Abt 737

Manufactured by Abbvie

Sourced in United States, Israel

ABT-737 is a small-molecule inhibitor of the Bcl-2 family of anti-apoptotic proteins. It is used in research settings to study the role of Bcl-2 proteins in cellular processes.

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Lab products found in correlation

Abt 199, by Abbvie (6 mentions) Bortezomib, by LC Laboratories (2 mentions) Abt 263, by Abbvie (2 mentions) Zvad fmk, by Avantor (2 mentions) Fluoro carbonyl cyanide phenylhydrazone (fccp), by Merck Group (2 mentions) Hoechst 33342, by AnaSpec (2 mentions) Antimycin a, by Merck Group (2 mentions) Staurosporine, by Merck Group (2 mentions) Bcl xl, by Cell Signaling Technology (2 mentions) A 1331852, by Abbvie (2 mentions) A 1210477, by Abbvie (2 mentions) Z vad fmk, by R&D Systems (1 mentions) Caspase glo 3 7, by Promega (1 mentions) Facscailbur, by BD (1 mentions) Mrt67307, by Merck Group (1 mentions) Wehi 539, by MedChemExpress (1 mentions) Dexamethasone (dex), by Merck Group (1 mentions) Propidium iodide, by Merck Group (1 mentions) Celltiter glo, by Promega (1 mentions) Polyethylene glycol 400, by Dow (1 mentions)

13 protocols using abt 737

Quantifying Cell Death Pathways

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Cell death was induced by exposure to ABT-737 (AbbVie), Dexamethasone (Sigma), WEHI-539 (MedChemExpress), or Etoposide (Hospira). Where indicated, cells were preincubated for 1 hr with MRT-67307 (Sigma) and for 15–30 min with ABT-737, followed by continuous exposure to Q-VD-Oph (SM Biochemicals) or zVAD.fmk (R&D Systems). Cell viability was quantified by CellTiterGlo (Promega) or flow cytometric analysis of cells excluding 5 µg/ml propidium iodide (PI) (Sigma) and, where indicated, cells also negative for AnnexinV-FITC (InvivoGen) binding using a FACSCailbur (BD) or LSRII (BD). Caspase activity was assayed by the addition of caspase3/7Glo (Promega) or by immunoblotting as described in the Extended Experimental Procedures.

White M.J., McArthur K., Metcalf D., Lane R.M., Cambier J.C., Herold M.J., van Delft M.F., Bedoui S., Lessene G., Ritchie M.E., Huang D.C, & Kile B.T. (2014). Apoptotic Caspases Suppress mtDNA-Induced STING-Mediated Type I IFN Production. Cell, 159(7), 1549-1562.

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Cell Culture and Reagent Preparation

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BCWM.1, MWCL-1 and RPCI-WM1 cells were maintained in RPMI 1640 supplemented with 10% fetal bovine serum, 2 mM L-glutamine, 100 I.U. penicillin/streptomycin, 1 mM sodium pyruvate and non-essential amino acids. Bortezomib was purchased from LC Laboratories (Woburn, MA). ATO was purchased from Sigma Aldrich (St. Louis, MO). ABT-737 and ABT-199 were generous gifts of Abbvie (North Chicago, IL).

Gaudette B.T., Dwivedi B., Chitta K.S., Poulain S., Powell D., Vertino P., Leleu X., Lonial S., Chanan-Khan A.A., Kowalski J, & Boise L.H. (2015). Low expression of pro-apoptotic Bcl-2 family proteins sets the apoptotic threshold in Waldenström Macroglobulinemia. Oncogene, 35(4), 479-490.

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In vivo Xenograft Treatment Protocol

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For in vivo studies, T-DM1 (Genentech) was administered i.p. at 10 mg/kg once per week. ABT-737 (AbbVie) was administered i.p. at 70 mg/kg once per day. ABT-263 (AbbVie) was administered p.o. at 70 mg/kg once per day. T-DM1 was prepared according to Genentech recommendations in sterile water for injection (Gibco). ABT-737 and ABT-263 were prepared according to AbbVie recommendations. ABT-737 in 30% propylene glycol (Sigma) plus 0.5% Tween 80 (Sigma) and 65% D5W (5% dextrose in water, Sigma) pH 3–4 and ABT-263 in 60% PHOSAL 50 PG (Lipoid) plus 30% polyethylene glycol 400 (Dow Chemical) and 10% ethanol. Matched control animals received vehicle alone in the same manner as drug-treated counterparts. All animals were randomized into groups and weighed before treatment. Individual weights were used for dose calculations. Weights were re-measured at the 14-day experimental end point. Weight reductions >20% prevented continuous treatments beyond 14 days.

