Xl147

Manufactured by Selleck Chemicals

Sourced in United States

The XL147 is a compact and versatile laboratory instrument designed for a range of analytical applications. It features precise temperature control and high-throughput capabilities to support efficient sample processing. The core function of the XL147 is to provide a reliable and consistent platform for various laboratory procedures.

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Lab products found in correlation

5 protocols using xl147

Combination Therapy Evaluation for Breast Cancer

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This study was approved by the Vanderbilt University Animal Care and Use Committee and meets the National Institutes of Health guidelines for animal welfare. BT474 cells or HR6 cells (10⁸) in 100μl Matrigel were injected in the inguinal mammary fat pads of female athymic nude mice (J:NU; Jackson Laboratories). Tumors grew to ≥200mm³. Tumor-bearing mice were treated twice weekly with the following drugs: control human IgG (10 mg/kg, IP; R&D Systems), trastuzumab (10 mg/kg, IP; Vanderbilt Pharmacy), paclitaxel (2.5 mg/kg, IP; Vanderbilt Pharmacy), XL147 (10 mg/kg, oral gavage; Selleckchem), trastuzumab + XL147, trastuzumab + paclitaxel, trastuzumab + paclitaxel + XL147. Tumor volume was calculated from caliper measurements of tumor length (L) and width (W), (L*W²)/2 twice a week.

Walsh A.J., Cook R.S., Sanders M.E., Aurisicchio L., Ciliberto G., Arteaga C.L, & Skala M.C. (2014). Quantitative optical imaging of primary tumor organoid metabolism predicts drug response in breast cancer. Cancer research, 74(18), 5184-5194.

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Ligands and Inhibitors for Cell Signaling

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Des[1–3]IGF-1 and recombinant human epidermal growth factor (EGF) were obtained from Cell Sciences (Canton, MA). alamarBlue, Dulbecco modified Eagle’s medium (DMEM)/F-12 media with HEPES, Roswell Park Memorial Institute (RPMI) 1640 media, and fetal bovine serum were obtained from Invitrogen (Carlsbad, CA). Hydrocortisone was purchased from Sigma–Aldrich (St. Louis, MO). OSI-906 and BMS754807 were obtained from Chemietek (Indianapolis, IN). Gefitinib, lapatinib, crizotinib, and cederanib were obtained from LC Laboratories (Woburn, MA). Dasatinib, BMS599626, NVP-BEZ235, PF-04691502, XL-147, MKK2206, GSK690693, temsirolimus, AT7867, foretinib, panobinostat, SAHA, diclofenac, serdemetan, and YM-155 were obtained from Selleck Chemicals (Houston, TX). PF-4708671 was obtained from Santa Cruz Biotechnology (Dallas, TX). PP242 was kindly provided by Dr. Michael Harding (University of Virginia, Charlottesville, VA). Anti-IGF-1Rβ, anti-AKT, anti-pAKT (S473), anti-pAKT (T308), anti-EGFR, and anti-pEGFR, were obtained from Cell Signaling Technology (Beverly, MA). Anti-pIGF-1R/pIR (Y1158/Y1162/Y1163) was obtained from Millipore (Bill-erica, MA).

Axelrod M.J., Mendez R.E., Khalil A., Leimgruber S.S., Sharlow E.R., Capaldo B., Conaway M., Gioeli D.G., Weber M.J, & Jameson M.J. (2015). Synergistic apoptosis in head and neck squamous cell carcinoma cells by co-inhibition of insulin-like growth factor-1 receptor signaling and compensatory signaling pathways. Head & neck, 37(12), 1722-1732.

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Investigating CDKL5 Overexpression and Combination Therapy in Glioblastoma

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Procedures related to animals were approved by the Ethical Committee of The First Affiliated Hospital of Dalian Medical University. The CDKL5 plasmid was constructed into the lentivirus vector LV‐3 (GenePharma). Stable cell lines with CDKL5 overexpression were selected with 4 μg·mL⁻¹ puromycin incubation for 7 days. Nude male BALB/c mice aged 4 weeks were subcutaneously injected with approximately the stable clones of U251 cells (4–6 × 10⁶ cells), transfected with CDKL5, in their flanks regardless of the presence of infection. Mice were treated intraperitoneally with 5 mg·kg⁻¹ cisplatin and 40 mg·kg⁻¹ XL147 (Selleckchem, Houston, TX, USA) two times per week for 30 days . Every group consisted of five mice, which were executed after 30 days, and the malignancies were cut off and weighed.

Jiang Z., Gong T, & Wei H. (2020). CDKL5 promotes proliferation, migration, and chemotherapeutic drug resistance of glioma cells via activation of the PI3K/AKT signaling pathway. FEBS Open Bio, 10(2), 268-277.

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Zebrafish Angiogenesis Assay Protocol

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Embryos were placed 5 per well in 48-well plates containing 400 µl of embryo medium/0.1% DMSO. Test compounds were added directly to the embryo medium. For intersegmental vessel (ISV) angiogenesis assay, embryos were treated from 6–24 hpf and from 2–5 dpf for hyaloid vessel (HV) angiogenesis assay [17] (link). Larvae were left to incubate with drugs at 28°C on a 14 h light/10 h dark cycle, euthanized and fixed with 4% paraformaldehyde (PFA) in PBS at room temperature for 2 hours before analysis. Drugs were purchased from the following: Rapamycin (Selleckchem S1039), NVP-BEZ235 (Selleckchem S1009), PI-103 (Selleckchem S1038), LY294002 (Sigma L9908), A66 (Selleckchem S2636), WYE125132 (Selleckchem S2661), Palomid 529 (Selleckchem S2238), XL147 (Selleckchem S1118) and XL765 (Selleckchem S1523). 2–5 dpf zebrafish larvae were euthanized in ice-cold PBS, or 4% PFA, or lysis buffer.

Sasore T, & Kennedy B. (2014). Deciphering Combinations of PI3K/AKT/mTOR Pathway Drugs Augmenting Anti-Angiogenic Efficacy In Vivo. PLoS ONE, 9(8), e105280.

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Evaluating Anti-Cancer Drug Responses in Cells

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RPMI-1640 medium, fetal bovin serum (FBS), penicillin and streptomycin were from Lonza (Lonza Milano SRL, Milan, Italy). Imatinib, Nilotinib, RAD001, GZD824, GSK690693, XL-147, MK-2206, ZSTK474, BGT226, KU0063794, CCI-779, AZD8055 and Torin-2 were provided by Selleck Chemicals (Houston, TX, USA). For cell viability determination, CellTiter 96(R) AQueous One Solution Assay (MTS) was purchased from Promega (Milan, Italy). Annexin V/7-AAD, Cell Cycle, Autophagy LC3 Activation detection kits were used for the analysis with the Muse™ Cell Analyzer from Merck-Millipore (Milan, Italy). All the antibodies were from Cell Signaling Technology (Danvers, MA, USA), including the rabbit secondary antibody. The mouse secondary antibody was from Sigma Aldrich (Milan, Italy). Signals were detected with the ECL Plus reagent purchased from Perkin Elmer (Boston, MA, USA).

Simioni C., Ultimo S., Martelli A.M., Zauli G., Milani D., McCubrey J.A., Capitani S, & Neri L.M. (2016). Synergistic effects of selective inhibitors targeting the PI3K/AKT/mTOR pathway or NUP214-ABL1 fusion protein in human Acute Lymphoblastic Leukemia. Oncotarget, 7(48), 79842-79853.

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