Tp 0903

Manufactured by Selleck Chemicals

Sourced in United States

TP-0903 is a laboratory instrument designed for the analysis and measurement of chemical samples. It is a precision tool used in various scientific and research applications.

Automatically generated - may contain errors

Lab products found in correlation

Afatinib, by Selleck Chemicals (2 mentions) Entinostat, by Selleck Chemicals (2 mentions) Fetal bovine serum (fbs), by Thermo Fisher Scientific (2 mentions) Mda mb 231, by American Type Culture Collection (2 mentions) Sorafenib, by Selleck Chemicals (1 mentions) Glutamine, by Thermo Fisher Scientific (1 mentions) Countess automated cell counter, by Thermo Fisher Scientific (1 mentions) Rpmi medium, by Merck Group (1 mentions) Niraparib, by Selleck Chemicals (1 mentions) Panobinostat, by Selleck Chemicals (1 mentions) Vorinostat, by Selleck Chemicals (1 mentions) Vinblastine, by Merck Group (1 mentions) Topotecan, by Merck Group (1 mentions) Pracinostat, by Selleck Chemicals (1 mentions) Marizomib, by Selleck Chemicals (1 mentions) Selisistat, by Selleck Chemicals (1 mentions) Gemcitabine, by Merck Group (1 mentions) Dasatinib, by Selleck Chemicals (1 mentions) Dinaciclib, by Selleck Chemicals (1 mentions) Vincristine, by Merck Group (1 mentions)

9 protocols using tp 0903

Cell line maintenance and RTKi assay

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The maintenance of SH-SY5Y and Kelly cell lines (DSMZ) was done in RPMI medium (Sigma-Aldrich, Italy) supplemented with FBS (fetal bovine serum; 10%), glutamine (1%) and antibiotics (1%; all from Gibco, Life Technologies, Italy). The number of the cells required for the analyses was preliminarily optimized for each experimental setting. The RTKi: Sorafenib, Afatinib and TP-0903 were all purchased from Selleck Chemicals (Germany). Cell count was done on the Countess™ automated cell counter (Invitrogen) using the trypan blue, and the cell viability was measured indirectly by the means of their metabolic activity using tetrazolium compound (MTT). The inhibitory concentration that reduced cell viability by 50% was determined as described in details previously [17 (link)].

Aveic S., Pantile M., Polo P., Sidarovich V., De Mariano M., Quattrone A., Longo L, & Tonini G.P. (2018). Autophagy inhibition improves the cytotoxic effects of receptor tyrosine kinase inhibitors. Cancer Cell International, 18, 63.

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Chemical Compounds for Cancer Research

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Panobinostat, vorinostat, pracinostat, trichostatin-A (TSA), RG2833, entinostat, bortezomib, marizomib, FK866, niraparib, selisistat, gefitinib, enzastaurin, dasatinib, dinaciclib, PI103, PD-0325901, HSP990, ABT737, (+)- JQ, TP0903, Bay11–7082, YM155, and cucurbitacin-I were purchased from Selleck Chemicals (Houston, TX). Vincristine, vinblastine, paclitaxel, topotecan, gemcitabine, 5-fluoruracil, and temozolomide were purchased from Sigma Aldrich (St. Louis, MO).

Jane E.P., Premkumar D.R., Thambireddy S., Golbourn B., Agnihotri S., Bertrand K.C., Mack S.C., Myers M.I., Chattopadhyay A., Taylor D.L., Schurdak M.E., Stern A.M, & Pollack I.F. (2020). Targeting NAD+ biosynthesis overcomes panobinostat and bortezomib-induced malignant glioma resistance. Molecular cancer research : MCR, 18(7), 1004-1017.

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Axl Inhibitor TP-0903 Treatment in H1299 Cells

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H1299 cells were treated with an Axl-specific inhibitor TP-0903 (Selleck Chemicals LLC, Houston, TX, USA) for 24 h (0.2 µmol/L)^{34 (link)}.

Kanzaki R., Naito H., Kise K., Takara K., Eino D., Minami M., Shintani Y., Funaki S., Kawamura T., Kimura T., Okumura M, & Takakura N. (2017). Gas6 derived from cancer-associated fibroblasts promotes migration of Axl-expressing lung cancer cells during chemotherapy. Scientific Reports, 7, 10613.

