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Pd173074

Manufactured by Cayman Chemical
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PD173074 is a small molecule that inhibits the activity of the fibroblast growth factor receptor (FGFR) tyrosine kinase. It is a tool compound used for research purposes.

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Lab products found in correlation

Aphidicolin, by Merck Group (2 mentions) Pd0325901, by Merck Group (2 mentions) Xav939, by Merck Group (2 mentions) Latrunculin a, by Cayman Chemical (2 mentions) Iwr 1, by Merck Group (2 mentions) Pd173074, by Merck Group (2 mentions) Azd4547, by Chemietek (2 mentions) Bgj 398, by Chemietek (2 mentions) Jnj 42756493, by Active Motif (2 mentions) Tki258, by LC Laboratories (2 mentions) Type 1 collagen, by BD (2 mentions) Fibroblast growth factor 2 (fgf2), by BD (2 mentions) Ebm 2 medium, by Lonza (2 mentions) U0126, by Cell Signaling Technology (1 mentions) Tgf β1, by Selleck Chemicals (1 mentions) Mk 2206, by Selleck Chemicals (1 mentions) Tgf β1, by R&D Systems (1 mentions) Fetal bovine serum (fbs), by Thermo Fisher Scientific (1 mentions) Rpmi 1640, by Cayman Chemical (1 mentions) Rpmi 1640, by Thermo Fisher Scientific (1 mentions)

10 protocols using pd173074

1

Modulation of BEAS-2B Cells by TGF-β1 and FGF2

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BEAS-2B cells were incubated with TGFβ1 (2 ng/ml) alone, FGF2 (2 nM) alone, PD173074 (0.1 μM, Cayman Chemical, MI, USA) alone or FGF2 (2 nM) and TGFβ1 with or without PD173074 for 4 days prior to collection of RNA. The dose of PD173074 used was based on our prior studies (53 (link)).
El-Baz L.M., Shoukry N.M., Hafez H.S., Guzy R.D, & Salem M.L. (2020). Fibroblast Growth Factor 2 Augments Transforming Growth Factor Beta 1 Induced Epithelial-mesenchymal Transition in Lung Cell Culture Model. Iranian journal of allergy, asthma, and immunology, 19(4), 348-361.
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2

Isolation and Culture of Primary Lung Fibroblasts

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Primary HLFs were isolated from explanted non-fibrotic human lungs unsuitable for transplantation and donated for research. Protocols were approved by the University of Chicago IRB. Fibroblasts were generated by mincing lung tissue into sub-millimeter pieces and allowing migration out on collagen-coated culture dishes. Fibroblasts were grown in DMEM with 10% FBS and used until passage 10.
For experiments, fibroblasts were grown to 90% confluence, serum-starved overnight in media containing 0.1% FBS, and treated with recombinant human low-molecular weight FGF2 + heparin sulfate (2 mg/ml), TGFβ1 (R&D, 2 ng/ml), or FGF2 + heparin + TGFβ1. When indicated, cells were treated with 0.1 μM PD173074 (Cayman Chemical) during the culture or pretreated with 20 μM U0126 (Cell Signaling) or 1 μM MK-2206 (Selleckchem) for 1 hour before the addition of FGF2 + heparin sulfate and/or TGFβ1.
Koo H.Y., El-Baz L.M., House S.L., Cilvik S.N., Dorry S.J., Shoukry N.M., Salem M.L., Hafez H.S., Dulin N.O., Ornitz D.M, & Guzy R.D. (2018). Fibroblast growth factor 2 decreases bleomycin-induced pulmonary fibrosis and inhibits fibroblast collagen production and myofibroblast differentiation. The Journal of pathology, 246(1), 54-66.
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3

