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ABT-737

ABT-737 is a small-molecule inhibitor of the apoptosis regulator proteins Bcl-2, Bcl-xL, and Bcl-w.
It has demonstrated potent anti-tumor activity in preclinical studies and is being investigated as a potential therapeutic agent for various types of cancer.
ABT-737 induces apoptosis by binding to and neutralizing the anti-apoptotic functions of Bcl-2 family proteins, thereby sensitizing cancer cells to apoptotic stimuli.
Reseachers can leverag PubCompare.ai's AI-driven platform to optimizie their ABT-737 research, easily locating relevant protocols from literature, pre-prints, and patents, while using AI-driven comparisons to identify the best protocols and products.
This can help achieve reproduciblle, accurate findings for ABT-737 studies with PubCompare.ai's intuitive tools.

Most cited protocols related to «ABT-737»

Apoptosis Induction in Cell Lines

Cited 18 times

HCT116 cells were purchased from ATCC (Manassas, VA) and AAV-293 cells from Stratagene (Cedar Creek, TX). Bax^−/− HCT116 cells were provided by Bert Vogelstein (Zhang et al 2000 (link)). WT, Bax^−/−, Bak^−/− and Bax^−/−Bak^−/− DKO MEF cells were provided by Stanley Korsmeyer (Wei et al 2001 ). Cells were cultured as described (Cleland et al 2011 (link)). 5-FU (fluorouracil), camptothecin, sulindac sulfate, cisplatin, TRAIL, indomethacin and staurosporine were purchased from Sigma (St. Louis, MO) and dissolved in DMSO for stock preparation. ABT-737 was purchased from Selleck Chemicals LLC (Houston, Texas).

Wang C, & Youle R.J. (2011). Predominant requirement of Bax for apoptosis in HCT116 cells is determined by Mcl-1’s inhibitory effect on Bak. Oncogene, 31(26), 3177-3189.

Publication 2011

ABT-737 Camptothecin Cells Cisplatin Fluorouracil HCT116 Cells Indomethacin Staurosporine Sulfates, Inorganic Sulfoxide, Dimethyl Sulindac TNFSF10 protein, human

Phosphorylation and Degradation of Mcl-1 in T-ALL

Cited 13 times

Expression plasmid constructs, proteins, antibodies and cell lines are described in the Methods. The sequences of various siRNA oligos used in this study are also listed in the Methods section. Mcl-1 in vivo phosphorylation was detected by mass spectrometry analysis, and the identified major GSK3 phosphorylation sites were examined by in vitro kinase assays. All mutants were generated using PCR and the sequences were verified. Fbw7-mediated Mcl-1 destruction and ubiquitination were examined by cell-based ubiquitination and degradation assays. Cell viability assays were used to detect the response of various T-ALL cell lines to sorafenib and ABT-737. Annexin V/7-AAD double staining was used to detect the percentage of cellular apoptosis. A detailed description of the experimental procedures is provided in the Methods section.

Inuzuka H., Shaik S., Onoyama I., Gao D., Tseng A., Maser R.S., Zhai B., Wan L., Gutierrez A., Lau A.W., Xiao Y., Christie A.L., Aster J., Settleman J., Gygi S.P., Kung A.L., Look T., Nakayama K.I., DePinho R.A, & Wei W. (2011). SCFFbw7 Regulates Cellular Apoptosis By Targeting Mcl-1 for Ubiquitination and Destruction. Nature, 471(7336), 104-109.