Zoeller J.J., Vagodny A., Taneja K., Tan B.Y., O’Brien N., Slamon D.J., Sampath D., Leverson J.D., Bronson R.T., Dillon D.A, & Brugge J.S. (2019). Neutralization of BCL-2/XL enhances the cytotoxicity of T-DM1 in vivo. Molecular cancer therapeutics, 18(6), 1115-1126.

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Kinase Inhibitor and Chemotherapeutic Protocols

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Kinase inhibitors were purchased from SYN kinase (Melbourne, Australia) and were used at 1 μM, unless otherwise specified, with dilutions performed in assay buffer containing 0.1% DMSO. Chemotherapeutics, diluted in PBS immediately prior to treatment, were obtained from the following suppliers: ABT-737 (AbbVie); Bortezomib (Janssen); Carboplatin, Doxorubicin, Etoposide, Vincristine (DBL); Docetaxel (Aventis); Gemcitabine (Ebewe, InterPharma); and, 7-ethyl-10-hydroxycamptothecin (SN-38) (LKT Laboratories).

McArthur K., D’Cruz A.A., Segal D., Lackovic K., Wilks A.F., O’Donnell J.A., Nowell C.J., Gerlic M., Huang D.C., Burns C.J, & Croker B.A. (2017). Defining a therapeutic window for kinase inhibitors in leukemia to avoid neutropenia. Oncotarget, 8(35), 57948-57963.

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Cytotoxic Effects of ABT-737 and Ruxolitinib

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HEL cells were incubated with different concentrations of ABT‐737 (AbbVie, Chicago, IL, USA) and ruxolitinib (Novartis, Basel, Switzerland) for 24 hrs (stock solutions in 10 mmol\L in Dimethyl sulfoxide (DMSO)). Leucocytes isolated from MPN patients were incubated with 2.5 µmol\L of ABT‐737 and 5 µmol\L of ruxolitinib in Iscove's Modified Dulbecco's Media (IMDM) (EuroClone, Milan, Italy) supplemented with 20% inactivated FBS for 24 hrs. The concentrations of ABT‐737 and ruxolitinib used to treat cells were chosen based on the results of the proliferation experiments (IC50) and the literature. After incubation, total RNA and proteins were extracted and proliferation and apoptosis were evaluated.

Petiti J., Lo Iacono M., Rosso V., Andreani G., Jovanovski A., Podestà M., Lame D., Gobbi M.D., Fava C., Saglio G., Frassoni F, & Cilloni D. (2020). Bcl‐xL represents a therapeutic target in Philadelphia negative myeloproliferative neoplasms. Journal of Cellular and Molecular Medicine, 24(18), 10978-10986.

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Comprehensive Cell Culture Reagents and Antibodies

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All cell culture reagents were from Invitrogen; and standard laboratory reagents were from Sigma-Aldrich or Fisher Scientific. Drugs were from: ABT737 (Abbvie); Antimycin A, Etoposide, FCCP, Nutlin-3a, Staurosporine (Sigma-Aldrich); zVAD-fmk (VWR Scientific); MitoQ (MedKoo Biosciences). Antibodies (clone or source): β-Actin (C4), BCL-2 (100), CH11 (Millipore), BAK (G-23), BAX (N20), BCL-xS/BCL-xL (S-18), MDM2 (SMP14), p53 (DO-1), BCL-2 (100), BIM (22-40), p21 (C-19), pH2A.X (JBW301), SOD-1 (FL-154), Cyclin D1, Chk1 (FL476), Chk1Ser317, Chk1Ser345 (133D3), GST (Z-5), ND1 (C-18), NDUFS1 (E-8), VDAC (FL-283), Cytochrome c (7H8). CellROX® and MitoSOX^™ were from Thermo Fisher Scientific, and Hoechst 33342 was from Anaspec.

