Plx4032

Manufactured by MedChemExpress

Sourced in United States, Germany

PLX4032 is a synthetic chemical compound used in laboratory research. It functions as a kinase inhibitor, specifically targeting the BRAF protein. The core purpose of PLX4032 is to facilitate the study of cellular signaling pathways and their implications in various biological processes.

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Lab products found in correlation

Ht 29, by MedChemExpress (2 mentions) Penicillin, by Capricorn (2 mentions) Streptomycin, by Capricorn (2 mentions) L glutamine, by Capricorn (2 mentions) Lgx818, by MedChemExpress (2 mentions) Gsk2118436a, by Selleck Chemicals (2 mentions) Plx8394, by MedChemExpress (2 mentions) Ht 29, by American Type Culture Collection (1 mentions) Hct116, by American Type Culture Collection (1 mentions) Caco 2, by American Type Culture Collection (1 mentions) A375 human melanoma cell line, by American Type Culture Collection (1 mentions) Rad001, by MedChemExpress (1 mentions) Dmem 4500, by Euroclone (1 mentions) Wm266 4, by American Type Culture Collection (1 mentions) Az628, by Selleck Chemicals (1 mentions) Ly3009120, by Selleck Chemicals (1 mentions) Tak 632, by Selleck Chemicals (1 mentions) Gdc 0879, by Selleck Chemicals (1 mentions) Azd6244, by Selleck Chemicals (1 mentions) E 100, by Alomone (1 mentions)

Close spelling variants of this product

Vemurafenib (PLX4032) (5 citations)

7 protocols using plx4032

Establishing Vemurafenib-Resistant Colon Cancer Cell Lines

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Human colon carcinoma cell lines RKO and HT-29 (BRAFV600E/KRASwt) were purchased from the ATCC and maintained in Dulbecco′s Modified Eagle′s medium (DMEM) or Minimum Essential Medium (MEM) supplemented with 10% foetal bovine serum (FBS), 2 mM L-glutamine, penicillin (100 U/mL) and streptomycin (100 µg/mL) (Capricorn Scientific, Ebsdorfergrund, Germany) in humified atmosphere with 5% CO₂ at 37 °C.
In order to eliminate molecular features of resistance that might be cell-line specific, we developed two vemurafenib (PLX4032)-resistant colon cancer cell lines derived from HT-29 and RKO cell lines by exposing the cells to successively increasing concentrations of PLX4032 (MedChemExpress, Monmouth Junction, NJ, USA) in the period of about 6 months until clinically relevant dose (11.52 µM) [7 (link)] was reached. Established resistance phenotypes were confirmed by the MTT assay showing an increase in the IC₅₀ values by 10- and 6.7-fold in the resistant RKO and HT-29 cells, respectively, in comparison with their sensitive counterparts (Supplementary Table S1).

Grbčić P., Eichmann T.O., Kraljević Pavelić S, & Sedić M. (2021). The Sphingosine Kinase 2 Inhibitor ABC294640 Restores the Sensitivity of BRAFV600E Mutant Colon Cancer Cells to Vemurafenib by Reducing AKT-Mediated Expression of Nucleophosmin and Translationally-Controlled Tumour Protein. International Journal of Molecular Sciences, 22(19), 10767.

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Generating Vemurafenib-Resistant Colon Cancer Cell Lines

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Human colon carcinoma cell lines Caco-2 (BRAF^wt/KRAS^wt), SW480 (BRAF^wt/KRAS^G12V), HCT 116 (BRAF^wt/KRAS^G13D) and HT-29 and RKO (BRAF^V600E/KRAS^wt) were purchased from the ATCC and maintained in Dulbecco′s Modified Eagle′s Medium (DMEM) or Minimum Essential Medium (MEM) supplemented with 10% fetal bovine serum (FBS), 2 mM L-glutamine, penicillin (100 U/mL) and streptomycin (100 µg/mL) (Capricorn Scientific, Ebsdorfergrund, Germany) in a humified atmosphere with 5% CO₂ at 37 °C.
In order to eliminate molecular features of resistance that might be cell line-specific, we developed two vemurafenib (PLX4032)-resistant colon cancer cell lines derived from HT-29 and RKO cell lines by exposing the cells to successively increasing concentrations of PLX4032 (MedChemExpress, Monmouth Junction, NJ, USA) in a period of about 6 months until a clinically relevant dose (11.52 µM) [41 (link)] was reached. Established resistance phenotypes were confirmed by the MTT assay showing an increase in the IC₅₀ values by 8- and 10-fold in the resistant HT-29 and RKO cells, respectively, in comparison with their sensitive counterparts (Supplementary Table S5).