Publication 2010

2',5'-oligoadenylate ABT-737 Annexin A5 Antibodies Apoptosis Biological Assay Cell Lines Cell Survival Glycogen Synthase Kinase 3 Mass Spectrometry Phosphorylation Phosphotransferases Plasmids Proteins RNA, Small Interfering Sorafenib Ubiquitination

Isolation and Culture of Primary Rat Hippocampal Neurons

Cited 5 times

Primary rat hippocampal neurons were prepared from rat feti (Sprague-Dawley, day 18 of gestation; Harlan, Indianapolis, IN, USA) as described previously^{13 (link), 52 (link), 53 (link)} with modifications specific for this study. After isolation of hippocampi from prenatal brains, neurons were dissociated and seeded (0.2 × 10⁶ cells/35 mm plate) onto plates containing medium with 5% FBS. After 2 h incubation, cells were maintained in neurobasal medium supplemented with B-27, glutamine and antibiotics (Invitrogen GIBCO Life Technologies, Carlsbad, CA, USA). Neurons were grown at 37 °C in 5% CO₂ and 20% O₂ in a humidified incubator, and assayed at DIV 20-22. Glutamate treatment: 20 μM Glutamate (Sigma-Aldrich, St. Louis, MO, USA) was freshly made in sterile PBS as an aqueous solution then added to the cell culture medium as described in relevant figure legends. Bcl-xL inhibitor treatment: a stock solution of ABT-737 (Selleckbio, Houston, TX, USA), or WEHI-539 (Apex Bio, Houston, TX, USA) were prepared in dimethyl sulfoxide (DMSO). ABT-737 (1 μM or 10 nM), WEHI-539 (5 μM or 10 nM) or the same volume of DMSO was added into the culture dishes 20 min prior to Glutamate treatment. Neurons were transfected at days in vitro (DIV) 7 using lipofectamin LTX with Plus Reagent (Invitrogen).

Park H.A., Licznerski P., Mnatsakanyan N., Niu Y., Sacchetti S., Wu J., Polster B.M., Alavian K.N, & Jonas E.A. (2017). Inhibition of Bcl-xL prevents pro-death actions of ΔN-Bcl-xL at the mitochondrial inner membrane during glutamate excitotoxicity. Cell Death and Differentiation, 24(11), 1963-1974.

Publication 2017

ABT-737 Antibiotics, Antitubercular Brain Cell Culture Techniques Cells Culture Media Fetus Glutamate Glutamine Hyperostosis, Diffuse Idiopathic Skeletal isolation Neurons Pregnancy Seahorses Sterility, Reproductive Sulfoxide, Dimethyl

Characterization of CRC cell lines

Cited 5 times

The human CRC cell lines (Table S1), including HCT116, RKO, DLD1, LoVo, Lim1215, Lim2405, SW480, SNU-C2B, LS411N, SW48, SW1463, SW837 and HCT-8 were obtained from the American Type Culture Collection (Manassas, VA). CCK-81, DiFi and NCI-H508 cells were obtained from Dr. Alberto Bardelli at University of Torino in Italy. Isogenic p53-KO, FBW7-KO, KRAS-KO (WT or G13D mutant allele), PIK3CA-KO (WT or H1047R or E545K mutant allele) HCT116 or DLD1 cell lines, as well as BRAF-KO (WT or V600E mutant allele) RKO and VACO432 cells, were obtained either from Dr. Bert Vogelstein at Johns Hopkins, or from Horizon Discovery (Cambridge, UK). The cell lines were last tested and authenticated for genotypes, drug response, morphology, and absence of mycoplasma in Feb, 2016. Loss of expression of targeted proteins was confirmed by western blotting and Mycoplasma testing was performed routinely by PCR. Regorafenib-resistant cell lines were generated by exposing regorafenib-sensitive HCT116, DLD1, RKO, SW480, Lim1215 and Lim2405 cells to 40 µM regorafenib for 3 days, followed by recovery for 5 days, and then repeated treatment/recovery for a total of 4 cycles.
All cell lines were maintained at 37°C in 5% CO₂ and cultured in McCoy's 5A modified media (Invitrogen) supplemented with 10% defined FBS (HyClone), 100 units/ml penicillin, and 100 μg/ml streptomycin (Invitrogen). For drug treatment, cells were plated in 12-well plates at 20% to 30% density 24 hr before treatment. The DMSO (Sigma) stocks of agents used, including regorafenib, sorafenib, TW-37, ABT-737, UCN-01, YM-155, roscovitine, sunitinib, crizotinib, VX680, etoposide, temsirolimus, and sulindac (Selleck Chemicals), were diluted to appropriate concentrations with the cell culture medium. TRAIL (XcessBio, San Diego, CA) was diluted with distilled water.

