Bmn673

Manufactured by Selleck Chemicals

Sourced in United States

BMN673 is a laboratory product designed for research purposes. It functions as a PARP inhibitor, which is a class of compounds that act on the Poly(ADP-ribose) polymerase (PARP) enzyme. The core function of BMN673 is to inhibit PARP activity, which can be utilized in various research applications.

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Lab products found in correlation

23 protocols using bmn673

Investigating PARP1 Regulation and Function

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Olaparib was purchased from LC laboratory. BMN-673, Veliparib, Niraparib, Rucaparib, MG-132 and Pomalidomide were obtained from Selleck. PDD 00017273 was purchased from Tocris. Peroxynitrite was purchased from Cayman Chemical. Antibodies against GAPDH and Poly-(ADP-Ribose) were purchased from Thermo and Trevigen, respectively. Antibodies against PARP1, SP1, H3, γH2A.X, CRBN, HA-Tag and VHL were purchased from Cell Signaling Technology. The PARP1-GFP plasmid was a gift from Dr. Xiaochun Yu (City of Hope). HA-Ub, lentiCRISPR-CRBN and control plasmids were constructed by standard molecular methods. All other chemicals and reagents were obtained from Sigma, unless stated otherwise.

Wang S., Han L., Han J., Li P., Ding Q., Zhang Q.J., Liu Z.P., Chen C, & Yu Y. (2019). Uncoupling of PARP1 Trapping and Inhibition Using Selective PARP1 Degradation. Nature chemical biology, 15(12), 1223-1231.

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BMN673 Blocks Cigarette Smoke-Induced Response

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100 μM BMN673 (S7048, Selleckchem, Houston, TX) was added to HBE cultures one hour before exposure to smoke of eight cigarettes. Control cells were given an identical concentration of the diluent DMSO, as found in the experimental samples. Cells were fractionated and processed for western blot analysis three hours after smoke exposure.

Künzi L, & Holt G.E. (2019). Cigarette smoke activates the parthanatos pathway of cell death in human bronchial epithelial cells. Cell Death Discovery, 5, 127.

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Evaluating Potent ATR Inhibitors

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The ATRi VE-821 and VX-970 were provided by Vertex Pharmaceuticals. Olaparib and BMN673 were purchased from Selleck Chemicals; cisplatin was purchased from Sigma.

Williamson C.T., Miller R., Pemberton H.N., Jones S.E., Campbell J., Konde A., Badham N., Rafiq R., Brough R., Gulati A., Ryan C.J., Francis J., Vermulen P.B., Reynolds A.R., Reaper P.M., Pollard J.R., Ashworth A, & Lord C.J. (2016). ATR inhibitors as a synthetic lethal therapy for tumours deficient in ARID1A. Nature Communications, 7, 13837.

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Evaluating PARP Inhibitors on Cellular Responses

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The following compounds were used at the indicated final concentrations: PJ-34 (10 μM, ALX-270-289-M001, Enzo Life Science), Olaparib (1-10 μM, AZD-2281, Selleckchem), Rucaparib (1-8 μM, AG-014699, Selleckchem), Talazoparib (6.25-50 nM, BMN673, Selleckchem), β-Nicotinamide adenine dinucleotide hydrate (20-200 μM, N7004, Sigma-Aldrich), hydrogen peroxide (0.02-0.5 mM, H3420, Sigma-Aldrich), Methyl methanesulfunate, MMS (0.01%, 129925, Sigma-Aldrich), PARG inhibitor (10 μM, PDD00017273, Tocris), FK866 (1 μM, F8557, Sigma-Aldrich), MG132 (10 μM, M7449, Sigma-Aldrich), cycloheximide (50 μM, C7698, Sigma-Aldrich).

Gatti M., Imhof R., Huang Q., Baudis M, & Altmeyer M. (2020). The Ubiquitin Ligase TRIP12 Limits PARP1 Trapping and Constrains PARP Inhibitor Efficiency. Cell Reports, 32(5), 107985.

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Multiparametric Analysis of Immune Responses

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GAPDH (AC033), STING (A3575), phosphorylated MEK1/2 (pMEK1/2) (AP0209), TBK1 (A14641), IRF3 (A11373) antibodies were from ABclonal. CD4 (ab183685), CD8 (ab209775), pERK1/2 (ab 214362), pSTAT1 (ab109461) and phosphorylated TBK1 (pTBK1) (ab 109272) antibodies were from Abcam. phosphorylated ERK1/2 (pERK1/2) (4370), pIRF3 (29047), STAT1 (14994) and phosphorylation of histone H₂AX at Ser139 (γH₂AX) (2577) antibodies were from Cell Signaling Technology.
Olaparib, BMN673, and trametinib were from Selleck. Cobimetinib, H151 and C176 were from MCE. Compounds were dissolved in DMSO and stored as 10 mM aliquots at instructions temperature. anti-PD-L1 antibody (BE0101, clone B7-H1) and IgG isotype control (BE0090) was from BioXcell. CD45 (BV605 30-F11), CD3e (APC-Cy7 145–2C11), mouse CD4 (FITC RM4–5), CD25 (PE-Cy7 PC61), Foxp3 (BV421 MF23), CD8a (PerCP-Cy5.5 53–6.7), Granzyme B (D2H2F), IFN-γ (PE XMG1.2), CD11c (PE-Cy HL3), I-A/I-E (BV421 M5/114.15.2), F4/80 (PE T45–2342), CD11b (FITC M1/70), CD49b (APC DX5), CD3e (APC-Cy7 145-2C11), ly-6G (PE 1A8), ly-6C (APC AL-21), Gr-1 (PerCP-Cy5.5), Fixable Viability Stain (BV510), Transcription Factor Buffer Set were from BD Biosciences.

