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Olaparib

Olaparib is a potent and selective inhibitor of the poly(ADP-ribose) polymerase (PARP) enzyme, which plays a crucial role in DNA repair.
It has demonstrated efficacy in the treatment of certain types of advanced ovarian, breast, and prostate cancers, particularly those with BRCA1 or BRCA2 mutations.
Olaparib is approved for use in various cancer indications and is the subject of extensive research to further optimize its therapeutic applications.
The PubCompare.ai platform can enhance Olaparib research by facilitating the identification of the most reporducible and accurate protocols from literature, preprints, and patents, using AI-driven comparisons to identify the best protocols and products.
This streamlines the research process and helps researchers optimize their Olaparib studies.

Most cited protocols related to «Olaparib»

1
Analyzing DNA Damage Responses in U2OS Cells
Cited 13 times
U2OS TRE cell line was described before as U2OS SCE 19 (20 (link)). In this cell line, 200 copies of pTRE/I-SceI were integrated in U2OS cells. Another U2OS 263 (a control cell line harboring 200 copies of the TRE element) (21 (link)) was used. Both cell lines were cultured in DMEM with 10% FBS at 37°C. Plasmids were transfected with Fugene-6 (Life Technology). The PARP inhibitors PJ34 (Sigma) or Olaparib (Sigma) were used. ROS scavengers NAC (500 mM/NaOH) (N-acetylcysteine) (Sigma), and MnTBAP (Enzo Life Science) were used. NAC (500 mM in NaOH) treatment was used with a 20 mM final concentration, and MnTBAP (100 mM/DMSO) was used with a 100 µM final concentration in PBS for 1 h. H2O2 (Sigma) treatment was used at the indicated concentration in PBS for 1 h. siFEN1 to target the UTR region (Thermo Scientific, A-010344-14) and siPARP1 (Thermo Scientific, E-006656-00) were transfected with DharmaFECT transfection regent (Thermo Scientific, T-2001-02). RNA polymerase II inhibitor 5,6-dichloro-1 -β-d-ribofuranosylbenzimidazole (DRB) (Sigma) stock concentration is 20 mM; final concentration used is 20 µM, added to cells for 24 h before irradiation or other treatment.
Lan L., Nakajima S., Wei L., Sun L., Hsieh C.L., Sobol R.W., Bruchez M., Van Houten B., Yasui A, & Levine A.S. (2013). Novel method for site-specific induction of oxidative DNA damage reveals differences in recruitment of repair proteins to heterochromatin and euchromatin. Nucleic Acids Research, 42(4), 2330-2345.
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Publication 2013
Acetylcysteine Cell Lines Cells FuGene Gas Scavengers manganese(III)-tetrakis(4-benzoic acid)porphyrin olaparib Peroxide, Hydrogen PJ-34 Plasmids Poly(ADP-ribose) Polymerase Inhibitors Radiotherapy RNA Polymerase II Sulfoxide, Dimethyl Transfection
2
Biomarker Studies for Precision Oncology
Cited 13 times
All biomarker studies were prospectively planned. Whole-exome sequencing and transcriptome studies were performed on DNA from fresh-frozen tumor-biopsy samples obtained before treatment; germline whole-exome sequencing was performed on DNA from saliva samples. These studies were conducted at the University of Michigan as previously described.3 (link),17 (link) Targeted next-generation sequencing studies were conducted at the Institute of Cancer Research18 (link),19 ; libraries were constructed with the use of the GeneRead DNAseq Panel (Qiagen) and run on a MiSeq sequencer (Illumina). Copy-number data were validated by means of droplet digital polymerase-chain-reaction (PCR) testing with the use of the QX100 Droplet Digital PCR System (Bio-Rad).19 Circulating tumor-cell counts were performed with the use of CellSearch (Janssen Diagnostics).20 (link) For the purpose of correlating the results of next-generation sequencing with the response to treatment, patients were classified as positive or negative for genomic defects in DNA-repair genes. A patient was considered to be biomarker-positive if a homozygous deletion or deleterious mutation was identified in a gene reported to be involved either in DNA damage repair or sensitivity to PARP inhibition.21 (link)–23 (link) PTEN and ERG protein expression was determined by means of immunohistochemical assessment24 (link) (for details, see the Supplementary Appendix).
Mateo J., Carreira S., Sandhu S., Miranda S., Mossop H., Perez-Lopez R., Nava Rodrigues D., Robinson D., Omlin A., Tunariu N., Boysen G., Porta N., Flohr P., Gillman A., Figueiredo I., Paulding C., Seed G., Jain S., Ralph C., Protheroe A., Hussain S., Jones R., Elliott T., McGovern U., Bianchini D., Goodall J., Zafeiriou Z., Williamson C.T., Ferraldeschi R., Riisnaes R., Ebbs B., Fowler G., Roda D., Yuan W., Wu Y.M., Cao X., Brough R., Pemberton H., A’Hern R., Swain A., Kunju L.P., Eeles R., Attard G., Lord C.J., Ashworth A., Rubin M.A., Knudsen K.E., Feng F.Y., Chinnaiyan A.M., Hall E, & de Bono J.S. (2015). DNA-Repair Defects and Olaparib in Metastatic Prostate Cancer. The New England journal of medicine, 373(18), 1697-1708.