Tong J., Tan S., Zou F., Yu J, & Zhang L. (2016). FBW7 mutations mediate resistance of colorectal cancer to targeted therapies by blocking Mcl-1 degradation. Oncogene, 36(6), 787-796.

Publication 2016

ABT-737 Alleles BRAF protein, human Cell Culture Techniques Cell Lines Cells Crizotinib Culture Media Etoposide Genotype Homo sapiens K-ras Genes Mycoplasma Penicillins Pharmaceutical Preparations PIK3CA protein, human regorafenib Roscovitine Sorafenib Streptomycin Sulfoxide, Dimethyl Sulindac Sunitinib temsirolimus TNFSF10 protein, human UCN 01 VX680 YM-155

Mcl1-deficient MEFs Reveal cGAS Binding

Cited 5 times

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Publication 2014

ABT-737 Chromogranin A Immunoprecipitation Internal Ribosome Entry Sites MCL1 protein, human Mus Oligonucleotides Plasmids Proteins quinoline-val-asp(OMe)-CH2-OPH

Most recents protocols related to «ABT-737»

Multi-Modality Apoptosis Assay Protocol

Alisertib (MLN8237) (catalog no.: S1133), danusertib (PHA-739358) (catalog no.: S1107), doxorubicin (adriamycin) HCl (catalog no.: S1208), and bortezomib (PS-341) (catalog no.: S1013) were purchased from SelleckChem and dissolved in dimethyl sulfoxide (DMSO). ABT-737 (catalog no.: 852808-04-9) and S63845 (catalog no.: 1799633-27-4) were purchased from ChemieTek and dissolved in DMSO. Camptothecin (catalog no.: 159732) and z-VAD-FMK (catalog no.: 03FK1090-CF) were purchased from MP Biomedicals and dissolved in DMSO. Human recombinant TRAIL was generated as previously described (51 (link)). 1,6-Bismaleimidohexane was purchased from Thermo Fisher Scientific (catalog no.: 22330). Annexin V-FITC was purchased from BioLegend (catalog no.: 640906). Propidium iodide (PI) solution was purchased from G-Biosciences (catalog no.: 786-1272).
Antibodies used for immunoblotting include anti-β-actin (Sigma–Aldrich; catalog no.: A5441), anti–caspase-3 (Santa Cruz Biotechnology; catalog no.: sc-56053), anti-GFP (Santa Cruz Biotechnology; catalog no.: sc-9996), anti-MCL-1 (Santa Cruz Biotechnology; catalog no.: sc-819), anti-BCL-2 (Cell Signaling Technology; catalog no.: 15071), anti-Bcl-xL (Cell Signaling Technology; catalog no.: 2762), anti-BCL-w (Cell Signaling Technology; catalog no.: 2724), anti-Bax (Cell Signaling Technology; catalog no.: 2772), anti-Bak (Cell Signaling Technology: catalog no.: 5023), anti-PUMA (Cell Signaling Technology; catalog no.: 12450), anti-Bid (36 (link)), anti-Bim-EL (Cell Signaling Technology; catalog no.: 2819), anti-BAD (Santa Cruz Biotechnology; catalog no.: sc-3044), anti-Noxa (Santa Cruz Biotechnology; catalog no.: sc-515840), anti-BIK (Cell Signaling Technology; catalog no.: 4592), anti–caspase-2 (Cell Signaling Technology; catalog no.: 2224), anti–caspase-8 (Cell Signaling Technology; catalog no.: 9746S), anti-p53 (Santa Cruz Biotechnology; catalog no.: sc-393), and anti-GFP (Santa Cruz Biotechnology; catalog no.: sc-459).
Secondary antibodies include anti-rabbit (Sigma–Aldrich; catalog no.: A6154) and antimouse (Jackson ImmunoResearch, Inc; catalog no.: 715-035-150).