Yang B., Li X., Fu Y., Guo E., Ye Y., Li F., Liu S., Xiao R., Liu C., Lu F., Huang J., Qin T., Han L., Peng G., Mills G.B., Sun C, & Chen G. (2021). MEK inhibition remodels the immune landscape of mutant KRAS tumors to overcome resistance to PARP and immune checkpoint inhibitors. Cancer research, 81(10), 2714-2729.

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Investigating PARP1 Regulation and Function

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Assessing PARP1 Inhibitor Efficacy in LCLs

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NHC1 lymphoblastoid cell lines (LCLs) harboring EBV B95.8 strain used in this study were cultured in 15% fetal bovine serum (FBS), 1% Penicillin/Streptomycin (Gibco) RPMI 1640 (Corning) at 37 °C and 5% CO₂. To assess the half maximal inhibitory concentration (IC50), LCL were treated with PARP1 inhibitor BMN-673 (Talazoparib, LT-673; Selleck Chemicals, Cat. No. S7048) for 72 hours (h), 5 days or 7 days at several doses (serial dilution from 10µM to 0.01 nM), or DMSO (MilliporeSigma, Cat. No. D8418). For the successive experiment, BMN-673 was used at 200nM, 100nM, 50nM and 20nM. PARP1 activity was validated by DB, as detailed below. For SCGE, cell was treated with 20 µM Etoposide (MilliporeSigma, Cat. No. E1383) for 4 h.

Napoletani G., Soldan S.S., Kannan T., Preston-Alp S., Vogel P., Maestri D., Caruso L.B., Kossenkov A., Sobotka A., Lieberman P.M, & Tempera I. (2023). PARP1 Inhibition Halts EBV+ Lymphoma Progression by Disrupting the EBNA2/MYC Axis. bioRxiv.

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Cisplatin-Resistant Lung Cancer Cells

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A549 (a human lung adenocarcinoma cell line), A549/DR (a cisplatin-resistant A549 cell line), and SK-MES-1 (a human lung squamous cell carcinoma cell line) were purchased from the Shanghai Institute for Biological Science (China). The cells were cultured in RPMT-1640 supplemented with 5% fetal bovine serum, 1% glutamine, 100μl/ml penicillin, 100μl/ml streptomycin. A549/DR cells were routinely maintained in culture media containing 0.5μg/ml cisplatin and growth in drug free media for 3 days before the experiment. Antibodies to the following antigen used in this study include: FANCD2, FAAP20, RAD51c, RAD51, Pol θ, Pol η, REV3, REV1, 53BP1, and gapdh were from Santa Cruz, BRCA2, p-ATM, p-CHK1 (S317), p-CHK2 (T68), p-KAP1(S824) were from Calibiochem, and γH2AX and H2AX were from Cell Signaling. Cisplatin was from Yangtze River Pharmaceutica, Carboplatin were from Qilu Pharmaceutical CO., Ltd, BMN673 was from Selleck Chemicals.

Dai C.H., Chen P., Li J., Lan T., Chen Y.C., Qian H., Chen K, & Li M.Y. (2016). Co-inhibition of pol θ and HR genes efficiently synergize with cisplatin to suppress cisplatin-resistant lung cancer cells survival. Oncotarget, 7(40), 65157-65170.

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Olaparib and BMN-673 Cytotoxicity Assay

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Olaparib (Sigma) in DMSO at 50 mM and BMN-673 (Selleck Chemicals) in DMSO at 10 mM were diluted in DMSO to make 1000X solutions and added directly to cell culture media, with 0.1% DMSO used as a control. 5-Bromo-2′-deoxyuridine (BrdU) (Sigma) at 1 mM in DMSO was diluted directly in cell culture media for a final concentration of 10 μM.

Scanlon S.E., Hegan D.C., Sulkowski P.L, & Glazer P.M. (2017). Suppression of homology-dependent DNA double-strand break repair induces PARP inhibitor sensitivity in VHL-deficient human renal cell carcinoma. Oncotarget, 9(4), 4647-4660.

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Combination Therapy Protocol for Cancer

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SAHA, olaparib, BMN-673, AGI-5198 and temozolomide were all obtained from SelleckChem, and dissolved in DMSO for cell culture experiments. For animal tumor studies, BMN-673 was diluted in a vehicle containing 10% dimethylacetamide, 6% Kolliphor HS 15 and 84% PBS. SAHA was diluted in PBS. Both were administered to mice via oral gavage five days a week, for three weeks. Octyl-2-HG ((2R)-octyl-alpha-hydroxyglutarate) (Cayman Chemical) and Octyl-α-KG (Sigma-Aldrich) were dissolved in DMSO. Horizon Dharmacon ON-TARGETplus Human BRCA1 and RAD51 siRNA were used at 20 nM for 72 hours.

Dow J., Krysztofiak A., Liu Y., Colon-Rios D.A., Rogers F.A, & Glazer P.M. (2021). Vulnerability of IDH1 mutant cancers to histone deacetylase inhibition via orthogonal suppression of DNA repair. Molecular cancer research : MCR.

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