Modulating Stem Cell Signaling Pathways

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To inhibit Notch signaling, 25 μM DAPT (Sigma Aldrich cat. no. D5942-5MG) was added to CLFBR media on day 2 of differentiation. To inhibit FGF signaling, PD0325901 (Stemgent 04-006) or PD173074 (Cayman Chemical cat. no. 219580-11-7) were added to CL or CLFBR media at the indicated concentrations. Wnt signaling was inhibited with the tankyrase inhibitors XAV939 (Sigma Aldrich cat. no. X3004) and IWR-1 (Sigma Aldrich cat. no. I0161) at 2μM and 12μM, respectively, in CLFBR medium. Cell division was blocked by arresting cells at early S phase with 5μM Aphidicolin (Sigma Aldrich cat. no. A0781) in CLFBR medium. Cells were pre-treated for 24 hours with Aphidicolin prior to imaging (during day 2). The onset of imaging was thus delayed by one day and started only on day 3. Aphidicolin was maintained in the medium throughout imaging. Latrunculin A (Cayman Chemical ca. no. 10010630), which inhibits actin polymerization and YAP signaling, was used at 350 nM in RHB basal media supplemented with CLFBR and 5% KSR. Mouse explants and micropatterned cultures were treated with PD0325901 (Sigma- concentration as described in the text) and PD173074 (Sigma - 250nM).
Diaz-Cuadros M., Wagner D.E., Budjan C., Hubaud A., Tarazona O.A., Donelly S., Michaut A., Al Tanoury Z., Yoshioka-Kobayashi K., Niino Y., Kageyama R., Miyawaki A., Touboul J, & Pourquié O. (2020). In vitro characterization of the human segmentation clock. Nature, 580(7801), 113-118.
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4

Culturing NSCLC and Bronchial Epithelial Cells

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NSCLC A549, SPC-A-1, 95D, and NCI-H520 cells and the tunica mucosa bronchiorum epithelium 16HBE cells were obtained from the American Type Culture Collection (Manassas, VA, USA) and maintained in our laboratory. The cells were grown in RPMI 1640 (Gibco, Grand Island, NY, USA) supplemented with 10% fetal bovine serum (Gibco, Grand Island, NY, USA) and 100 units/mL streptomycin/penicillin and cultured at 37°C in a humidified atmosphere with 5% CO2. For the PD173074 experiments, A549 and A549- pLenti-shRNA1 cells were grown in serum-free and epidermal growth factor (EGF)-free medium (SITA: RPMI 1640 supplemented with 5 µg/mL insulin, 10 µg/mL transferrin, 30 nmol/L sodium selenite, and 0.25% bovine serum albumin) supplemented with PD173074 (dissolved in DMSO, Cayman, USA) at a final concentration of 1 µΜ. The growth media for the control cells were supplemented with equivalent volumes of DMSO without inhibitor.
Lei J., Li W., Yang Y., Lu Q., Zhang N., Bai G., Zhong D., Su K., Liu B., Li X., Wang Y, & Wang X. (2014). TC-1 Overexpression Promotes Cell Proliferation in Human Non-Small Cell Lung Cancer that Can Be Inhibited by PD173074. PLoS ONE, 9(6), e100075.
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5

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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6

NC Induction Optimization and Signaling

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For induction into the NC fate, KC were cultured at a density of 8‐10 × 103 cells/cm2 in collagen type I coated dishes (10 μg collagen type I per cm2; BD Biosciences) in the presence of NC induction medium (NCIM), comprising basal medium (EBM‐2 medium; Lonza, Basel, Switzerland) plus 2% (v/v) FBS, 10 μg per ml heparin (Lonza), 100 μg per ml ascorbic acid (Lonza), and 0.5 μg per ml hydrocortisone (Lonza), 1× Gentamicin/Amphotericin‐B (Lonza) and supplemented with 10 ng/mL fibroblast growth factor 2 (FGF2; BD Biosciences) and 10 ng/mL insulin‐like growth factor 1 (IGF1, Lonza). FGF2 and IGF1 concentrations were optimized in previous studies in our lab.17 For our signaling pathways investigation, the following inhibitors were used: PD173074 (Cayman Chemical, Ann Arbor, MI, USA, concentration: 1 μM), CH5183284 (Sellechem, Boston, MA, USA, concentration: 0.5 μM), SB431542 (Sigma, concentration: 10 μM). All inhibitors were dissolved in DMSO.
Tseropoulos G., Moghadasi Boroujeni S., Bajpai V.K., Lei P, & Andreadis S.T. (2018). Derivation of neural crest stem cells from human epidermal keratinocytes requires FGF‐2, IGF‐1, and inhibition of TGF‐β1. Bioengineering & Translational Medicine, 3(3), 256-264.
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7

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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8