Li J., Chen C.H., O’Neill K.L., Fousek-Schuller V.J., Black A.R., Black J.D., Zhang J, & Luo X. (2023). Combined inhibition of aurora kinases and Bcl-xL induces apoptosis through select BH3-only proteins. The Journal of Biological Chemistry, 299(2), 102875.

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Publication 2023

ABT-737 Actins Adriamycin alisertib Antibodies BCL2 protein, human benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone Bortezomib Camptothecin CASP2 protein, human Caspase-8 Caspase 3 danusertib Doxorubicin FITC-annexin A5 Homo sapiens MLN 8237 PHA 739358 Propidium Iodide PS 341 Puma Rabbits S63845 Sulfoxide, Dimethyl TNFSF10 protein, human

Apoptosis Assay with Annexin V and PI

Cells were seeded into 48‐well plates in phenol‐free RPMI 1640 medium supplemented with 10% foetal calf serum (FCS) at a density of 6 × 10⁴ cells per well. Cells were allowed to equilibrate under humidified 10% CO₂ at 37°C for 1 h before the medium was supplemented with 1:500 dilution of AlexaFluor488‐conjugated Annexin V (ThermoFisher Scientific) and 0.5 μg/ml propidium iodide (PI) (Sigma). Cells were treated with combinations of the following agonists/antagonists: 100 ng/ml recombinant human TNF (produced in‐house¹⁸), 500 nM Smac‐mimetic/compound A (Tetralogic Pharmaceuticals¹⁹), 5 μM IDN‐6556 (Idun Pharmaceuticals), 100 μg/ml cycloheximide (Sigma), 1 μM ABT‐737 (Abbott) and 0.1 μM Mcl‐1 inhibitor (also known as S63485; SYNthesis MedChem). Cells were transferred to an IncuCyte S3 System (Essen Bioscience) and imaged over time using the 10× objective and the default bright‐field, green and red channel settings. The number of Annexin V/PI‐positive cells per mm² over time was quantified using IncuCyte S3 v2018A software (Essen Bioscience).

Martin K.R., Day J.A., Hansen J.A., D'Silva D.B., Wong H.L., Garnham A., Sandow J.J., Nijagal B., Wilson N, & Wicks I.P. (2023). CD98 defines a metabolically flexible, proinflammatory subset of low‐density neutrophils in systemic lupus erythematosus. Clinical and Translational Medicine, 13(1), e1150.

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Publication 2023

ABT-737 agonists Anabolism Annexin A5 antagonists Cells Cycloheximide Etanercept Fetal Bovine Serum IDN 6556 Pharmaceutical Preparations Phenol Propidium Iodide Technique, Dilution

