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Ly2603618

Manufactured by Selleck Chemicals
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LY2603618 is a laboratory product that serves as a tool for scientific research. It is a chemical compound that can be used in various experimental procedures. The core function of LY2603618 is to facilitate specific research activities, but a detailed description of its intended use would require further information that is not available at this time.

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Lab products found in correlation

Mk 8776, by Selleck Chemicals (5 mentions) Azd7762, by Selleck Chemicals (5 mentions) Ve 821, by Selleck Chemicals (3 mentions) Etoposide, by Merck Group (3 mentions) Hydroxyurea, by Merck Group (3 mentions) Roscovitine, by Selleck Chemicals (3 mentions) Azd6738, by MedKoo Biosciences (2 mentions) Ve 822, by MedKoo Biosciences (2 mentions) Plv ef1a rnaseh1 ires blast lentivirus, by Addgene (2 mentions) Carboplatin, by Merck Group (2 mentions) Cisplatin, by Merck Group (2 mentions) Oxaliplatin, by Merck Group (2 mentions) Bafilomycin a1, by Merck Group (2 mentions) Penicillin streptomycin, by Thermo Fisher Scientific (2 mentions) Fetal bovine serum (fbs), by Thermo Fisher Scientific (2 mentions) Bleomycin, by Selleck Chemicals (2 mentions) Ku55933, by Selleck Chemicals (2 mentions) 5 fluorouracil, by Merck Group (2 mentions) Ucn 01, by Merck Group (2 mentions) Pf 477736, by Selleck Chemicals (2 mentions)

Spelling variants of this product

Chk1 inhibitor LY2603618 (2 citations)

37 protocols using ly2603618

1

Cell Line-Based Anticancer Drug Evaluation

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AZD6738 and VE-822 were purchased from MedKoo Biosciences (Morrisville, NC, USA), MK-8776 and LY2603618 from Selleckchem (Munich, Germany), and MMC and 5-FU from Sigma-Aldrich (Hamburg, Germany). Oxaliplatin and carboplatin were kindly donated from the cytostatic drug department of the University Hospital Marburg. AZD6738, used in the xenograft in vivo assay, was purchased from AdooQ Bioscience (Irvine, CA, USA).
Job A., Tatura M., Schäfer C., Lutz V., Schneider H., Lankat-Buttgereit B., Zielinski A., Borgmann K., Bauer C., Gress T.M., Buchholz M, & Gallmeier E. (2020). The POLD1R689W variant increases the sensitivity of colorectal cancer cells to ATR and CHK1 inhibitors. Scientific Reports, 10, 18924.
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2

Evaluating ATR and CHK1 Inhibitors in EWS-FLI1 Knockdown

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350,000 cells were seeded in 6-well plates, 24 hours prior to drug treatment. Cells were treated with varying doses of ATR kinase inhibitor VE-821 (Selleckchem) or CHK1 inhibitor LY2603618 (Selleckchem) for 3 days at the end of which cells were counted to determine fractional cell survival. For dox-inducible EWS-FLI1 knockdown in A673 cells, shRNA was induced by treatment with 1μg/ml dox for 72 hours prior to ATR or CHK1 inhibitor treatment. For RNAseH1 experiments, A673 cells were infected with pLV-EF1a-RNAseH1-IRES-Blast lentivirus (derived from Addgene plasmid #85133) or empty vector and selected for stably infected cells.
Menon S., Breese M.R., Lin Y.P., Allegakoen H., Perati S., Heslin A., Horlbeck M.A., Weissman J., Sweet-Cordero E.A., Bivona T.G, & Tulpule A. (2023). FET fusion oncoproteins disrupt physiologic DNA repair networks and induce ATR synthetic lethality in cancer. Research Square.
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3

Generation and Characterization of Cell Lines

Cited 4 times
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Cell line origins and their cell growth media can be found in Supplementary Methods Table S1. mESC, FaDu and A549 ATM-knockout cell lines were generated as described before (37 (link),38 (link)). mESC Cdc25a KO clones #4/5 were kindly provided by Oscar Fernández-Capetillo (24 (link)) and U2-OS T-Rex GFP-RNase H1(D210N) (RNH1(D210N)-GFP) or GFP-RNase H1 (RNH1-GFP) cells by Pavel Janscak (39 (link)). mESCs were cultured on 0.1% gelatin-coated tissue culture flasks, and Cas9-expressing cell lines were maintained in blasticidin (10 μg/ml mESC and U2-OS, 5 μg/ml HAP-1). AZD6738 and AZD1775 were made by AstraZeneca. DRB (5,6-dichloro-1-beta-ribo-fuanosyl benzimidazole), actinomycin D, aphidicolin, hydroxyurea, carboplatin and etoposide were obtained from Sigma-Aldrich. XL413 (S7547), VE-822 (S27102), LY2603618 (S2626) and LY2606368 (S7178) were obtained from SelleckChem. CX-5461 (509265) was obtained from Merck Millipore, and BRD-6989 (6438) from Tocris. Final assay DMSO concentrations were normalised to 1:1000 as required. Recombinant human IFNγ was obtained from Peprotech (300–02) and used at a final concentration of 2.5 ng/ml.
Lloyd R.L., Urban V., Muñoz-Martínez F., Ayestaran I., Thomas J.C., de Renty C., O’Connor M.J., Forment J.V., Galanty Y, & Jackson S.P. (2021). Loss of Cyclin C or CDK8 provides ATR inhibitor resistance by suppressing transcription-associated replication stress. Nucleic Acids Research, 49(15), 8665-8683.
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4

