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Dabrafenib

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Dabrafenib is a small-molecule inhibitor that targets the BRAF kinase. It is a white to slightly colored crystalline solid used in research applications.

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Lab products found in correlation

Vemurafenib, by MedChemExpress (2 mentions) Dabrafenib, by Merck Group (1 mentions) Vemurafenib, by Merck Group (1 mentions) Tween 80, by Merck Group (1 mentions) Encorafenib, by MedChemExpress (1 mentions) Normal human epidermal keratinocytes, by PromoCell (1 mentions) Keratinocyte growth medium 2, by PromoCell (1 mentions) 7 hydroxyflavone, by Merck Group (1 mentions) 3 methoxy 4 nitroflavone, by Merck Group (1 mentions) Antibiotics antimycotics, by PAN Biotech (1 mentions) Tapinarof, by MedChemExpress (1 mentions) Vemurafenib, by Selleck Chemicals (1 mentions) Dulbecco modified eagle medium (dmem), by PAN Biotech (1 mentions) Fetal bovine serum (fbs), by PAN Biotech (1 mentions) Trametinib, by MedChemExpress (1 mentions) Crizotinib, by Selleck Chemicals (1 mentions) Doxycycline, by Merck Group (1 mentions) Alisertib, by Selleck Chemicals (1 mentions) Ferrostatin, by Selleck Chemicals (1 mentions) Polybrene, by Santa Cruz Biotechnology (1 mentions)

7 protocols using dabrafenib

1

Evaluation of BRAF and STING Agonists

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BRAF inhibitors Dabrafenib (Cat No. HY-14660), Vemurafenib (Cat No. HY-12057) and diABZI STING agonist-1 trihydrochloride (Cat No. HY-112921B) were procured form MedChem Express. CDDO-methyl ester (SMB00376) was purchased from Sigma Aldrich and used at a concentration of 500 nM. Dabrafenib, Vemurafenib and diABZI were used at their given IC50 concentrations 0.6, 31, and 21 nM respectively.
Chipurupalli S., Ganesan R., Dhanabal S.P., Kumar M.S, & Robinson N. (2020). Pharmacological STING Activation Is a Potential Alternative to Overcome Drug-Resistance in Melanoma. Frontiers in Oncology, 10, 758.
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2

Dabrafenib Administration After Spinal Cord Injury

Cited 2 times
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Mice were randomly assigned to vehicle-treated and Dabrafenib-treated groups. Dabrafenib (MedChemExpress, Monmouth Junction, NJ, USA) was suspended in an aqueous mixture of 0.5% hydroxypropyl methyl cellulose (HPMC) and 0.2% Tween 80 (Sigma-Aldrich, St. Louis, MO, USA). The suspended drug (200 µL) was administered by oral gavage to mice in the Dabrafenib-treated group at 100 mg/kg of Dabrafenib at 4, 24, and 48 h after SCI [30 (link),37 (link)]. In the vehicle-treated mice, an equivalent volume of the vehicle was administrated by oral gavage, as described previously [30 (link),37 (link)].
Sugaya T., Kanno H., Matsuda M., Handa K., Tateda S., Murakami T., Ozawa H, & Itoi E. (2019). B-RAFV600E Inhibitor Dabrafenib Attenuates RIPK3-Mediated Necroptosis and Promotes Functional Recovery after Spinal Cord Injury. Cells, 8(12), 1582.
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3

Culturing and Treating HaCaT Keratinocytes

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HaCaT keratinocytes were cultured in DMEM (PAN Biotech, Aidenbach, Germany) supplemented with 10% fetal bovine serum (PAN Biotech) and 1% antibiotics/antimycotics (PAN Biotech). The generation of HaCaT-EV and HaCaT-shAHR keratinocytes has been previously described [16 (link)]. The culture medium of HaCaT-EV and HaCaT-shAHR keratinocytes was supplemented with G418 (Carl Roth, Karlsruhe, Germany). Normal human epidermal keratinocytes were obtained from PromoCell (Heidelberg, Germany) and cultured in Keratinocyte Growth Medium 2 (PromoCell). All cells were cultured at 37 °C in a humidified atmosphere containing 5% CO2. UV exposure of cells was carried out by using the BS-02 irradiation chamber (Opsytec Dr. Gröbel, Ettlingen Germany) equipped with individually controllable UVA Actinic and UVB bulbs and respective sensors. For both, UV and sham irradiation, cell culture medium was replaced by PBS. For cell treatment, 6-formylindolo[3,2-b]carbazole (Biomol, Hamburg, Germany), tapinarof, dabrafenib, encorafenib (MedChem Express, Monmouth Junction, NJ, USA), 3’-methoxy-4′-nitroflavone (a kind gift from I. Meyer, Symrise AG, Holzminden, Germany), 7-hydroxyflavone (Sigma-Aldrich, Munich, Germany) and vemurafenib (Selleck Chemicals, Houston, TX, USA) were dissolved in dimethyl sulfoxide.
Rolfes K.M., Sondermann N.C., Vogeley C., Dairou J., Gilardino V., Wirth R., Meller S., Homey B., Krutmann J., Lang D., Nakamura M, & Haarmann-Stemmann T. (2021). Inhibition of 6-formylindolo[3,2-b]carbazole metabolism sensitizes keratinocytes to UVA-induced apoptosis: Implications for vemurafenib-induced phototoxicity. Redox Biology, 46, 102110.
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4