Kinetics and Modes of Macrophage Cell Death

To assess the kinetics and modes of cell death induced in LPS‐primed BMDMs in response to BH3‐mimetics, 5 × 10⁴ macrophages were seeded into wells of a 96‐well Thermo Scientific™ Nunc™ Edge 2.0 plate. After an overnight incubation to allow cell adhesion, culture medium was replaced with fresh DMEM (supplemented with 20% LCCM, 4 mM L‐glutamine, 1 mM sodium pyruvate, and 100 U/ml penicillin/streptomycin) containing PI (200 ng/ml), SPY505‐DNA (1×, Spirochrome) and, where indicated, LPS (50 ng/ml). After 2.5 h cells were pre‐treated, as indicated, with Q‐VD‐OPh (40 μM, In Vitro Technologies), MCC950 (5 μM, CP‐456773 sodium salt, PZ0280), and/or GSK'872 (5 μM, MedChemExpress), rat anti‐mouse TNF (XT‐22 20 μg/ml) or rat anti‐mouse IgG1 (GL113 Isotype control) monoclonal antibodies for 30 min prior to treatment with ABT‐737 (500 nM) and S63845 (10 μM). To assess the kinetics of NOMV‐induced monocyte cell death, sorted Ly6C^hi monocytes were labelled with 100 nM Cell Tracker Green (CTG) (Invitrogen) for 10 min at 37°C in serum‐free DMEM. Cells were then washed and seeded at 0.5–1 × 10⁵ cells/well in 96‐well flat bottom tissue culture‐treated plates (Greiner). Monocyte cultures were pre‐treated, as indicated, for 15–30 min with Q‐VD‐OPh (40 μM), MCC950 (5 μM), and GSK'872 (1 μM), prior to treatment with 50 μg/ml of NOMVs. Monocytes were then exposed to 200 ng/ml PI and imaged every 30 min on an IncuCyte® S3 or SX5 Live‐Cell Analysis System (Sartorius) at 10× magnification for up to 14 h. BMDM and monocyte images were analysed, and the % of dead cells was calculated by dividing the number of PI‐positive cells by the total cell number (based on CTG⁺ or SPY505‐DNA⁺ cells), as quantified by the IncuCyte® Analysis Software.

Speir M., Tye H., Gottschalk T.A., Simpson D.S., Djajawi T.M., Deo P., Ambrose R.L., Conos S.A., Emery J., Abraham G., Pascoe A., Hughes S.A., Weir A., Hawkins E.D., Kong I., Herold M.J., Pearson J.S., Lalaoui N., Naderer T., Vince J.E, & Lawlor K.E. (2023). A1 is induced by pathogen ligands to limit myeloid cell death and NLRP3 inflammasome activation. EMBO Reports, 24(11), e56865.

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Publication 2023

5-chloromethylfluorescein diacetate ABT-737 Cell Adhesion Cell Death Cells CP-456773 Culture Media Glutamine IgG1 Immunoglobulin Isotypes Kinetics Macrophage MCC-950 Monoclonal Antibodies Monocytes Mus Penicillins PI 200 Pyruvate quinoline-val-asp(OMe)-CH2-OPH S63845 Serum Sodium Sodium Chloride Streptomycin Tissues

Quantifying Caspase-3 Activity in BMDMs

To assess caspase‐3 activity, 1 × 10⁵ BMDMs were plated per well in 96‐well flat‐bottom tissue culture‐treated plates (BD Falcon), primed with LPS (50 ng/ml) for 3 h and then treated, as indicated with Q‐VD‐OPh (40 μM), ABT‐737 (500 nM) and S63845 (10 μM). All stimulations were staggered in a reverse time course fashion to ensure identical LPS priming and QVD incubation periods across treatments. At experimental endpoint, supernatants were discarded after cell centrifugation and BMDMs lysed in 70 μl DISC lysis buffer (20 mM Tris, 150 mM NaCl, 2 mM EDTA, 1% TritonX‐100, 10% Glycerol, H₂O) for 1 h at room temperature with rotation. 10 μl of cell lysate was used for protein quantification (Pierce™ BCA Protein Assay Kit, Thermo Fisher Scientific) according to manufacturer's instruction, and 50 μl was transferred to an opaque‐walled, clear bottom 96‐well flat bottom plate. DEVDase substrate (Ac‐DEVD‐AMC, BD Pharmingen™ Cat) was prepared to working concentration (20 μM) in assay buffer (20 mM HEPES pH 7.5, 10% Glycerol, 2 mM Dithiothreitol (DTT)). 200 μl of prepared DEVDase substrate reagent was added to each well containing lysates and allowed to incubate overnight with rotation in the absence of light. After incubation, caspase AMC fluorescence was detected using a CLARIOstar Plus (BMG Labtech). Protein concentrations obtained from the BCA were used to normalise the AMC fluorescence intensity across samples.

