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Azd4547

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AZD4547 is a compound used for research purposes. It is a selective inhibitor of the fibroblast growth factor receptor (FGFR) tyrosine kinase. AZD4547 can be utilized in various in vitro and in vivo research applications to study the role of FGFR signaling.

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Lab products found in correlation

Bgj 398, by Chemietek (2 mentions) Pd173074, by Cayman Chemical (2 mentions) Jnj 42756493, by Active Motif (2 mentions) Tki258, by LC Laboratories (2 mentions) Mission shrna, by Merck Group (2 mentions) Effectene, by Qiagen (2 mentions) Recombinant fgf2, by R&D Systems (2 mentions) Mg63 human osteosarcoma cells, by American Type Culture Collection (2 mentions) Fulvestrant, by Merck Group (1 mentions) Cell titer glo luminescence cell viability kit, by Promega (1 mentions) Spectramax m5e, by Thermo Fisher Scientific (1 mentions)

5 protocols using azd4547

1

NSCLC Cell Lines and Compounds

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NSCLC 201T, 273T and 128-88T cell lines were established in our laboratory as previously described [27 (link)]. A549 and H23 cell lines were purchased from American Type Culture Collection (ATCC; Manassas, VA). Cells were cultured in either BME +10% FBS or RPMI 1640 +10% FBS (ATCC; Manassas, VA). Cell lines were authenticated by genotyping with a multiplex STR assay (Genetica) within 3 months of performed studies. E2 and fulvestrant were purchased from Sigma-Aldrich (St. Louis, MO) and diluted in DMSO to 100mM or 5μM stocks, respectively for in vitro use. AZD4547 was purchased from ChemieTek (Indianapolis, IN) and diluted in DMSO to a 10mM stock for in vitro studies.
Siegfried J.M., Farooqui M., Rothenberger N.J., Dacic S, & Stabile L.P. (2017). Interaction between the estrogen receptor and fibroblast growth factor receptor pathways in non-small cell lung cancer. Oncotarget, 8(15), 24063-24076.
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2

Xenograft Model of FGFR Inhibition

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NSG (NOD.Cg-Prkdcscid Il2rgtm1Wjl/SzJ) mice (obtained from the Jackson Laboratories), were maintained as a breeding colony. All experiments were conducted under Augusta University IACUC approved protocols. Female, 6–8 week old mice were used in all xenograft experiments. Mice were engrafted with 1–2 × 106 cells via tail vein injection. All mice were treated with either drug, or vehicle control (PEG300:acetic buffer = 1:1), orally using a gavage needle once per day. All treatments were performed 5 days per week for 4 weeks.
Ponatinib was provided by Ariad Pharmaceuticals Inc. (Cambridge, MA). PD173074 was purchased from Cayman Chemical, AZD4547 and BGJ398 from ChemieTek, JNJ-42756493 from Active Biochem and TKI258 from LC Laboratories. E3810 was provided by EOS pharmaceuticals. All drugs were dissolved in DMSO and stored at −80°C before use. For drug treatments, cells were seeded at 3,000–10,000 cells/well, depending on the cell line, in 96-well plates and incubated overnight. Cells were then treated with either DMSO (control) or different FGFR inhibitors as indicated in the results section at concentrations defined by the experiments. Cell viability was determined using CellTiter-Glo® luminescence cell viability kits (Promega) and a SpectraMax® M5e (Molecular Probes) luminescence plate reader as described previously.8 (link)
Cowell J.K., Qin H., Hu T., Wu Q., Bhole A, & Ren M. (2017). Mutation in the FGFR1 tyrosine kinase domain or inactivation of PTEN is associated with acquired resistance to FGFR inhibitors in FGFR1-driven leukemia/lymphomas. International journal of cancer, 141(9), 1822-1829.
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3

