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Veliparib abt 888

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Veliparib (ABT-888) is a small-molecule inhibitor of the poly(ADP-ribose) polymerase (PARP) enzyme. It is used in research applications to study the role of PARP in various cellular processes.

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Lab products found in correlation

Rucaparib, by Selleck Chemicals (4 mentions) Olaparib, by MedChemExpress (2 mentions) Talazoparib bmn 673, by Selleck Chemicals (2 mentions) Olaparib, by Selleck Chemicals (2 mentions) Talazoparib, by Selleck Chemicals (2 mentions) Olaparib azd2281, by Selleck Chemicals (2 mentions) Ab6160, by Abcam (2 mentions) Ab6734, by Abcam (2 mentions) Camptothecin cpt, by Merck Group (2 mentions) Obt0030g, by Bio-Rad (2 mentions) A11077, by Thermo Fisher Scientific (2 mentions) A11036, by Thermo Fisher Scientific (2 mentions) Abc738, by Merck Group (2 mentions) Mca1522g, by Merck Group (2 mentions) A31628, by Thermo Fisher Scientific (2 mentions) Peroxide h2o2, by Thermo Fisher Scientific (2 mentions) Mabe1016, by Merck Group (2 mentions) A39571, by Thermo Fisher Scientific (2 mentions) A11001, by Thermo Fisher Scientific (2 mentions) Dimethyl sulfoxide (dmso), by Thermo Fisher Scientific (2 mentions)

Spelling variants of this product

Veliparib (59 citations) ABT-888 (24 citations)

14 protocols using veliparib abt 888

1

Cell Culture and Transfection Protocol

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U2OS, HCT116, RPE1-hTert and PT67 cell lines were maintained in DMEM supplemented with 10% foetal calf serum (FCS). HOC7, OVCA 429, HEY, SKOV 3, OVCAR 3, OVCAR 8, IGROV 1 and OVCA 433 cell lines were maintained in DMEM supplemented with 10% FCS. U2OS DRGFP and EJ5GFP cells were maintained in DMEM without sodium pyruvate supplemented with 10% FCS [48] (link). Exponentially growing cells were transfected with siRNAs (Qiagen, sequences available upon request) using Lipofectamine RNAiMax (Invitrogen) according to the manufacturer's instructions. Plasmids were transfected using Fugene 6 (Promega) or Lipofectamine 2000 (Invitrogen) according to the manufacturer's instructions. Bleomycin (MedChemExpress), mitomycin C (Sigma), cisplatin (Sigma), NU-7441 (Selleckchem), olaparib (AZD-2281, Enzo/Axxora), rucaparib (AG-014699, Selleckchem), veliparib (ABT-888, Selleckchem) and KU-55933 (Calbiochem/Merck) were added as indicated.
Gundogdu R., Erdogan M.K., Ditsiou A., Spanswick V., Garcia-Gomez J.J., Hartley J.A., Esashi F., Hergovich A, & Gomez V. (2021). hMOB2 deficiency impairs homologous recombination-mediated DNA repair and sensitises cancer cells to PARP inhibitors. Cellular Signalling, 87, 110106.
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2

Comprehensive Synthetic Compound Library

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Olaparib (Catalog# A4154), cisplatin (Catalog# A8321), carboplatin (Catalog# A2171), and 5-fluorouracil (Catalog# A4071) were all purchased from APExBIO company. UPF 1096 (Catalog# S8038), NMS-P118(Catalog# S8363), stenoparib (E7449) (Catalog# S8419), niraparib (Catalog# S2741), rucaparib (Catalog# S4948), and veliparib (ABT-888) (Catalog# S1004) were all purchased from Selleckchem.
cisplatin (Catalog# A10221) was purchased from AdooQ Bioscience. ART-558(Catalog# HY-141520), DNA-PK inhibitors PIK-75 hydrochloride (Catalog# HY-13281), Nedisertib (Catalog# HY-101570) and AZD-7648 (Catalog# HY-111783), RAD51 Inhibitor B02 (Catalog# HY-101462), and Olaparib (for in vivo experiment: Catalog# HY-10162) were all purchased from MCE (MedChem Express). ART-812 was synthetized by Dr. Wayne Childers at Temple University School of Pharmacy. All compounds were dissolved, aliquoted, and stored following the manufacturer’s instructions.
Li H., Chatla S., Liu X., Vekariya U., Kim D., Walt M., Lian Z., Morton G., Feng Z., Yang D., Liu H., Reed K., Childers W., Yu X., Madzo J., Chitrala K.N., Skorski T, & Huang J. (2023). Haploinsufficiency of ZNF251 causes DNA-PKcs-dependent resistance to PARP inhibitors in BRCA1-mutated cancer cells. Research Square.
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3