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Publication 2023

ABT-737 Ac-aspartyl-glutamyl-valyl-aspartyl-aminomethylcoumarin Biological Assay Buffers Caspase Caspase 3 Cells Centrifugation DEVDase Dithiothreitol Edetic Acid Fluorescence Glycerin HEPES Proteins quinoline-val-asp(OMe)-CH2-OPH S63845 Sodium Chloride Tissues TNFSF14 protein, human Tromethamine

Quantification of Mitochondrial DNA in Cellular Fractions

HEK293T WT or HEK293T ATG5 KO cells were transfected with ARF1 WT, ARF1 R99C or empty vector. Alternatively, HEK293T WT cells were transfected with ARF1 WT, ARF1 R99C or empty together with VCP or empty vector. 24 h later, cells were treated with 10 µM of ABT-737 (SYNkinase, 1001) and 10 µM Quinoline-Val-Asp-Difluorophenoxymethylketone (Q-VD-OPH, Cayman Chemical, 15260) as a positive control. In the case of primary human dermal fibroblasts, cells from four healthy donors or from patient AGS460 were used. On the next day, the cells were harvested and isolation and quantification of DNA from cytosolic, mitochondrial and nuclear fractions was performed as described previously^{68 (link)} (basic protocol 2). Briefly, half of the cells were lysed in SDS lysis buffer (20 mM Tris, pH 8, 1% (v/v) SDS, protease inhibitors) to obtain WCLs for normalisation, whereas the other half was used for fractionation. Cytosolic, mitochondrial and nuclear extracts were isolated by subsequently incubating the cells with saponin lysis buffer (1x PBS, pH 7.4, 0.05% saponin, protease inhibitors), NP-40 lysis buffer (50 mM Tris, pH 7.5, 150 mM NaCl, 1 mM EDTA, 1% (v/v) NP-40, 10% (v/v) glycerol, protease inhibitors) and SDS lysis buffer (20 mM Tris, pH 8, 1% (v/v) SDS, protease inhibitors), respectively. Purity of the fractions was determined by immunoblotting for GAPDH (cytosolic extract), TFAM (mitochondrial extract), and Lamin B1 (nuclear extract). DNA extraction of the fractions and WCLs was performed using phenol-chloroform. DNA concentrations were determined by photometry (Nanodrop) and equal amounts of DNA were used to perform qPCR for mitochondrial DNA (MT-Dloop) and nuclear DNA (KCNJ10) (see primers in Table 2). qPCR was performed using PowerUP SYBR Green (Applied Biosystems, A25742) and the relative cytosolic mtDNA was calculated using the ΔΔCT method.

Hirschenberger M., Lepelley A., Rupp U., Klute S., Hunszinger V., Koepke L., Merold V., Didry-Barca B., Wondany F., Bergner T., Moreau T., Rodero M.P., Rösler R., Wiese S., Volpi S., Gattorno M., Papa R., Lynch S.A., Haug M.G., Houge G., Wigby K.M., Sprague J., Lenberg J., Read C., Walther P., Michaelis J., Kirchhoff F., de Oliveira Mann C.C., Crow Y.J, & Sparrer K.M. (2023). ARF1 prevents aberrant type I interferon induction by regulating STING activation and recycling. Nature Communications, 14, 6770.