Publication 2015
Biological Markers Biopsy Deletion Mutation Diagnosis DNA Repair Freezing Genes Genome Germ Line Homozygote Hypersensitivity Malignant Neoplasms Mutation Neoplasms Patients Polymerase Chain Reaction Proteins Psychological Inhibition PTEN protein, human Saliva Transcriptome
3
Biopsy-Driven Exploration of mCRPC
Cited 11 times
Subjects with mCRPC who were receiving standard-of-care therapy or treatment in a clinical trial [including trials combining AR therapies with other agents, a trial of the PARP inhibitor olaparib (37 (link)), and a trial of the Aurora kinase A inhibitor alisertib in patients with neuroendocrine features (14 (link))] and who had disease amenable to biopsy under radiographic guidance were considered for inclusion at one of seven SU2C-PCF (Stand Up to Cancer/Prostate Cancer Foundation) International Prostate Cancer Dream Team consortium sites (Dana-Farber Cancer Institute, Karmanos Cancer Institute, Memorial Sloan Kettering Cancer Center, Royal Marsden, University of Michigan, University of Washington, and Weill Cornell Medicine) (5 (link)). All subjects included in this study provided written consent for research use of tumor tissue with institutional review board approvals or appropriate waivers (Office of Human Research Studies at the Dana-Farber Cancer Institute, Wayne State University Institutional Review Board, Memorial Sloan Kettering Cancer Center Institutional Review Board/Privacy Board, Royal Marsden Ethics Committee, University of Michigan Medical School Institutional Review Board, University of Washington Institutional Review Board, and Weill Cornell Medicine Institutional Review Board). Clinical data, including treatment history, duration of therapy, and survival, were collected using a web-based electronic data capture. All samples and clinical data were deidentified.
Abida W., Cyrta J., Heller G., Prandi D., Armenia J., Coleman I., Cieslik M., Benelli M., Robinson D., Van Allen E.M., Sboner A., Fedrizzi T., Mosquera J.M., Robinson B.D., De Sarkar N., Kunju L.P., Tomlins S., Wu Y.M., Nava Rodrigues D., Loda M., Gopalan A., Reuter V.E., Pritchard C.C., Mateo J., Bianchini D., Miranda S., Carreira S., Rescigno P., Filipenko J., Vinson J., Montgomery R.B., Beltran H., Heath E.I., Scher H.I., Kantoff P.W., Taplin M.E., Schultz N., deBono J.S., Demichelis F., Nelson P.S., Rubin M.A., Chinnaiyan A.M, & Sawyers C.L. (2019). Genomic correlates of clinical outcome in advanced prostate cancer. Proceedings of the National Academy of Sciences of the United States of America, 116(23), 11428-11436.
Publication 2019
alisertib Aurora Kinase A Biopsy Dreams Ethics Committees Ethics Committees, Research Homo sapiens Malignant Neoplasms Neoplasms Neurosecretory Systems olaparib Patients Pharmaceutical Preparations Poly(ADP-ribose) Polymerase Inhibitors Prostate Cancer Tissues X-Rays, Diagnostic
4
Cell Lines for PARP Inhibitor Resistance
Cited 9 times
UWB1.289 and UWB1.289 + BRCA1 were obtained from American Type Culture Collection (ATCC) and maintained in RPMI1640 (ATCC) and MEGM bullet kit (1:1; Lonza) with 3% FBS and 1% penicillin/streptomycin (DelloRusso et al. 2007 (link)). SYr-resistant cell lines were derived from the parental UWB1.289 line after 45 d of selection with 1.0 µM PARPi (olaparib; SelleckChem) or following passages with incremental increases of PARPi (olaparib) from 0.025 to 1.0 µM. T2 (non-BRCA), BR5 (BRCA1Δ11/Δ11, exon 11 deleted), and resistant BR5-R1 cell lines are FVB mouse-derived ovarian tumor cell lines (Xing and Orsulic 2006 (link)) and were maintained in DMEM supplemented with 10% FBS, 1% penicillin/streptomycin, and 1% L-glutamine. BR5-R1 was derived through incremental increases of PARPi (olaparib) from 0.025 to 1.0 µM. HCC1937 and HCC1937 + BRCA1 cells were maintained in RPMI-1640 supplemented with 10% FBS and 1% penicillin/streptomycin. RPE-hTERT cells were maintained in DMEM supplemented with 10% FBS, 1% penicillin/streptomycin, and 1% L-glutamine. Primary human ovarian tumor cells were collected from ascites or pleural fluid of ovarian cancer patients that had tested positive for malignant cells by cytological analysis. Human ovarian tumor cells were maintained in RPMI-1640 with 10% FBS, 1% L-glutamine, 1% penicillin/streptomycin, and supernatant from patient-matched ascites/pleural fluid. All cells were grown at 37°C and 5% CO2.
Yazinski S.A., Comaills V., Buisson R., Genois M.M., Nguyen H.D., Ho C.K., Todorova Kwan T., Morris R., Lauffer S., Nussenzweig A., Ramaswamy S., Benes C.H., Haber D.A., Maheswaran S., Birrer M.J, & Zou L. (2017). ATR inhibition disrupts rewired homologous recombination and fork protection pathways in PARP inhibitor-resistant BRCA-deficient cancer cells. Genes & Development, 31(3), 318-332.
Publication 2017
Ascites Ascitic Fluid BRCA1 protein, human Cell Lines Cells Exons Glutamine Homo sapiens Mus olaparib Ovarian Cancer Ovarian Neoplasm Parent Patients Penicillins Pleura Streptomycin
5
Chemotherapy Resistance in Cancer Cells
Cited 9 times