Comprehensive Anticancer Compound Evaluation

Cited 1 time
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CB-839, mitomycin C, cryptotanshinone, altretamine, GSK583, liproxstatin-1, spautin-1, PD-1/PD-L1 inhibitor 2, RVX-208, selinexor, ferrostatin-1, diacerein, LY2603618, and patupilone were purchased from Selleckchem (Houston, TX). Cisplatin, carboplatin and oxaliplatin were purchased from Sigma-Aldrich (St. Louis, MO). Olaprib, niraparib, veliparib were purchased from Cayman Chemical (Ann Arbor, MI). As2O3 was purchased from BioTang (Lexington, MA). C1–27 is a GSTO1 inhibitor previously identified and synthesized by our laboratory (5 (link)).
Xu Y., Bankhead A I.I.I., Tian X., Tang J., Ljungman M, & Neamati N. (2020). Deletion of Glutathione S-Transferase Omega 1 Activates Type I Interferon Genes and Downregulates Tissue Factor. Cancer research, 80(17), 3692-3705.
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5

Multimodal Senescence Assessment Protocol

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ATM inhibitor KU-55933 (#SML1109), Hoechst 33258 (#14530), E64d (#516485), bafilomycin A1 (#B1793), 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazoliumbromide, MTT (#M2128), blasticidine (#3513-03-9), Fluoromount (#F4680), puromycin (#58-58-2), Quinoline-Val-Asp-Difluorophenoxymethyl Ketone, QVD-OPH (# SML0063) and doxycycline (Dox) (#D9891) were purchased from Sigma-Aldrich. Pepstatin A methyl ester (#516485) and epoxomycin (# 134381-21-8) were obtained from Calbiochem. Tetramethyl rhodamine methyl ester perchlorate dye (#T-668) and carboxyfluorescein succinimidyl ester (CFSE) (#C34554) were purchased from Molecular Probes. LY2603618 (#S2626) was purchased from Selleckchem. 20A was synthesized as previously described (compound #3 in (20 (link))). Sentragor (#AR8850020) for antibody-enhanced detection of senescence cells was provided by Arriani Pharmaceuticals.
Beauvarlet J., Bensadoun P., Darbo E., Labrunie G., Rousseau B., Richard E., Draskovic I., Londono-Vallejo A., Dupuy J.W., Nath Das R., Guédin A., Robert G., Orange F., Croce S., Valesco V., Soubeyran P., Ryan K.M., Mergny J.L, & Djavaheri-Mergny M. (2019). Modulation of the ATM/autophagy pathway by a G-quadruplex ligand tips the balance between senescence and apoptosis in cancer cells. Nucleic Acids Research, 47(6), 2739-2756.
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6

Cell Culture and Inhibitor Treatments

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Human NCI-H460 and A549 lung cancer (ATCC) and U2OS osteosarcoma cells were cultured in DMEM (Dulbecco's modified Eagle’s) medium, and SW900 lung cancer and Reh pre-B cell leukemia cells in RPMI (Roswell Park Memorial Institute) medium (both media from Life Technologies), at 37°C in a humidified atmosphere with 5% CO2. The media were supplemented with 10% fetal bovine serum (origin South America, Life Technologies) and 1% Penicillin/Streptomycin (Life Technologies). All cell lines (except Reh) were verified by STR (short tandem repeat) technology as described previously [43 (link)]. The Wee1 inhibitor MK1775 (AZD1775) was from Merck Calbiochem. The Chk1 inhibitors AZD7762, LY2603618 and MK8776 were from Selleck Chemicals, UCN01 was a gift from R.J. Schultz, National Cancer Institute, and the Chk2 inhibitor PV1019 was from Millipore. The dual CDK1/CDK2 inhibitor Roscovitine and the CDK2 inhibitor CVT-313 were from Cell Signaling, and the CDK1 inhibitor RO-3306 from Merck Calbiochem.
Hauge S., Naucke C., Hasvold G., Joel M., Rødland G.E., Juzenas P., Stokke T, & Syljuåsen R.G. (2016). Combined inhibition of Wee1 and Chk1 gives synergistic DNA damage in S-phase due to distinct regulation of CDK activity and CDC45 loading. Oncotarget, 8(7), 10966-10979.
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7