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Publication 2023

ABT-737 Buffers Caimans Chloroform Cloning Vectors Cytosol DNA, Mitochondrial Donors Edetic Acid Fibroblasts GAPDH protein, human Glycerin Homo sapiens isolation lamin B1 Mitochondrial Inheritance Nonidet P-40 Oligonucleotide Primers Patients Phenol Photometry Protease Inhibitors quinoline-val-asp(OMe)-CH2-OPH Quinolines Radiotherapy Dose Fractionations Saponin Sodium Chloride SYBR Green I TFAM protein, human Tromethamine

Top products related to «ABT-737»

Abt 737 by Selleck Chemicals

Sourced in United States, Germany

ABT-737 is a laboratory compound used in scientific research. It functions as a selective inhibitor of the Bcl-2 family of anti-apoptotic proteins. The core function of ABT-737 is to modulate apoptosis, a fundamental cellular process.

Abt 737 by Abbott

Sourced in United States

ABT-737 is a laboratory equipment product manufactured by Abbott. It is a small-molecule inhibitor that selectively binds to the anti-apoptotic proteins Bcl-2, Bcl-xL, and Bcl-w. The core function of ABT-737 is to induce apoptosis in cells, which can be used for research purposes.

Abt 199 by Selleck Chemicals

Sourced in United States, Germany

ABT-199 is a small molecule inhibitor that targets the BCL-2 protein. It is primarily used for research purposes in the laboratory setting.

Abt 737 by Santa Cruz Biotechnology

Sourced in United States, Germany

ABT-737 is a small molecule inhibitor that targets the Bcl-2 family of proteins, which are involved in the regulation of apoptosis or programmed cell death. It is a laboratory reagent for research purposes.

Abt 263 by Selleck Chemicals

Sourced in United States, Germany, China

ABT-263 is a laboratory research chemical produced by Selleck Chemicals. It is a small molecule inhibitor. The core function of ABT-263 is to inhibit apoptosis regulators.

Abt 737 by Cayman Chemical

Sourced in United States

ABT-737 is a synthetic small-molecule inhibitor that targets the Bcl-2 family of proteins. It functions by binding to and inhibiting the anti-apoptotic proteins Bcl-2, Bcl-xL, and Bcl-w, which are involved in regulating the intrinsic apoptosis pathway.

Cycloheximide (chx) by Merck Group

Sourced in United States, Germany, United Kingdom, China, Italy, Sao Tome and Principe, France, Macao, Japan, Spain, Canada, Switzerland, India, Israel, Brazil, Poland, Portugal, Australia, Morocco, Sweden, Austria, Senegal, Belgium

Cycloheximide is a laboratory reagent commonly used as a protein synthesis inhibitor. It functions by blocking translational elongation in eukaryotic cells, thereby inhibiting the production of new proteins. This compound is often utilized in research applications to study cellular processes and mechanisms related to protein synthesis.

Obatoclax by Selleck Chemicals

Sourced in United States, Germany

Obatoclax is a laboratory compound that functions as a pan-Bcl-2 inhibitor. It is used in research settings to study cellular processes related to apoptosis and cell survival.

Fetal bovine serum (fbs) by Thermo Fisher Scientific

Sourced in United States, China, United Kingdom, Germany, Australia, Japan, Canada, Italy, France, Switzerland, New Zealand, Brazil, Belgium, India, Spain, Israel, Austria, Poland, Ireland, Sweden, Macao, Netherlands, Denmark, Cameroon, Singapore, Portugal, Argentina, Holy See (Vatican City State), Morocco, Uruguay, Mexico, Thailand, Sao Tome and Principe, Hungary, Panama, Hong Kong, Norway, United Arab Emirates, Czechia, Russian Federation, Chile, Moldova, Republic of, Gabon, Palestine, State of, Saudi Arabia, Senegal

Fetal Bovine Serum (FBS) is a cell culture supplement derived from the blood of bovine fetuses. FBS provides a source of proteins, growth factors, and other components that support the growth and maintenance of various cell types in in vitro cell culture applications.

Abt 737 by Merck Group

Sourced in United States, Germany

ABT-737 is a small molecule compound developed by Merck Group. It is designed to inhibit the activity of the Bcl-2 family of proteins, which play a key role in regulating apoptosis, or programmed cell death. The compound has been used in research settings to study the effects of Bcl-2 inhibition on various cell types and disease models.