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Publication 2013
ABT 888 Acid Phosphatase Antibiotics, Antitubercular Atmosphere AZD 2281 Bicarbonate, Sodium Biological Assay Cell Culture Techniques Cell Lines Cells Cell Survival Cytotoxin Glutamine Insulin olaparib Pharmaceutical Preparations Pharmacotherapy Pyruvate Resistance, Drug Sodium Sulfoxide, Dimethyl Technique, Dilution veliparib

Most recents protocols related to «Olaparib»

1
Modeling Acquired Olaparib Resistance
Ovarian cancer cell lines were subjected to a gradual increase in the concentration of Olaparib (from 0.5 to 20 µM) to allow for the development of acquired resistance. Cells with acquired resistance to Olaparib (designated as OlaR) were developed after 3–4 months in drug media. The established Olaparib resistance models were maintained in culture medium with low-concentration Olaparib, and dosing was temporarily ceased prior to conducting experiments.
Liu C., Li J., Xu F., Chen L., Ni M., Wu J., Zhao H., Wu Y., Li J., Wu X, & Chen X. (2024). PARP1-DOT1L transcription axis drives acquired resistance to PARP inhibitor in ovarian cancer. Molecular Cancer, 23, 111.
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Publication 2024
2
Synergistic GSC Radiosensitization by PARP1 Inhibitor
PARP1 inhibitor Olaparib/Lynparza/AZD2281 (Adooq Bioscience, A10111; PARPi) and TMZ (Sigma Aldrich, T2577) was diluted with DMSO to make 10 mM stocks, which were stored at −20 °C. DMSO was added as a vehicular control to maintain consistent DMSO concentrations. DMSO, Olaparib and TMZ were diluted in GSC culture media to the final intended concentrations and 1 mL of the drug/DMSO dilutions was added to the desired wells. To firstly determine the inhibitory dose of Olaparib, 3D GSCs were incubated with Olaparib for 1 h followed by ionizing radiation (IR) or sham irradiated using a Caesium-137 (137Cs) Irradiator (CIS IBL437c) to a total dose of 5 Gy. SDS-PAGE analysis of subsequent lysates determined inhibition through loss of αPARylation (500 nM) in response to IR. For combination chemosensitisation studies, 3D GSCs were treated with DMSO or Olaparib (500 nM) and incubated for one hour before TMZ (5 mM) was added (where required) followed by exposure to TTFields (72 h, 200 kHz, 1.33 V/cm RMS), or incubated at 37 °C for the untreated ‘sham irradiated’ control. Cell survival was determined as detailed above.
Jones C.G., Vanderlinden A., Rominiyi O, & Collis S.J. (2024). Development and Optimisation of Tumour Treating Fields (TTFields) Delivery within 3D Primary Glioma Stem Cell-like Models of Spatial Heterogeneity. Cancers, 16(5), 863.
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Publication 2024
3
Generating Olaparib-Resistant Cell Lines