Transgenic Osteoblast and Chondrocyte Cell Lines

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All general laboratory reagents were purchased from Sigma Chemical Co. (Poole, UK) unless otherwise stated. All cells were cultured in α–MEM containing 10% batch-tested FCS (Lonza, Slough, UK), antibiotics (penicillin 50U/ml, streptomycin 50μg/ml) and L-glutamine (5mM). The tetracycline-inducible osteoblastic AT9.2 and chondroblastic DT12.4 cell lines were cultured as previously described19 (link),26 (link) in the presence of 10 μg/ml (AT9.2) or 1μg/ml (DT12.4) tetracycline to inhibit transgene expression, and c-Fos was induced following withdrawal of tetracycline for 48h. DT8.6 cells represent a subclone of ATDC5 chondrocytes constitutively overexpressing c-Fos26 (link) and P1.15, P1.7, 131 P cells are clonal osteosarcoma cell lines derived from c-Fos murine transgenic osteosarcomas12 (link). Primary mouse osteoblasts were obtained from newborn mouse calvariae as described19 (link) and MG63 human osteosarcoma cells were purchased from American Type Culture Collection (ATCC). All cell lines were mycoplasma-negative. Recombinant FGF2 was purchased from R&D Systems (Abingdon, UK). Transfections were performed using Effectene (Qiagen, Crawley, UK) and clones were selected in gentamycin (G418). Lentiviral shRNA vectors for FGFR1 were obtained from MISSION™ shRNA (Sigma). The FGFR inhibitor AZD4547 was purchased from ChemieTek (Indianapolis, IN).
Weekes D., Kashima T.G., Zandueta C., Perurena N., Thomas D.P., Sunters A., Vuillier C., Bozec A., El-Emir E., Miletich I., Patiño-Garcia A., Lecanda F, & Grigoriadis A.E. (2015). Regulation of osteosarcoma cell lung metastasis by the c-Fos/AP-1 target FGFR1. Oncogene, 35(22), 2852-2861.
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4

Preparation of Targeted Kinase Inhibitors

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AZD4547 and BGJ398 were purchased from the ChemieTek, JNJ42756493 from Active Biochem, TKI258 from LC Laboratories and PD173074 from Cayman Chemical. All drugs were diluted in DMSO, aliquoted and stored as 10 mM stocks at −80°C.
Wu Q., Bhole A., Qin H., Karp J., Malek S., Cowell J.K, & Ren M. (2016). Targeting FGFR1 to suppress leukemogenesis in syndromic and de novo AML in murine models. Oncotarget, 7(31), 49733-49742.
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5

Transgenic Osteoblast and Chondrocyte Cell Lines

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All general laboratory reagents were purchased from Sigma Chemical Co. (Poole, UK) unless otherwise stated. All cells were cultured in α–MEM containing 10% batch-tested FCS (Lonza, Slough, UK), antibiotics (penicillin 50U/ml, streptomycin 50μg/ml) and L-glutamine (5mM). The tetracycline-inducible osteoblastic AT9.2 and chondroblastic DT12.4 cell lines were cultured as previously described19 (link),26 (link) in the presence of 10 μg/ml (AT9.2) or 1μg/ml (DT12.4) tetracycline to inhibit transgene expression, and c-Fos was induced following withdrawal of tetracycline for 48h. DT8.6 cells represent a subclone of ATDC5 chondrocytes constitutively overexpressing c-Fos26 (link) and P1.15, P1.7, 131 P cells are clonal osteosarcoma cell lines derived from c-Fos murine transgenic osteosarcomas12 (link). Primary mouse osteoblasts were obtained from newborn mouse calvariae as described19 (link) and MG63 human osteosarcoma cells were purchased from American Type Culture Collection (ATCC). All cell lines were mycoplasma-negative. Recombinant FGF2 was purchased from R&D Systems (Abingdon, UK). Transfections were performed using Effectene (Qiagen, Crawley, UK) and clones were selected in gentamycin (G418). Lentiviral shRNA vectors for FGFR1 were obtained from MISSION™ shRNA (Sigma). The FGFR inhibitor AZD4547 was purchased from ChemieTek (Indianapolis, IN).
Weekes D., Kashima T.G., Zandueta C., Perurena N., Thomas D.P., Sunters A., Vuillier C., Bozec A., El-Emir E., Miletich I., Patiño-Garcia A., Lecanda F, & Grigoriadis A.E. (2015). Regulation of osteosarcoma cell lung metastasis by the c-Fos/AP-1 target FGFR1. Oncogene, 35(22), 2852-2861.
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