Cobimetinib

Manufactured by Genentech

Sourced in United States

Cobimetinib is a small molecule inhibitor that targets the MEK1 and MEK2 kinases. It is designed to inhibit the activity of the MEK enzymes, which are involved in the regulation of cell growth and survival.

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Lab products found in correlation

Gdc 0973, by Genentech (1 mentions) Vemurafenib, by Genentech (1 mentions) Everolimus, by Novartis (1 mentions)

4 protocols using cobimetinib

Cell Viability Assay for Inhibitor Treatments

Cited 1 time

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The inhibitors pictilisib (GDC-0941), apitolisib (GDC-0980) and cobimetinib (GDC-0973) were obtained from Genentech, Inc. 1 × 10⁴ cells/well were plated into flat-bottomed, 96-well plates and allowed to attach overnight. All drug treatments including combinations were tested in triplicate during a 5-day incubation period with serial dilutions of drug in a final volume of 200 uL. Drug-free controls were included in each assay. DMSO controls were also performed for each assay. Plates were incubated at 37 °C in a humidified atmosphere with 5% CO₂ and cell viability was determined using an acid phosphatase assay as described previously [16 (link), 17 (link)].

Aslan O., Cremona M., Morgan C., Cheung L.W., Mills G.B, & Hennessy B.T. (2018). Preclinical evaluation and reverse phase protein Array-based profiling of PI3K and MEK inhibitors in endometrial carcinoma in vitro. BMC Cancer, 18, 168.

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Inhibiting MEK Pathway in Cancer

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Cobimetinib, vemurafenib, and compounds with the GDC-prefix were manufactured at Genentech (South San Francisco, CA, USA). The PD0325901 MEK inhibitor was purchased from Selleck Chemicals (Houston, TX, USA).

Wagle M.C., Kirouac D., Klijn C., Liu B., Mahajan S., Junttila M., Moffat J., Merchant M., Huw L., Wongchenko M., Okrah K., Srinivasan S., Mounir Z., Sumiyoshi T., Haverty P.M., Yauch R.L., Yan Y., Kabbarah O., Hampton G., Amler L., Ramanujan S., Lackner M.R, & Huang S.M. (2018). A transcriptional MAPK Pathway Activity Score (MPAS) is a clinically relevant biomarker in multiple cancer types. NPJ Precision Oncology, 2, 7.

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Combination Treatment of Melanoma Cell Lines

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Vemurafenib (Absource Diagnostics GmbH, München, Deutschland), molecular weight 489.92 g/mol, cobimetinib (Genentech, Roche Group, San Francisco, California, USA), molecular weight 531.32 g/mol, and everolimus (Novartis Pharma AG, Basel, Switzerland), molecular weight 958.22 g/mol were dissolved in dimethyl sulfoxide (DMSO). DCA (Sodium dichloroacetate, Sigma-Aldrich, St. Louis, Missouri, USA), molecular weight 128.94 g/mol, was dissolved in distilled water (dH2O) and filtered, with a 0.22 µm filter. To treat melanoma cell lines, drugs were added to the respective culture medium and incubated during 48 and 72 h. For control, cell lines were incubated with the respective culture medium and culture medium with DMSO and/or dH2O, according to the drug solvent.

Pópulo H., Domingues B., Sampaio C., Lopes J.M, & Soares P. (2021). Combinatorial Therapies to Overcome BRAF/MEK Inhibitors Resistance in Melanoma Cells: An in vitro Study. Journal of Experimental Pharmacology, 13, 521-535.

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Xenograft model of MCL-1 knockdown

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HT29 cells containing stable expression of control (#293) or MCL-1 (#50) shRNA were injected (2 × 10⁶ cells per injection) into the right flank of male immunodeficient nu/nu, SCID mice (Charles River Laboratories) at 6–8 weeks of age. When flank tumors reached approximately 100 mm³, cobimetinib (Genentech) at a dose of 15 mg/kg or vehicle (5% DMSO/30% PEG 300/5% Tween 80/ddH₂O) was administered once every 3 days by oral gavage for 14 consecutive days. A replicate of 8 mice for vehicle and 6 mice for cobimetinib treatment per experimental condition were utilized. Two mice from vehicle groups were sacrificed before treatment to examine the baseline efficiency of MCL-1 knockdown. Tumor volume was calculated using the following formula: length × width² × 0.5. All animals were sacrificed at 72 hrs post last treatment dose and tumor tissue was snap frozen at −80°C for immunoblotting experiments. All the animal experiments were performed under an animal protocol approved by the Mayo Clinic Institutional Animal Care and Use Committee.

Kawakami H., Huang S., Pal K., Dutta S.K., Mukhopadhyay D, & Sinicrope F.A. (2016). Mutant BRAF upregulates MCL-1 to confer apoptosis resistance that is reversed by MCL-1 antagonism and cobimetinib in colorectal cancer. Molecular cancer therapeutics, 15(12), 3015-3027.

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