Modulating Stem Cell Signaling Pathways

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To inhibit Notch signaling, 25 μM DAPT (Sigma Aldrich cat. no. D5942-5MG) was added to CLFBR media on day 2 of differentiation. To inhibit FGF signaling, PD0325901 (Stemgent 04-006) or PD173074 (Cayman Chemical cat. no. 219580-11-7) were added to CL or CLFBR media at the indicated concentrations. Wnt signaling was inhibited with the tankyrase inhibitors XAV939 (Sigma Aldrich cat. no. X3004) and IWR-1 (Sigma Aldrich cat. no. I0161) at 2μM and 12μM, respectively, in CLFBR medium. Cell division was blocked by arresting cells at early S phase with 5μM Aphidicolin (Sigma Aldrich cat. no. A0781) in CLFBR medium. Cells were pre-treated for 24 hours with Aphidicolin prior to imaging (during day 2). The onset of imaging was thus delayed by one day and started only on day 3. Aphidicolin was maintained in the medium throughout imaging. Latrunculin A (Cayman Chemical ca. no. 10010630), which inhibits actin polymerization and YAP signaling, was used at 350 nM in RHB basal media supplemented with CLFBR and 5% KSR. Mouse explants and micropatterned cultures were treated with PD0325901 (Sigma- concentration as described in the text) and PD173074 (Sigma - 250nM).
Diaz-Cuadros M., Wagner D.E., Budjan C., Hubaud A., Tarazona O.A., Donelly S., Michaut A., Al Tanoury Z., Yoshioka-Kobayashi K., Niino Y., Kageyama R., Miyawaki A., Touboul J, & Pourquié O. (2020). In vitro characterization of the human segmentation clock. Nature, 580(7801), 113-118.
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9

Neural Crest Induction from Keratinocytes

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For induction into the NC fate, KC were cultured at a density of 10-15×103 cells/ cm2 in collagen type I coated dishes (10µg collagen type I per cm2; BD Biosciences) in the presence of neural crest induction medium (NCIM) comprising of basal medium (EBM-2 medium; Lonza) plus 2% (v/v) FBS, 10 µg per ml heparin, 100 µg per ml ascorbic acid and 0.5 µg per ml hydrocortisone, 1x Gentamicin/Amphotericin-B supplemented with 10 ng/ml fibroblast growth factor 2 (FGF2, BD Biosciences), 10 ng/ml Insulin like growth factor 1 (IGF1, BD Biosciences). Other induction factors and inhibitors tested were EGF, WNT1 (Life Technologies), Chir99021 (Tocris), NRG1 (Sigma), BMP4 (Gibco), and PD173074 (Cayman).
Bajpai V.K., Kerosuo L., Tseropoulos G., Cummings K.A., Wang X., Lei P., Liu B., Liu S., Popescu G., Bronner M.E, & Andreadis S.T. (2017). Reprogramming postnatal human epidermal keratinocytes toward functional neural crest fates. Stem cells (Dayton, Ohio), 35(5), 1402-1415.
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10

Regulation of Heparanase and FGF2 Signaling

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Human recombinant FGF2 was purchased from PeproTech (Rocky Hill, NJ, USA). The anti-FGF2 neutralizing monoclonal antibody, clone bFM-1, and the control monoclonal antibody, clone 1E2.2, were purchased from Millipore (Billerica, MA, USA), and the anti-Actin (C-2) antibody from Santa Cruz Biotechnology, Inc. Antibodies to doubly phosphorylated ERK1/2 (pTEY-ERK) and general ERK (tERK), were obtained from Sigma Israel (Rehovot, Israel). The latent 65 kDa heparanase precursor was purified (to at least 95% purity) from the culture medium of heparanase-transfected HEK-293 cells, essentially as described 33 .
For Western blot we applied anti-heparanase polyclonal antibody (#1453) that was raised against the entire 65 kDa heparanase precursor 34, 35 . The heparanase inhibitor PG545 was kindly provided Dr. Edward Hammond (Progen pharmaceuticals, Brisbane, Australia) 36 . The FGFR inhibitor, PD173074 was from Cayman Chemical (Ann Arbor, MI).
Gibor G., Ilan N., Journo S., Sharabi A., Dreyer J., Gertel S., Singh P., Menachem A., Snir N., Elkayam O., Vlodavsky I, & Arad U. (2018). Heparanase is expressed in adult human osteoarthritic cartilage and drives catabolic responses in primary chondrocytes. Osteoarthritis and cartilage, 26(8).
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