Trametinib

Manufactured by ChemScene

Sourced in United States

Trametinib is a chemical compound used in scientific research and laboratory settings. It is a protein kinase inhibitor that specifically targets the MEK protein, which plays a role in cellular signaling pathways. Trametinib is commonly used in cell culture and biochemical assays to study the effects of MEK inhibition on cellular processes.

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Lab products found in correlation

Capmatinib, by Selleck Chemicals (1 mentions) Lorlatinib, by Selleck Chemicals (1 mentions) Lapatinib, by Selleck Chemicals (1 mentions) Captisol, by ChemScene (1 mentions) Dimethyl sulfoxide (dmso), by Merck Group (1 mentions) Neratinib, by LC Laboratories (1 mentions) Dabrafenib, by LC Laboratories (1 mentions) Osimertinib, by LC Laboratories (1 mentions) Erlotinib, by Roche (1 mentions) Shp099, by MedChemExpress (1 mentions)

4 protocols using trametinib

Synthesis and Characterization of Anti-Cancer Compounds

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Alectinib was synthesized by Chugai Pharmaceutical Co., Ltd. (Tokyo, Japan). Erlotinib was provided by F. Hoffmann-La Roche Ltd. (Basel, Switzerland). Infrigatinib (BGJ398), osimertinib, neratinib, and dabrafenib were obtained from LC Laboratories (Woburn, MA, USA). AZD4547 and trametinib were obtained from ChemScene (Monmouth Junction, NJ, USA). Lorlatinib, capmatinib, and lapatinib were obtained from Selleck Chemicals (Houston, TX, USA). The anti-cancer compound library was obtained from TargetMol (Boston, MA, USA). All agents were dissolved in dimethyl sulfoxide (DMSO: Sigma-Aldrich, St. Louis, MO, USA) for in vitro assays and in a 6% (w/v) solution of Captisol (ChemScene) for in vivo assays. DMSO and Captisol were used as vehicle controls. Recombinant human FGF1, FGF2, FGF7, and FGF12 proteins were obtained from R&D Systems (Minneapolis, MN, USA) and dissolved in phosphate-buffered saline (PBS, Sigma-Aldrich). Recombinant human FGF9 and FGF18 proteins were obtained from Abcam (Cambridge, UK) and dissolved in distilled water. Recombinant human FGF11 protein was obtained from LifeSpan Biosciences (Seattle, WA, USA) and dissolved in Tris buffer (Horizon Discovery, Cambridge, UK).

Furugaki K., Fujimura T., Mizuta H., Yoshimoto T., Asakawa T., Yoshimura Y, & Yoshiura S. (2023). FGFR blockade inhibits targeted therapy-tolerant persister in basal FGFR1- and FGF2-high cancers with driver oncogenes. NPJ Precision Oncology, 7, 107.

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Trametinib Preparation for In Vitro and In Vivo Studies

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Trametinib was purchased from ChemScene (Monmouth Junction, NJ). For the in vitro experiments, the reagent was reconstituted in dimethyl sulfoxide (DMSO) to yield a final concentration of 10 mmol/L and stored at –80°C for up to 6 mo before addition to culture media. For the in vivo experiments, the drug was reconstituted in 200 μL vehicle (corn oil).

Tada S., Anazawa T., Shindo T., Yamane K., Inoguchi K., Fujimoto N., Nagai K., Masui T., Okajima H., Takaori K., Sumi S, & Uemoto S. (2020). The MEK Inhibitor Trametinib Suppresses Major Histocompatibility Antigen-mismatched Rejection Following Pancreatic Islet Transplantation. Transplantation Direct, 6(9), e591.

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Inhibition of Oncogenic Signaling Pathways

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Trametinib (MEK inhibitor) was obtained from ChemScene, SHP099 (SHP-2 inhibitor) from MedChem Express, and calpeptin (cell-penetrating calpain inhibitor) from Calbiochem.

Harigai R., Sato R., Hirose C., Takenouchi T., Kosaki K., Hirose T., Saya H, & Arima Y. (2022). Mutation of PTPN11 (Encoding SHP-2) Promotes MEK Activation and Malignant Progression in Neurofibromin-Deficient Cells in a Manner Sensitive to BRAP Mutation. Cancers, 14(10), 2377.

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Pharmacological Inhibition of MEK1/2 and RAF

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The MEK1/2 inhibitor, trametinib (GSK12021101), and a dual Raf/MEK inhibitor, CH5126766 (RO5126766), were purchased from ChemScene and Selleckchem, respectively. Both these drugs were solubilized in DMSO to prepare stock solutions, per the manufacturer’s protocol.

Tomida A., Yagyu S., Nakamura K., Kubo H., Yamashima K., Nakazawa Y., Hosoi H, & Iehara T. (2021). Inhibition of MEK pathway enhances the antitumor efficacy of chimeric antigen receptor T cells against neuroblastoma. Cancer Science, 112(10), 4026-4036.

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