-myc (catalog C3956) antibodies were from Sigma-Aldrich. The anti–human KLF4 (catalog 12173), anti-ERK (catalog 9107), anti–phospho-ERK (catalog 4370), and anti–phospho-threonine/proline (catalog 9391) antibodies were from Cell Signaling Technology. The anti-T7 antibody was from Abcam (catalog ab9138). The anti-HA antibody was from Santa Cruz Biotechnology (catalog sc-805). The secondary antibodies used were alkaline phosphatase–conjugated mouse IgG (catalog S372B), rabbit IgG (catalog S373B), and goat IgG (V115A) from Promega. Live C. acnes was prepared as previously described (63 (link)).

Satoh T.K., Mellett M., Meier-Schiesser B., Fenini G., Otsuka A., Beer H.D., Rordorf T., Maul J.T., Hafner J., Navarini A.A., Contassot E, & French L.E. (2020). IL-36γ drives skin toxicity induced by EGFR/MEK inhibition and commensal Cutibacterium acnes. The Journal of Clinical Investigation, 130(3), 1417-1430.

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Synthesis and Characterization of SR4 Compound

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SR4 was synthesized according to a previously validated protocol at the Chemical GMP Synthesis Facility, Translational Medicinal Chemistry Laboratory, Beckman Research Institute of the City of Hope [25 (link)]. The BRAF inhibitor vemurafenib was purchased from ApexBio (Houston, TX, USA). Antibodies against AMPKα, phospho-AMPKα (Thr¹⁷²), ACC, phospho-ACC (Ser⁷⁹), p70S6 kinase (S6K), phospho-S6K (Thr³⁸⁹), ERK 1/2 (p44/42 MAPK), phospho-ERK (Thr²⁰²/Tyr²⁰⁴), Raptor, phospho-Raptor (Ser⁷⁹²), MEK, phospho-MEK (Ser²¹⁷/Ser²²¹), p38, phospho-p38 (Thr¹⁸⁰/Tyr¹⁸²), LKB1 and β-actin were obtained from Cell Signaling Technology (Danvers, MA, USA). Unless otherwise noted, all other chemicals and reagents, including niclosamide, were purchased from Sigma-Aldrich (St. Louis, MO, USA).

Figarola J.L., Singhal J., Singhal S., Kusari J, & Riggs A. (2018). Bioenergetic modulation with the mitochondria uncouplers SR4 and niclosamide prevents proliferation and growth of treatment-naïve and vemurafenib-resistant melanomas. Oncotarget, 9(97), 36945-36965.

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