What is ABT-737 and how does it work?

ABT-737 is a small-molecule inhibitor that targets the apoptosis regulator proteins Bcl-2, Bcl-xL, and Bcl-w. It has demonstrated potent anti-tumor activity in preclinical studies and is being investigated as a potential therapeutic agent for various types of cancer. ABT-737 induces apoptosis by binding to and neutralizing the anti-apoptotic functions of Bcl-2 family proteins, thereby sensitizing cancer cells to apoptotic stimuli.

How can PubCompare.ai help with ABT-737 research?

PubCompare.ai's AI-driven platform can help optimize your ABT-737 research in several ways. First, it allows you to screen protocol literature more efficiently, helping you easily locate relevant protocols from literature, pre-prints, and patents. Second, the platform's AI-driven analysis can help you leverage Critical Insights to identify the most effective protocols related to ABT-737 for your specific research goals. This enables you to choose the best option for reproducibility and accuracy in your ABT-737 studies.

What are the different variations or types of ABT-737?

ABT-737 is a specific small-molecule inhibitor, and there are no major variations or types of this compound. It is a well-defined chemical entity that has been extensively studied in preclinical research for its apoptosis-inducing effects on cancer cells. Researchers may use different concentrations, treatment durations, or combinations with other agents when studying ABT-737, but the core compound remains the same.

What are the specific applications of ABT-737?

ABT-737 has been investigated as a potential therapeutic agent for a variety of cancer types, including leukemia, lymphoma, small cell lung cancer, and solid tumors. Its ability to induce apoptosis in cancer cells by targeting the Bcl-2 family of proteins makes it a promising candidate for cancer treatment. Researchers are exploring the use of ABT-737 both as a monotherapy and in combination with other anti-cancer agents to enhance its efficacy.

What are some common usage challenges with ABT-737?

One of the main challenges with ABT-737 is its relatively poor solubility, which can make it difficult to formulate and deliver effectively. Researchers may need to explore different solvents or delivery systems to overcome this limitation. Additionally, the specificity of ABT-737 for Bcl-2 family proteins means that it may not be effective in all cancer types or indvidual patients, depending on the specific genetic and molecular profile of the tumor. Careful selection of patient populations and combination therapies may be needed to optimize the use of ABT-737.

More about "ABT-737"

ABT-737 is a small-molecule inhibitor that targets the Bcl-2 family of apoptosis regulator proteins, including Bcl-2, Bcl-xL, and Bcl-w.
This compound has demonstrated potent anti-tumor activity in preclinical studies, making it a promising therapeutic agent for various types of cancer.
ABT-737 induces apoptosis, or programmed cell death, by binding to and neutralizing the anti-apoptotic functions of Bcl-2 family proteins, thereby sensitizing cancer cells to apoptotic stimuli.
Researchers can leverage PubCompare.ai's AI-driven platform to optimize their ABT-737 research.
This intuitive tool allows users to easily locate relevant protocols from literature, pre-prints, and patents, while utilizing AI-driven comparisons to identify the best protocols and products.
This can help achieve reproducible and accurate findings for ABT-737 studies.
In addition to ABT-737, researchers may also be interested in exploring other related compounds such as ABT-199 (Venetoclax) and ABT-263 (Navitoclax), which are also Bcl-2 family inhibitors.
Cycloheximide, an antibiotic, and Obatoclax, another Bcl-2 inhibitor, may also be of interest in the context of apoptosis and cancer research.
Additionally, fetal bovine serum (FBS) is a commonly used supplement in cell culture media and can play a role in cell viability and apoptosis studies.
By utilizing PubCompare.ai's AI-powered tools and exploring the broader landscape of Bcl-2 inhibitors and apoptosis-related compounds, researchers can optimize their ABT-737 studies and unlock valuable insights for cancer therapeutics.