DNA Damage Response in MCF-7 Cells

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MCF-7 cells were obtained from ATCC and cultured in Dulbecco’s Modified Eagle Medium (DMEM, high glucose, Invitrogen) supplemented with 10% fetal bovine serum (FBS, Invitrogen) and 1% penicillin/streptomycin (P/S, Invitrogen) in T-75 flasks until they reached sub-confluence (~90% or ~10 million cells). Cells were treated with DNA damaging agents: cisplatin (Biotang Inc.), methylmethane sulfonate (Acros Organics), zeocin (Invivogen) or a phosphate buffered saline (PBS, Invitrogen) control for 24 hr (or 1 hr in the case of MMS followed by 23 hr of recovery due to rapid DNA damage induction in the case of MMS due to a higher rate of interaction with the DNA as compared to other drugs) before harvesting. Cells were treated with the PARP inhibitor veliparib (ABT-888) (Selleckchem) or PBS containing DMSO (1μg/ml) 24 hr prior to other drug treatments. Stock solution for all drugs, except for veliparib which was in DMSO, were prepared in PBS. All experiments were performed in three independent, biological replicates.
Bhute V.J, & Palecek S.P. (2015). Metabolic responses induced by DNA damage and poly (ADP-ribose) polymerase (PARP) inhibition in MCF-7 cells. Metabolomics : Official journal of the Metabolomic Society, 11(6), 1779-1791.
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4

Comprehensive Pharmacological Toolkit

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The following compounds were used during this study: MMC (Tocris), ACT (Sigma-Aldrich), hydroxyurea (Sigma-Aldrich), etoposide (Selleckchem), cisplatin and actinomycin D (Thermo Fisher Scientific), camptothecin (Sigma-Aldrich), olaparib (Syncom), talazoparib (BMN-673, Selleckchem), veliparib (ABT-888, Selleckchem), doxycycline (Sigma-Aldrich), and dTAG-13 (Tocris).
Mazouzi A., Moser S.C., Abascal F., van den Broek B., Del Castillo Velasco-Herrera M., van der Heijden I., Hekkelman M., Drenth A.P., van der Burg E., Kroese L.J., Jalink K., Adams D.J., Jonkers J, & Brummelkamp T.R. (2023). FIRRM/C1orf112 mediates resolution of homologous recombination intermediates in response to DNA interstrand crosslinks. Science Advances, 9(22), eadf4409.
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5

Antibodies and Inhibitors in DNA Repair

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Antibodies and suppliers were as follows: mouse anti-cyclin A2 (1:5,000, E23.1, Abcam); mouse anti-actin (1:5,000, A5441/clone AC-15, Sigma-Aldrich); mouse anti-MRE11 (1:100, SC-135992, SantaCruz); rabbit anti-RAD51 (Calbiochem, PC130), horseradish peroxidase-conjugated anti-mouse or anti-rabbit immunoglobulin G (Cell Signaling Technology). Veliparib (ABT-888) and olaparib (AZD2281) were purchased from Selleck Chemicals. siRNAs designed to target human cyclin A2 was purchased from Dharmacon. An siRNA targeting luciferase that has no specificity to any human genes was used as the negative transfection control throughout the experiments.
Gu W.W., Lin J, & Hong X.Y. (2017). Cyclin A2 regulates homologous recombination DNA repair and sensitivity to DNA damaging agents and poly(ADP-ribose) polymerase (PARP) inhibitors in human breast cancer cells. Oncotarget, 8(53), 90842-90851.
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6

Pharmacological Inhibitors for Cell Studies

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Olaparib (MedChem Express), veliparib (ABT888; Selleck), rucaparib (AG014699; Selleck), talazoparib (BMN673; Selleck), VE822 (MedChem Express), AZ20 (MedChem Express), VE821 (Selleck), KU55933 (Selleck), BKM120 (Selleck), and TMZ (Sigma) were dissolved in dimethyl sulfoxide (DMSO). bpV(phen) (Millipore) was dissolved in water for stock. Chemicals were diluted with medium for in vitro studies.
Ning J.F., Stanciu M., Humphrey M.R., Gorham J., Wakimoto H., Nishihara R., Lees J., Zou L., Martuza R.L., Wakimoto H, & Rabkin S.D. (2019). Myc targeted CDK18 promotes ATR and homologous recombination to mediate PARP inhibitor resistance in glioblastoma. Nature Communications, 10, 2910.
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7