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Evaluating AXL Inhibitor TP-0903 for Cancer

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The library was cherry picked for cancer indication from a larger Selleckchem collection. The AXL inhibitor TP-0903 was from Selleckchem (Cat#S7846) and auranofin was from Sigma (Cat#A6733).

Saei A.A., Beusch C.M., Chernobrovkin A., Sabatier P., Zhang B., Tokat Ü.G., Stergiou E., Gaetani M., Végvári Á, & Zubarev R.A. (2019). ProTargetMiner as a proteome signature library of anticancer molecules for functional discovery. Nature Communications, 10, 5715.

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Cardiomyoblast Response to Gas6 and LPS

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Cardiomyoblasts (H9C2 cells) obtained from the Chinese Academy of Sciences Cell Bank were cultured in Dulbecco's modified Eagle's medium supplemented with 10% fetal bovine serum (Gibco; Thermo Fisher Scientific, Inc.), 100 IU/ml penicillin and 100 mg/ml streptomycin at 37°C in an atmosphere containing in 5% CO₂. Cells were seeded onto 6-well plates at a density of 1.5×10⁵ cells/well. Recombinant mouse Gas6 (100 ng/ml) (R&D Systems, Inc.) was added 2 h prior to stimulation with LPS (10 µg/ml; from Escherichia coli; Sigma-Aldrich; Merck KGaA). Inhibitors TP-0903 (15 nM) and Wortmannin (3 nM) (Selleck Chemicals, LLC) were administered 15 min prior to Gas6 administration. Cells were incubated for 15 min-24 h with LPS at 37°C and were then harvested for analysis.

Li M., Ye J., Zhao G., Hong G., Hu X., Cao K., Wu Y, & Lu Z. (2019). Gas6 attenuates lipopolysaccharide-induced TNF-α expression and apoptosis in H9C2 cells through NF-κB and MAPK inhibition via the Axl/PI3K/Akt pathway. International Journal of Molecular Medicine, 44(3), 982-994.

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Trastuzumab-resistant Breast Cancer Models

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The BC cell lines BT474, SKBR3, AU565, HCC1954, and MDA-MB-231 were purchased from the American Type Culture Collection (Manassas, VA, USA). All cell lines were maintained as recommended by the suppliers. TP-0903 was purchased from Selleckchem (#S7846, Houston, TX, USA). Trastuzumab was obtained from Roche Pharma (Basel, Switzerland). Trastuzumab-resistant cell lines (AU565R, BT474R, and SKBR3R) were obtained from F.R.’s group at the Fundación Jiménez Díaz Hospital. Cells were established by treating with Trastuzumab for 6 months, starting at 10 μg/ml Trastuzumab for the first 30 days and increasing the dose at each passage until resistant clones emerged. The final Trastuzumab concentration was 15 μg/ml (51 (link)). In vitro Trastuzumab treatment was maintained at 15 μg/ml. TP-0903 was given at IC₅₀ for each cell line for 72 hours.

Adam-Artigues A., Arenas E.J., Martínez-Sabadell A., Brasó-Maristany F., Cervera R., Tormo E., Hernando C., Martínez M.T., Carbonell-Asins J., Simón S., Poveda J., Moragón S., Zazo S., Martínez D., Rovira A., Burgués O., Rojo F., Albanell J., Bermejo B., Lluch A., Prat A., Arribas J., Eroles P, & Cejalvo J.M. (2022). Targeting HER2-AXL heterodimerization to overcome resistance to HER2 blockade in breast cancer. Science Advances, 8(20), eabk2746.

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Inhibitory Effects of TAS-115 and Kinase Inhibitors