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Publication 2024
4
Generating Olaparib-Resistant Cell Line
To generate olaparib-resistant cells, C1 cells were treated with 0.75 mM MMS for 1 h and then continuously cultured in the presence of 1–20 μM olaparib for approximately 5 months. Olaparib-resistant clones were maintained in MEM supplemented with 10% FBS, 1% non-essential amino acids, 1% penicillin-streptomycin, and 1 μM olaparib. An isolated single clone#(2–4)9 was designated as C1/OLA cells.
Sasaki Y., Inouchi T., Nakatsuka R., Inoue A., Masutani M, & Nozaki T. (2024). Activated NAD+ biosynthesis pathway induces olaparib resistance in BRCA1 knockout pancreatic cancer cells. PLOS ONE, 19(4), e0302130.
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Publication 2024
5
Olaparib-Treated Cell Line Characterization
The UWB1.289 (CRL-2945; female) cell line was accessed from internal GSK collections and was obtained from ATCC. The cell line was additionally authenticated using the Promega Cell ID system. The generated short tandem repeat (STR) profiles matched exactly the expected STR profiles of the ATCC lines. Reagents were obtained from Gibco unless stated otherwise. Cells were cultured at 37 °C, 5% CO2 in 1:1 RPMI:MEGM (Lonza, #CC-3151), 3% fetal bovine serum (FBS, Gibco), MEGM SingleQuots supplements (Lonza, #CC-4136) used without gentamycin-amphotericin. For the Olaparib (CAS: 763113-22-0) treatment, three 15 cm dishes per condition were prepared by seeding 3‒4 × 106 cells per plate; 24 h later medium was removed and 25 ml fresh medium containing dimethylsulfoxide (DMSO, Sigma) or 4uM Olaparib was applied to the cells. Cells were incubated for the indicated time (24 h) at 37 °C, 5% CO2. Cells were collected by trypsinization, washed twice with PBS, and counted using a Casy Cell Counter (OMNI Life Science). Cell pellets were generated containing 1–2 million cells for either proteomic and phosphoproteomic or transcriptomic analysis. Three independent replicates were generated per data point per readout.
Burtscher M.L., Gade S., Garrido-Rodriguez M., Rutkowska A., Werner T., Eberl H.C., Petretich M., Knopf N., Zirngibl K., Grandi P., Bergamini G., Bantscheff M., Fälth-Savitski M, & Saez-Rodriguez J. (2024). Network integration of thermal proteome profiling with multi-omics data decodes PARP inhibition. Molecular Systems Biology, 20(4), 458-474.
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Publication 2024

Top products related to «Olaparib»