Generating BRAF-inhibitor Resistant Clones

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BRAF inhibitors, vemurafenib and dabrafenib (MedChemExpress, Monmouth Junction, NJ, USA), were added in the cell culture medium using measured IC50 concentration for 72 h before detecting cell viability. The resistant clones were developed using IC50 concentration for selection and subcultured for at least 2 passages.
Tseng C.H., Lu P.H., Wang Y.P, & Chang J.Y. (2022). Enrichment of SOX2-Positive Cells in BRAF V600E Mutated and Recurrent Ameloblastoma. Journal of Personalized Medicine, 12(1), 77.
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5

Dabrafenib and Trametinib Combination Therapy

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Mice received combination therapy with a dose of 30mg/kg dabrafenib and 1mg/kg trametinib (Medchem Express). dabrafenib and trametinib were initially dissolved in dimethylsulphoxide (DMSO) and subsequently diluted into carboxymethylcellulose (CMC, 0.5% w/v), Tween 80 (0.05% v/v) in sterile water and administered to mice daily by oral gavage.
Kim D., An L., Moon J., Maymi V.I., McGurk A.I., Rudd B.D., Fowell D.J, & White A.C. (2023). Ccr2+ monocyte-derived macrophages influence trajectories of acquired therapy resistance in Braf-mutant melanoma. Cancer research, 83(14), 2328-2344.
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6

Comprehensive Cell Culture Toolkit

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DMEM High Glucose (Gibco), RPMI 1640 (Gibco), Trypsin 0.05% (Gibco), penicillin/streptomycin 1X (Gibco), Glutamine (Gibco), Matrigel (Corning), Polybrene (Santa Cruz Biotechnology), Polyethylenimine (Sigma-Aldrich), BRD2 antibody (Bethyl Laboratories), β-actin (Cell Signaling Technology), Osimertinib (MedchemExpress, Selleck), CID compound (Takara 635088), Doxycycline (Sigma), Alisertib (Selleck), Trametinib (Medko), Dabrafenib (MedchemExpress), Crizotinib (Selleck), AMG510 (Selleck), RSL3(Selleck), NEO2734(Selleck), ARV-771(Selleck), CC90010 (Selleck), ABT-263 (Selleck), Ferrostatin (Selleck), Z-VAD-FMK (Selleck), N-acetylcysteine amide (Sigma).
Chen M., Mainardi S., Lieftink C., Velds A., de Rink I., Yang C., Kuiken H.J., Morris B., Edwards F., Jochems F., van Tellingen O., Boeije M., Proost N., Jansen R.A., Qin S., Jin H., Koen van der Mijn J.C., Schepers A., Venkatesan S., Qin W., Beijersbergen R.L., Wang L, & Bernards R. (2024). Targeting of vulnerabilities of drug-tolerant persisters identified through functional genetics delays tumor relapse. Cell Reports Medicine, 5(3), 101471.
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7

Establishing BRAF-Inhibitor Resistant Cell Lines

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Cell lines were obtained from the American Type Culture Collection (ATCC). All cells were cultured in RMPI-1640, supplemented with 10% FBS, penicillin/streptomycin, and L-glutamine and grown at 37°C in a humidified chamber with 5% CO2. A375 parental and resistant lines were authenticated by short tandem repeat profiling. Cells were verified to be mycoplasma free (MycoAlert PLUS, Lonza). Chemical inhibitors were dissolved in DMSO for in vitro studies: vemurafenib (LC Labs), cobimetinib (MedChem Express), ponatinib (LC Labs), NVP-BGJ398 (MedChem Express), PD173074 (Selleckchem), dabrafenib (MedChem Express), and trametinib (LC Labs). A375 cells were treated with vemurafenib, cobimetinib or the combination starting at IC50 concentration and escalated weekly. Once resistant populations had been established, they were maintained at 2 μM for vemurafenib, 0.5 μM for cobimetinib, and 1.5/0.5 μM for the combination respectively.
Wang V.E., Xue J.Y., Frederick D.T., Cao Y., Lin E., Wilson C., Urisman A., Carbone D.P., Flaherty K.T., Bernards R., Lito P., Settleman J, & McCormick F. (2019). Adaptive Resistance to Dual BRAF/MEK Inhibition in BRAF-Driven Tumors Through Autocrine FGFR Pathway Activation. Clinical cancer research : an official journal of the American Association for Cancer Research, 25(23), 7202-7217.
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