Elkholi R., Abraham-Enachescu I., Trotta A.P., Rubio-Patiño C., Mohammed J.N., Luna-Vargas M.P., Gelles J.D., Kaminetsky J.R., Serasinghe M.N., Zou C., Ali S., McStay G.P., Pfleger C.M, & Chipuk J.E. (2019). MDM2 integrates cellular respiration and apoptotic signaling through NDUFS1 and the mitochondrial network.. Molecular cell, 74(3), 452-465.e7.

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Apoptosis Regulators Characterization

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Imatinib, nilotinib and dasatinib were from Selleck Chemicals (Houston, TX, USA). ABT-737, ABT-199, A-1331852 and A-1210477 were kindly provided by AbbVie (North Chicago, IL, USA). Antibodies against BIM, PUMA, BMF, BIK, BAD, BCL-X_L and BCL-w were from Cell Signaling Technology (Danvers, MA, USA), GAPDH and MCL-1 from Santa Cruz Biotechnology (Santa Cruz, CA, USA), NOXA from Calbiochem (Darmstadt, Germany), BCL-2 from Dako (Ely, UK), BAX and BAK from Millipore (Watford, UK), HRK from Aviva Systems Biology (San Diego, CA, USA) and BID and BFL-1 were from Prof J Borst (The Netherlands Cancer Institute, Amsterdam, The Netherlands). All other reagents, unless mentioned otherwise, were from Sigma-Aldrich (St Louis, MO, USA).

Lucas C.M., Milani M., Butterworth M., Carmell N., Scott L.J., Clark R.E., Cohen G.M, & Varadarajan S. (2016). High CIP2A levels correlate with an antiapoptotic phenotype that can be overcome by targeting BCL-XL in chronic myeloid leukemia. Leukemia, 30(6), 1273-1281.

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Evaluating Cell Death Pathways

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All cell culture reagents were from Invitrogen; and standard laboratory reagents were from Sigma-Aldrich or Fisher Scientific. Drugs were from: PLX4032, GSK1120212, A1210477 (Selleck); ABT737 (Abbvie); FCCP, Antimycin A, Staurosporine (Sigma-Aldrich), zVAD-fmk (VWR Scientific). Antibodies (clone or source): ERK^Total & ERK^℗ (Cell Signaling); Actin (C4), BCL-2 (100), MCL-1 (Rockland), BAK (NT), BAX (N20), BCL-xL (S18). MitoTracker Green and TMRE were from Invitrogen, and Hoechst 33342 was from Anaspec.

Serasinghe M.N., Gelles J.D., Li K., Zhao L., Abbate F., Syku M., Mohammed J.N., Badal B., Rangel C.A., Hoehn K.L., Celebi J.T, & Chipuk J.E. (2018). Dual suppression of inner and outer mitochondrial membrane functions augments apoptotic responses to oncogenic MAPK inhibition. Cell Death & Disease, 9(2), 29.

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Anticancer Compounds from Diverse Sources

Cited 5 times

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ABT-737, ABT-263, ABT-199, A-1331852 and A-1210477 were kindly provided by AbbVie Inc. (North Chicago, IL, USA). Compounds 10, 20, 21, 22, 36, 37 and 41 were provided by Dr. Z Nikolovska-Coleska (University of Michigan, Ann Arbor, MI, USA).^{8 (link)} Compound 9 was custom-synthesised and purchased from Molport (Riga, Latvia).^{6 (link)} MIM-1 and the stapled peptides against MCL-1 and NOXA were kindly provided by Dr. L Walensky (Dana-Farber Cancer Institute, Boston, MA, USA).^{7 (link), 16 (link)} Maritoclax was provided by Professor H-G Wang (Pennsylvania State University College of Medicine, Hershey, PA, USA).^{10 (link)} Apogossypol, Sabutoclax and BI112D1 were provided by Professor M. Pellecchia (Sanford-Burnham Institute, La Jolla, CA, USA).^{11 (link), 12 (link)} Gossypol, Obatoclax and TW-37 were obtained from Selleck Chemicals Co. (Houston, TX, USA).

Milani M., Byrne D.P., Greaves G., Butterworth M., Cohen G.M., Eyers P.A, & Varadarajan S. (2017). DRP-1 is required for BH3 mimetic-mediated mitochondrial fragmentation and apoptosis. Cell Death & Disease, 8(1), e2552-.

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Cell Culture and Reagent Preparation

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