Grbčić P., Fučkar Čupić D., Gamberi T., Kraljević Pavelić S, & Sedić M. (2021). Proteomic Profiling of BRAFV600E Mutant Colon Cancer Cells Reveals the Involvement of Nucleophosmin/c-Myc Axis in Modulating the Response and Resistance to BRAF Inhibition by Vemurafenib. International Journal of Molecular Sciences, 22(12), 6174.

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Melanoma Cell Lines and Treatments

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In this study, we used A375 human melanoma cell lines, obtained from American Type Culture Collection (ATCC, Rockville, MD, USA). In some experiments we used also the human melanoma cell lines WM266-4 (from ATCC) and M21 (kindly provided by Dr. Antony Montgomery, The Scripps Research Institute, La Jolla, CA, USA). Melanoma cells were cultivated in Dulbecco’s Modified Eagle Medium high glucose (DMEM 4500, EuroClone, Milan, Italy) supplemented with 10% fetal bovine serum (FBS, Boerhinger Mannheim, Binger Strasse, Ingelheim am Rhein, Germany), at 37 °C in a humidified atmosphere containing 90% air and 10% CO₂. Viability of the cells was determined using a trypan blue exclusion test. Cultures were periodically monitored for mycoplasma contamination using Chen’s fluorochrome test [26 (link)].
A375 melanoma cells resistant to PLX4032 were kindly provided by Laura Poliseno from University of Pisa and they were obtained as explained in Reference [27 (link)]. PLX4032-resistant A375 melanoma cells were maintained without PLX4032 overnight before the start of the experiment.
According to the experiments, cells were treated with Oleuropein glucoside (purity ≥ 90%) (Extrasynthese S.A., Lyon, Nord-Genay, France), DTIC (Sigma Aldrich, Milan, Italy), RAD001 (MedChem Express, Stockholm, Sweden) or PLX4032 (MedChem Express, Stockholm, Sweden).

Ruzzolini J., Peppicelli S., Andreucci E., Bianchini F., Scardigli A., Romani A., la Marca G., Nediani C, & Calorini L. (2018). Oleuropein, the Main Polyphenol of Olea europaea Leaf Extract, Has an Anti-Cancer Effect on Human BRAF Melanoma Cells and Potentiates the Cytotoxicity of Current Chemotherapies. Nutrients, 10(12), 1950.

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Comparative Analysis of BRAF and MEK Inhibitors

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BRAFi used are as follows: PLX4032 (vemurafenib; MedChemExpress, #HY-12057), LGX818 (encorafenib; MedChemExpress, #HY-15605), GSK2118436A (dabrafenib; Selleckchem, #S2807), PLX8394 (MedChemExpress, #HY-18972), AZ628 (Selleckchem, #S2746), GDC0879 (Selleckchem, #S1104), LY3009120 (Selleckchem, #S7842), and TAK632 (Selleckchem, #S7291). MEKi used are as follows: AZD6244 (selumetinib; Selleckchem, #S1008), BAY86-9766 (refametinib; MedChemExpress, #HY-102156), and benzyl-coelenterazine (NanoLight, #301).

Röck R., Mayrhofer J.E., Torres-Quesada O., Enzler F., Raffeiner A., Raffeiner P., Feichtner A., Huber R.G., Koide S., Taylor S.S., Troppmair J, & Stefan E. (2019). BRAF inhibitors promote intermediate BRAF(V600E) conformations and binary interactions with activated RAS. Science Advances, 5(8), eaav8463.