Breast Cancer Cell Lines and PARP Inhibitors

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We studied 14 human breast cancer cell lines: 3 BRCA1 mutant lines with BRCA1 allelic loss (HCC-1947, MDA-MB-436, and SUM-149PT), 1 BRCA2 mutant line with BRCA2 allelic loss (HCC-1428), 9 BRCA wild-type lines with BRCA1 allelic loss (MCF-7, ZR75, MDA-MB-361, BT-474, SKBR3, MDA-MB-231, BT-549, MDA-MB-468 and BT-20), and 1 BRCA wild-type line without BRCA1 allelic loss (T47D). T47D, MCF-7, ZR75, MDA-MB-361, BT-474, SKBR3, MDA-MB-231, BT-549, MDA-MB-468, and BT-20 cells were cultured at 37°C in DMEM supplemented with 10% FBS in a humid incubator with 5% CO2. SUM-149PT cells were cultured in Ham’s F-12 supplemented with 5% FBS, insulin, and hydrocortisone. The PARP inhibitors veliparib (ABT-888), olaparib (AZD2281), and iniparib (BSI-201) were purchased from Selleck Chemicals (Houston TX, USA).
Arun B., Akar U., Gutierrez-Barrera A.M., Hortobagyi G.N, & Ozpolat B. (2015). The PARP inhibitor AZD2281 (Olaparib) induces autophagy/mitophagy in BRCA1 and BRCA2 mutant breast cancer cells. International Journal of Oncology, 47(1), 262-268.
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8

NHEJ Inhibitors to Enhance HDR

Cited 1 time
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The following NHEJ inhibitors were used to enhance HDR: vanillin (12 (link)) reconstituted in H2O, 300µM final concentration (Sigma cat#V1104); SCR7-X in DMSO, 1µM final (Xcess Biosciences cat#M60082). Since we purchased SCR7-X from Xcess Biosciences we refer to this compound as “SCR7-X” as recently suggested (13 (link)). Rucaparib/AG-014699/PF-01367338, in DMSO, 1µM final (Selleckchem cat#S1098); veliparib/ABT-888 in DMSO, 5µM final (Selleckchem cat#S1004); RS-1 (14 ) in DMSO, 7.5µM final (MerckMillipore cat# 553510); RS-1 in DMSO, 7.5µM final, (Sigma cat#R9782); Luminespib/AUY-922/NVP-AUY922 in DMSO, 1µM final (Selleckchem cat#S1069); L-755,507 in DMSO, 5µM final (Tocris cat#2197); vanillin derivatives (12 (link)) 6-nitroveratraldehyde in DMSO, 3µM final (Maybridge cat#11427047), 4,5-dimethoxy-3-iodobenzaldehyde in DMSO, 3µM final (Maybridge cat#11328426); 6-bromoveratraldehyde in DMSO, 3µM final (Maybridge cat#11480124).
Kornete M., Marone R, & Jeker L.T. (2018). Highly Efficient and Versatile Plasmid-Based Gene Editing in Primary T Cells. The Journal of Immunology Author Choice, 200(7), 2489-2501.
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9

Clonal Isolation and Veliparib Treatment

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Clonal isolation was performed by serial dilution in 96 well plates. Single clones of HCC1937 and BRCA1c were cultured for 3 weeks in IMDM (Gibco, USA)+ 15% FBS (GeminiBio, USA) + 0.15 mg/mL geneticin (G418) (Gibco, USA) antibiotic in either DMSO (Thermo Fisher, USA) or 3.6 μM veliparib (ABT-888) (Selleckchem,USA) dissolved in DMSO. Cells were seeded at 1:10 and re-treated every 24 hrs. Once the cells reached 80–90% confluence, cells were trypsinized and passaged 1:10 and treated with fresh. After 3 weeks of treatment, clonal isolation was again performed by serial dilution in 96 well plates, followed by expansion.
Alvarado-Cruz I., Mahmoud M., Khan M., Zhao S., Oeck S., Meas R., Clairmont K., Quintana V., Zhu Y., Porciuncula A., Wyatt H., Ma S., Shyr Y., Kong Y., LoRusso P.M., Laverty D., Nagel Z.D., Schalper K.A., Krauthammer M, & Sweasy J.B. (2020). Differential immunomodulatory Effect of PARP Inhibition in BRCA1 deficient and competent tumor cells. Biochemical pharmacology, 184, 114359.
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10

PARP Inhibitor Pharmacology Protocol

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Imatinib, temozolomide, bendamustine, cisplatin, oxaliplatin, paclitaxel, docetaxel, veliparib (ABT-888) and talazoparib (BMN 673) were purchased from Selleck Chemicals. Olaparib (AZD2281, KU-0059436) and CO-338 (PF-01367338-BW, rucaparib camsylate salt) were obtained from AstraZeneca and Clovis Oncology through MTAs, respectively. 4-HC was kindly provided by Drs. Michael Colvin and Susan Ludeman (Duke University, NC). Structures of PARP1 inhibitors used are shown in Suppl. Fig. 1.
Liu X., Jiang Y., Nowak B., Hargis S, & Plunkett W. (2016). Mechanism-based drug combinations with the DNA-strand-breaking nucleoside analog, CNDAC. Molecular cancer therapeutics, 15(10), 2302-2313.
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