Olaparib

Manufactured by Calibre Scientific

Sourced in Germany

Olaparib is a small molecule inhibitor that targets the PARP (Poly(ADP-ribose) polymerase) enzyme, which is involved in the repair of DNA damage. It is used as a laboratory research tool for studying the PARP pathway and its role in cellular processes.

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Lab products found in correlation

Niraparib, by Selleck Chemicals (1 mentions) Pamiparib, by Selleck Chemicals (1 mentions) Veliparib, by Selleck Chemicals (1 mentions) Topotecan, by Apexbio (1 mentions) Dimethyl sulfoxide (dmso), by Merck Group (1 mentions) Metformin, by Merck Group (1 mentions) Zvad fmk, by Bachem (1 mentions)

4 protocols using olaparib

Olaparib and Carboplatin Cytotoxicity in PBLs

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To assess the response to the PARP inhibitor olaparib (Biozol, Eching, Germany), PBLs were treated with various olaparib concentrations (0.5–512 μmol/L) or carboplatin (0.125–2048 µmol/L) for 24 hr and subsequently re‐cultivated in fresh medium for 24 hr. Cell viabilities after the different treatments were determined in duplicate using the 3‐(4,5‐dimethylthiazol‐2‐yl)‐2,5‐diphenyltetrazolium bromide (MTT) assay as described (Deniz, 2017).

Keupp K., Hampp S., Hübbel A., Maringa M., Kostezka S., Rhiem K., Waha A., Wappenschmidt B., Pujol R., Surrallés J., Schmutzler R.K., Wiesmüller L, & Hahnen E. (2019). Biallelic germline BRCA1 mutations in a patient with early onset breast cancer, mild Fanconi anemia‐like phenotype, and no chromosome fragility. Molecular Genetics & Genomic Medicine, 7(9), e863.

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Translational Drug Library Screening

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The following compounds were used: entinostat (Biomol GmbH, M4693-15A.25), idasanutlin (TargetMol; T6254), olaparib (BIOZOL; S1060), ribociclib (supplier), selinexor (BioCat; T6106-TM), vinblastinesulfate (Selleckchem; S4505), doxorubicin in 0.9% NaCl (UKHD pharmacy), niraparib (Selleckchem; S2741), pamiparib (Selleckchem; S8592), veliparib (Selleckchem; S1004). The translational drug library for initial drug selection comprised 74 compounds [19 (link)].

Vollmer J., Ecker J., Hielscher T., Valinciute G., Ridinger J., Jamaladdin N., Peterziel H., van Tilburg C.M., Oehme I., Witt O, & Milde T. (2023). Class I HDAC inhibition reduces DNA damage repair capacity of MYC-amplified medulloblastoma cells. Journal of Neuro-Oncology, 164(3), 617-632.

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Evaluating Tumor Cell Viability

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Tumor cell lines MB 594, MB 794, MB 1197, and control cell lines NSPC1 and NSCP2 were plated in 6-well plate for 10 h and then treated either with 10 µM B02 (Sigma-Aldrich, SML0364) or 10 µM Ri1 (Merck Millipore, 553514) or 5 µM Olaparib (Biozol, AZD2281) or 100 nM Topotecan (Apex Bio, B4982) or a combination of B02, Olaparib and Topotecan or a combination of Ri1, Olaparib and Topotecan at the above-mentioned concentrations for 24 h, 48 h, or 72 h. For each time point, cell viability was measured by cell viability analyzer Vi-Cell XR (Beckman Couter).

Ratnaparkhe M., Wong J.K., Wei P.C., Hlevnjak M., Kolb T., Simovic M., Haag D., Paul Y., Devens F., Northcott P., Jones D.T., Kool M., Jauch A., Pastorczak A., Mlynarski W., Korshunov A., Kumar R., Downing S.M., Pfister S.M., Zapatka M., McKinnon P.J., Alt F.W., Lichter P, & Ernst A. (2018). Defective DNA damage repair leads to frequent catastrophic genomic events in murine and human tumors. Nature Communications, 9, 4760.

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Olaparib, zVAD-fmk, and Metformin Treatments

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Olaparib (Tocris/Biozol, Eching, Germany) was dissolved at 100 mM in DMSO (Sigma-Aldrich, Taufkirchen, Germany) and used at 100 nM in culture medium. zVAD-fmk (Bachem, Bubendorf, Switzerland) was dissolved at 20 mM in DMSO/ethanol (Sigma-Aldrich) and used at 50 µM final concentration in culture medium. Metformin (Sigma-Aldrich) was reconstituted to 500 mM in phosphate-buffered saline (PBS) and diluted to 5 mM in culture medium. Drugs were applied during medium change directly before irradiation and were not removed until the end of the experiment.

Schoetz U., Klein D., Hess J., Shnayien S., Spoerl S., Orth M., Mutlu S., Hennel R., Sieber A., Ganswindt U., Luka B., Thomsen A.R., Unger K., Jendrossek V., Zitzelsberger H., Blüthgen N., Belka C., Unkel S., Klinger B, & Lauber K. (2021). Early senescence and production of senescence-associated cytokines are major determinants of radioresistance in head-and-neck squamous cell carcinoma. Cell Death & Disease, 12(12), 1162.

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