Senescence Induction and Drug Interactions

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Doxorubicin (Sigma-Aldrich, D1515) was used to induce senescence at 50 nM (20 nM for H460). Etoposide (Sigma-Aldrich, E1383) was used at 500 nM (125 nM for H460). Camptothecin (Cayman Chemical, 11694) was used at 30 nM (for A549) and 20 nM (for HCT116 and H460). Bleomycin (Selleck Chemicals, S1214) was used at 5 uM (for A549 and H460) and 100 nM (for HCT116). Nutlin-3a (Sigma-Aldrich, SML0580) was used at 10 μM as pretreatment or at indicated concentrations as co-treatment. KU-55933 (Selleck Chemicals, S1092) was used at 10 uM. LY2603618 (Selleck Chemicals, S2626) was used at 5 uM. Bortezomib (Selleck Chemicals, S1013) was used at 40 nM.
Hsu C.H., Altschuler S.J, & Wu L.F. (2019). Patterns of early p21 dynamics determine proliferation-senescence cell fate after chemotherapy. Cell, 178(2), 361-373.e12.
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8

Preparation of Anticancer Drug Stocks

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Solid stocks were purchased from the indicated suppliers and prepared as concentrated stock solutions in the appropriate solvent: gemcitabine (Apin Chemicals Inc), 20 mM in H2O; camptothecin (LC Laboratories), 5 mM in DMSO; cisplatin (David Bull Laboratories), 3.33 mM in 1% NaCl in H2O; oxaliplatin (Tocris), 5 mM in H2O; etoposide (Selleckchem), 20 mM in DMSO; doxorubicin (Selleckchem), 5 mM in DMSO; 5-fluorouracil (Sigma), 50 mM in DMSO; LY2603618 (Selleckchem), 20 mM in DMSO and MK-8776 (ChemieTek), 20 mM in DMSO.
Rawlinson R, & Massey A.J. (2014). γH2AX and Chk1 phosphorylation as predictive pharmacodynamic biomarkers of Chk1 inhibitor-chemotherapy combination treatments. BMC Cancer, 14, 483.
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9

Chk1 Inhibitor Sensitivity Assay

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TH-302 was from Syngene, AZD7762 and LY2603618 were from Selleck Chemicals, and PF477736 was from Tocris Bioscience. RIPA was from Sigma. Protease inhibitor cocktails were from Thermo Scientific. ChemiGlow substrate was from Proteinsimple. ECL reagent, Rad51 mAb, actin mAb, goat anti-rabbit HRP, goat anti-mouse HRP, and cell cycle reagents were from EMD Millipore. γH2AX mAb was from Epitomics. Antibodies against phospho-Histone H3, phospho-Cdc2 Y15 antibody, total Chk1, phospho-Chk1 (S296) were from Cell Signaling. Total Cdc2 p34 antibody was from Santa Cruz Biotechnology. FITC-conjugated goat anti-mouse secondary antibody and AlamarBlue cell viability reagent were from Life Technologies. Comet assay kit was from Trevigen. Caspase Glo 3/7 assay system was from Promega. Isogenic p53 proficient and deficient cell line pairs were from Horizon Discovery. All other cell lines were from ATCC.
Meng F., Bhupathi D., Sun J.D., Liu Q., Ahluwalia D., Wang Y., Matteucci M.D, & Hart C.P. (2015). Enhancement of hypoxia-activated prodrug TH-302 anti-tumor activity by Chk1 inhibition. BMC Cancer, 15, 422.
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10

Neonatal Mouse Ovary Culture with CHK1 Inhibitor

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Neonatal mouse ovaries were harvested and cultured, as previously reported [51 (link)]. Briefly, ovaries were placed in prewarmed dissection media (Leibowitz L15 [Sigma-Aldrich] with 3mg/mL of BSA) and, under the stereomicroscope, they were trimmed with forceps, eliminating the remains of the bursal sac, the oviduct, and the uterus. Ovaries were transferred to UV- sterilized polycarbonate membrane (Whatman) sitting on a 24-well plate containing prewarmed culture media (α-Minimum Essential Medium (Thermofisher) with 3mg/mL of BSA). The samples were treated with 1 μM or 5 μM of the CHK1 inhibitor LY2603618 (Selleckchem), dissolved in DMSO. Control samples were treated with equivalent volumes of DMSO. All ovaries were cultured in an incubator at 37°C supplied with 5% CO2 for five days. After this time, ovaries were processed as previously mentioned to obtain ovarian sections.
Martínez-Marchal A., Huang Y., Guillot-Ferriols M.T., Ferrer-Roda M., Guixé A., Garcia-Caldés M, & Roig I. (2020). The DNA damage response is required for oocyte cyst breakdown and follicle formation in mice. PLoS Genetics, 16(11), e1009067.
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