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TAS‐115 [4‐[2‐fluoro‐4‐[[[(2‐phenylacetyl)amino]thioxomethyl]amino]‐phenoxy]‐7‐methoxy‐N‐methyl‐6‐quinolinecarboxamide] was provided by Taiho Pharmaceutical Co., Ltd. (Tsukuba, Japan). CP‐673451 (PDGFR inhibitor), TP‐0903 (AXL inhibitor), and quizartinib [Fms‐like tyrosine kinase 3 (FLT‐3) inhibitor] were purchased from Selleck Chemicals (Houston, TX, USA). According to the manufacturer’s instructions, TAS‐115, CP‐673451, TP‐0903, and quizartinib were prepared in dimethyl sulfoxide (DMSO; Sigma‐Aldrich), before their addition to the cell cultures for the in vitro experiments. TAS‐115 was diluted in water with 2‐hydroxypropyl‐β‐cyclodextrin (HPβCD) to the appropriate concentrations for the in vivo experiments, according to the manufacturer’s instructions. Antibodies against platelet‐derived growth factor receptor alpha (PDGFRα) (#3174), p‐PDGFRα (Tyr⁸⁴⁹; #3170), p‐AXL ( #5724), AXL ( #8661), FLT‐3 (#3462), p‐FLT‐3 (#3461), poly(ADP‐ribose) polymerase (PARP) (#9542), CD31 (PECAM‐1) (#77699), and β‐actin (#4970), and anti‐rabbit IgG horseradish peroxidase‐linked secondary antibody (#7074) were purchased from Cell Signaling Technology, Inc. (Danvers, MA, USA). The antibody against AXL (ab32828) was purchased from Abcam (Cambridge, UK).

Yasuda N., Takenaka S., Nakai S., Nakai T., Yamada S., Imura Y., Outani H., Hamada K., Yoshikawa H, & Naka N. (2020). TAS‐115 inhibits PDGFRα/AXL/FLT‐3 signaling and suppresses lung metastasis of osteosarcoma. FEBS Open Bio, 10(5), 767-779.

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Evaluating Targeted Therapies in Lung Cancer Cell Lines

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A549 and H2009 cell lines were obtained from and authenticated by the
American Type Culture Collection, and routinely maintained in RPMI-1640 medium
supplemented 10% FBS, penicillin (100 units/mL) and streptomycin
(100μg/mL) in aired with 5% CO² at 37 °C. The absence
of Mycoplasma contamination was validated using DAPI staining.
These cells were treated with TP-0903 and/or ruxolitinib (SelleckChem) at
appropriate doses over 72 hr. The CellTiter-Glo Luminescent Cell Viability assay
was used to determine cell responsiveness. shRNA knockdown was performed in A549
cells by using lentiviral delivery of short-hairpin AXL or
vehicle plasmid pLKO.1 puro in two biological repeats (Addgene; Supplementary Table S2) (29 (link)).

Taverna J.A., Hung C.N., DeArmond D.T., Chen M., Lin C.L., Osmulski P.A., Gaczynska M.E., Wang C.M., Lucio N.D., Chou C.W., Chen C.L., Nazarullah A., Lampkin S.R., Qiu L., Bearss D.J., Warner S., Whatcott C.J., Mouritsen L., Wade M., Weitman S., Mesa R.A., Kirma N.B., Chao W.T, & Huang T.H. (2020). Single-cell Proteomic Profiling Identifies Combined AXL and JAK1 Inhibition as a Novel Therapeutic Strategy for Lung Cancer. Cancer research, 80(7), 1551-1563.

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Breast Cancer Cell Line Drug Sensitivity

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Breast cancer cell lines CAMA-1, T47D, MCF7, ZR-75-1, MDA-MB-231, BT549, HCC38, HCC1143, and HCC1395 were all obtained from ATCC. BGB324 was obtained from BerGenBio. The following drugs were all purchased from Selleckchem s including: chemotherapy drugs (Doxorubicin, Carboplatin, and Paclitaxel), AXL inhibitors (BGB324 and TP-0903), Wnt/CBP inhibitor (ICG-001,), Hedgehog inhibitor (vismodegib), CDK8 inhibitor (senexinA), CDK4/6 inhibitor (ribociclib and abemaciclib), FGFR inhibitor (AZD4547), EGFR inhibitors (afatinib and gefitinib), ALDH inhibitor (disulfiram, DSF), pan-HDAC inhibitor belinostat, Class I HDAC inhibitor entinostat, and specific HDAC inhibitors SantacruzanateA (HDAC2i), RGFP966 (HDAC3i), PCI-34051 (HDAC8i), LMK-235 (HDAC4/5i), CAY10603 (HDAC6i).

Chi F., Liu J., Brady S.W., Cosgrove P.A., Nath A., McQuerry J.A., Majumdar S., Moos P.J., Chang J.T., Kahn M., & Bild A.H. (2020). A ‘one-two punch’ therapy strategy to target chemoresistance in estrogen receptor positive breast cancer.

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