1
Olaparib by Selleck Chemicals
Sourced in United States, Germany, United Kingdom, China, France, Japan
Olaparib is a laboratory chemical product. It is a poly(ADP-ribose) polymerase (PARP) inhibitor. Olaparib functions by inhibiting the activity of PARP enzymes, which are involved in DNA repair processes.
2
Olaparib by MedChemExpress
Sourced in United States, China, Sweden
Olaparib is a lab equipment product manufactured by MedChemExpress. It is a chemical compound used for research purposes.
3
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.
4
Talazoparib by Selleck Chemicals
Sourced in United States, United Kingdom, Germany, China
Talazoparib is a poly(ADP-ribose) polymerase (PARP) inhibitor. It is a laboratory research tool used to investigate the role of PARP enzymes in cellular processes.
5
Cisplatin by Merck Group
Sourced in United States, Germany, United Kingdom, China, Sao Tome and Principe, Macao, Italy, France, Canada, Japan, Spain, Czechia, Poland, Australia, India, Switzerland, Sweden, Belgium, Portugal
Cisplatin is a platinum-based medication used as a chemotherapeutic agent. It is a crystalline solid that can be dissolved in water or saline solution for administration. Cisplatin functions by interfering with DNA replication, leading to cell death in rapidly dividing cells.
6
Dimethyl sulfoxide (dmso) by Merck Group
Sourced in United States, Germany, United Kingdom, China, Italy, Sao Tome and Principe, France, Macao, India, Canada, Switzerland, Japan, Australia, Spain, Poland, Belgium, Brazil, Czechia, Portugal, Austria, Denmark, Israel, Sweden, Ireland, Hungary, Mexico, Netherlands, Singapore, Indonesia, Slovakia, Cameroon, Norway, Thailand, Chile, Finland, Malaysia, Latvia, New Zealand, Hong Kong, Pakistan, Uruguay, Bangladesh
DMSO is a versatile organic solvent commonly used in laboratory settings. It has a high boiling point, low viscosity, and the ability to dissolve a wide range of polar and non-polar compounds. DMSO's core function is as a solvent, allowing for the effective dissolution and handling of various chemical substances during research and experimentation.
7
Rucaparib by Selleck Chemicals
Sourced in United States, Germany
Rucaparib is a lab equipment product that serves as a PARP inhibitor. It is a small molecule designed to inhibit the activity of PARP enzymes, which play a crucial role in DNA repair processes.
8
Olaparib by Merck Group
Sourced in United States
Olaparib is a laboratory product manufactured by Merck Group. It is a poly(ADP-ribose) polymerase (PARP) inhibitor used in research applications.
9
Veliparib by Selleck Chemicals
Sourced in United States, United Kingdom, China, Germany
Veliparib is a laboratory chemical used in research applications. It is a PARP inhibitor, a class of compounds that play a role in various cellular processes. The core function of Veliparib is to inhibit the activity of PARP enzymes, which are involved in DNA repair and other cellular pathways. This product is intended for research use only and its specific applications should be determined by the end user.
10
Olaparib by AstraZeneca
Sourced in United Kingdom, United States
Olaparib is a lab equipment product manufactured by AstraZeneca. It is a poly(ADP-ribose) polymerase (PARP) inhibitor. The core function of Olaparib is to inhibit the activity of PARP enzymes, which play a role in DNA repair.

More about "Olaparib"

Olaparib, a potent and selective inhibitor of the poly(ADP-ribose) polymerase (PARP) enzyme, plays a crucial role in DNA repair.
This PARP inhibitor has demonstrated efficacy in the treatment of certain types of advanced ovarian, breast, and prostate cancers, particularly those with BRCA1 or BRCA2 mutations.
Olaparib is approved for use in various cancer indications and is the subject of extensive research to further optimize its therapeutic applications.
To enhance Olaparib research, the PubCompare.ai platform utilizes AI-driven comparisons to identify the most reproducible and accurate protocols from literature, preprints, and patents.
This streamlines the research process and helps researchers optimize their Olaparib studies, including the use of related compounds like Talazoparib, Rucaparib, and Veliparib.
When conducting Olaparib research, researchers may also explore the use of cell culture media like Fetal Bovine Serum (FBS) and the incorporation of solvents like Dimethyl Sulfoxide (DMSO) to solubilize and deliver the drug.
Additionally, Olaparib may be studied in combination with other anticancer agents, such as Cisplatin, to investigate synergistic effects.
By leveraging the insights and tools provided by PubCompare.ai, researchers can streamline their Olaparib studies, enhance reproducibility, and optimize their research outcomes, ultimately advancing the understanding and therapeutic potential of this PARP inhibitor in the fight against cancer.