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Nvp bgj398

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NVP-BGJ398 is a potent and selective inhibitor of fibroblast growth factor receptor (FGFR) kinases. It exhibits high selectivity for FGFR1, FGFR2, FGFR3, and FGFR4. NVP-BGJ398 is a useful tool for the study of FGFR signaling pathways.

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Lab products found in correlation

Huvecs, by Merck Group (1 mentions) Huvecs, by American Type Culture Collection (1 mentions) Dabrafenib, by MedChemExpress (1 mentions) Cobimetinib, by MedChemExpress (1 mentions) Mycoalert plus, by Lonza (1 mentions) Pd173074, by Selleck Chemicals (1 mentions)

2 protocols using nvp bgj398

1

Modulating miR-146a in HUVECs

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HUVECs were obtained from the American Type Culture Collection (Manassas, VA, USA) and cultured in RPMI 1640 at 37 °C in a humidified atmosphere of 5% CO2. For lentivirus generation, a recombinant lentivirus carrying the human miR-146a precursor sequence was constructed by homologous recombination between the expression cosmid cassette and the parental virus genome in HEK293 cells. The recombinant lentivirus was then used to stably infect HUVECs as previously described11 . HUVECs were infected with lentiviral vectors encoding shFGFBP1 and FGFBP1 cDNA as previously reported21 (link). miR-146 overexpressing HUVECs were treated with FGF2 neutralizing antibody (F-5537, 8.8 μg/ml, Sigma, Deisenhofen, Germany) and FGFR inhibitor (NVP-BGJ398, 0.2 μM/ml, medchem express, Princeton, NJ, USA to evaluate the growth, migration and Tube formation effect, respectively.
Zhu H.Y., Bai W.D., Liu J.Q., Zheng Z., Guan H., Zhou Q., Su L.L., Xie S.T., Wang Y.C., Li J., Li N., Zhang Y.J., Wang H.T, & Hu D.H. (2016). Up-regulation of FGFBP1 signaling contributes to miR-146a-induced angiogenesis in human umbilical vein endothelial cells. Scientific Reports, 6, 25272.
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2

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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