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Evaluating BRAF inhibitor combinations

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The reagents used included PLX4032 (vemurafenib; MedChemExpress, HY-12057), LGX818 (encorafenib; MedChemExpress, HY-15605), GSK2118436A (dabrafenib; Selleckchem, S2807), PLX8394 (MedChemExpress, HY-18972), Benzyl-coelenterazine (Nanolight, 301), and human EGF (Alomone Labs, E-100).

Mayrhofer J.E., Enzler F., Feichtner A., Röck R., Fleischmann J., Raffeiner A., Tschaikner P., Ogris E., Huber R.G., Hartl M., Schneider R., Troppmair J., Torres-Quesada O, & Stefan E. (2020). Mutation-oriented profiling of autoinhibitory kinase conformations predicts RAF inhibitor efficacies. Proceedings of the National Academy of Sciences of the United States of America, 117(49), 31105-31113.

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Generation of Vemurafenib-Resistant Melanoma Cell Lines

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Three human melanoma cell lines that harbor the BRAF V600E mutation (SK-MEL-5, SK-MEL-28, and A375) were obtained from American Tissue Culture Collection (Manassas, VA, USA). The cells were cultured in Dulbecco modified Eagle medium (DMEM) (Invitrogen; Thermo Fisher Scientific, Inc., Waltham, MA, USA) supplemented with 10% fetal bovine serum (FBS) (Invitrogen) and 1% penicillin/streptomycin (Invitrogen) and incubated at 37°C in 5% carbon dioxide. Vemurafenib (PLX4032)-resistant melanoma cell lines were generated by adding escalating concentrations of PLX4032 (MedChemExpress, Inc., Monmouth Junction, NJ, USA) into SK-MEL-5, SK-MEL-28, and A375 cells for >6 months. 17 The final concentrations for generating SK-MEL-5, SK-MEL-28, and A375 cells with acquired resistance to PLX4032 (SK-MEL-5R, SK-MEL-28R, and A375R) were 1 μmol/L, 1 μmol/L, and 2 μmol/L, respectively.

Liu X., Mi J., Qin H., He S., Li Z., Chai J., Li M., Xu J., & Wu J. (2020). SOX4 Mediates BRAF Inhibitor Resistance in Melanoma through Regulation of IGF-1R Signaling: In Vitro Study. International Journal of Dermatology and Venereology, 3(3), 156-165.

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Establishment of BRAF Inhibitor-Resistant Melanoma Cells

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Establishment of BRAFi-resistant melanoma cells A2058 cells were inoculated in a culture ask, and a high dose of vemurafenib(PLX4032, Cat#HY-L032) (MedChemExpress, USA) was used for treatment. When most of the cells had died, the dead cells were washed away and the medium was changed to a drug-free medium. Post reaching con uence, the cells were digested and re-inoculated into a new culture ask, and some cells were cryopreserved for RNA-seq. The cells were treated with high density vemurafenib until the cells reached 30% con uence. This process was repeated 3 times, and we obtained R0, R1, R2, and R3 cells, which were then used for RNA-seq analysis. Melanoma cells in the exponential growth phase were inoculated into culture bottles. After 48 h, the cells were transferred to a drug-free medium and expanded until the next mitotic phase. Then, the above steps were repeated using vemurafenib that was two times more concentrated. At the same time, cell death was observed every day, the fresh complete medium containing vemurafenib was replaced, and CCK8 analysis was performed regularly until melanoma cells grew stably in the medium. This process lasted for six months, and transcriptome sequencing was performed once every two months; thus, 4 samples (R0, R1, R2, and R3) were obtained.

Ren M., Wang L., Deng X., Gao Z., Wang Q., Tao M., Shen K., Ding Y., Liu Q., Wei C., & Gu J. (2021). Overcoming Chemoresistance to Vemurafenib in Melanoma via Targeted Inhibition of PCK1 Using 3-mercaptopropionic Acid.

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