Prexasertib

Manufactured by Merck Group

Prexasertib is a laboratory instrument manufactured by Merck Group. It is designed for use in scientific research and analysis. The core function of Prexasertib is to perform advanced analytical tasks, but a detailed description of its intended use or capabilities is not available.

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Lab products found in correlation

Olaparib, by Merck Group (2 mentions) Dimethyl sulfoxide (dmso), by Merck Group (2 mentions) Olaparib, by Selleck Chemicals (2 mentions) Hp β cyclodextrin, by Merck Group (1 mentions) Hydroxyurea hu, by Merck Group (1 mentions) Adh 1, by Merck Group (1 mentions) Adh 1, by MedChemExpress (1 mentions) Rucaparib, by Selleck Chemicals (1 mentions) Prexasertib, by MedChemExpress (1 mentions) Rucaparib, by Merck Group (1 mentions) Dulbecco s modified eagle s medium, by Corning (1 mentions) γh2ax, by Cell Signaling Technology (1 mentions) Rad51, by Cell Signaling Technology (1 mentions) Fancd2, by Cell Signaling Technology (1 mentions) Pf 477736, by Merck Group (1 mentions) P chk1 317, by Cell Signaling Technology (1 mentions) Hct116, by American Type Culture Collection (1 mentions) Penicillin streptomycin, by Corning (1 mentions) 5 iodo 2 deoxyuridine idu, by Merck Group (1 mentions) Ht 29, by American Type Culture Collection (1 mentions)

4 protocols using prexasertib

Targeting Ctdnep1-Deficient Brain Tumors

Cited 1 time

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Ctdnep1-deficient Tumors cells were subcutaneously injected into eight-week-old female athymic BALB/c nude mice or NSG mice. Tumors will be harvested after 6–10 weeks and quantified. 1 × 10⁵ NPCs in a 5 μl with 2 μl matrigel were stereotactically injected into the NSG mouse cerebellum. Animals were monitored weekly and euthanized when they showed signs of brain tumor. The mouse brain tissue with tumor was embedded in paraffin and sectioned at a thickness of 5 μm for H/E and immunohistochemistry assays. Ctdnep1 cKO tumors exhibit the large cell/anaplastic morphology observed in MYC-driven Group 3 MB, which was confirmed by a neuropathologist Dr. Christina Fuller. The NSG mice with Ctdnep1-cKO NPC tumors in the cerebellum were randomized into different groups and administered Prexasertib (15 mg/kg) and/or JQ1 (50 mg/kg) or vehicle (10% DMSO in 10% HP-β-Cyclodextrin, Sigma) on alternating days via intraperitoneal injection for 14 days^{64 (link)}.

Luo Z., Xin D., Liao Y., Berry K., Ogurek S., Zhang F., Zhang L., Zhao C., Rao R., Dong X., Li H., Yu J., Lin Y., Huang G., Xu L., Xin M., Nishinakamura R., Yu J., Kool M., Pfister S.M., Roussel M.F., Zhou W., Weiss W.A., Andreassen P, & Lu Q.R. (2023). Loss of phosphatase CTDNEP1 potentiates aggressive medulloblastoma by triggering MYC amplification and genomic instability. Nature Communications, 14, 762.

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Preparation and Storage of PARP Inhibitors

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Olaparib (#S1060) and rucaparib (#S1098) were purchased from Selleck Chemicals, Houston, TX. Hydroxyurea (HU; #H8627) was from Sigma-Aldrich. ADH-1 (N-cadherin inhibitor; #HY-13541) and prexasertib (CHK1 inhibitor; #HY-18174) were from MedChemExpress (Monmouth Junction, NJ). 100 mM of Olaparib, 10 mM of rucaparib, HU, ADH-1, and prexasertib were prepared as stocks in dimethyl sulfoxide (DMSO; #S-002-M, Sigma-Aldrich, Saint Louis, MO). All drugs were stored in aliquots at −80 °C until use.

Huang T.T., Burkett S.S., Tandon M., Yamamoto T.M., Gupta N., Bitler B.G., Lee J.M, & Nair J.R. (2022). Distinct roles of treatment schemes and BRCA2 on the restoration of homologous recombination DNA repair and PARP inhibitor resistance in ovarian cancer. Oncogene, 41(46), 5020-5031.

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CRC Cell Line Culturing and Compound Characterization

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Human CRC cell lines HCT-116 and HT-29 were acquired from ATCC (Manassas, VA). Both cells were grown in Dulbecco's modified Eagle's medium (Corning, Manassas, VA) supplemented with 10% fetal bovine serum (FBS) (Omega Scientifics, Tarzana, CA) and 1× penicillin/streptomycin (Corning, Manassas, VA). Cell lines were tested for mycoplasma contamination before each experiment. F10 compound was synthesized according to methods described previously [21] (link). 5-FU and Chk1 inhibitors PF-477736 and prexasertib were purchased from Sellechem (Houston, TX). Both the PF-477736 and prexasertib were dissolved in dimethyl sulfoxide (DMSO) (Sigma, St. Louis, MO), whereas F10 was dissolved in sterile H₂O. 5-Chloro-2′-deoxyuridine (CldU) and 5-iodo-2′-deoxyuridine (IdU) were purchased from Sigma (St. Louis, MO) and dissolved in growth media. The following antibodies were used in this study: Santa Cruz Biotechnology (Dallas, TX): FANCD2 (catalog no. sc-20022), GAPDH (catalog no. sc-32233), Chk1 (catalog no. sc-8408), and Rad51 (catalog no. 8349); Cell Signaling (Beverly, MA): pChk1-317 (catalog no. 2344) and γH2AX (catalog no. 2577).

Mani C., Pai S., Papke C.M., Palle K, & Gmeiner W.H. (2018). Thymineless Death by the Fluoropyrimidine Polymer F10 Involves Replication Fork Collapse and Is Enhanced by Chk1 Inhibition. Neoplasia (New York, N.Y.), 20(12), 1236-1245.

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Preparation of Drugs for In Vitro and In Vivo Studies

Cited 2 times

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For in vitro assays, olaparib (#S1060), prexasertib (#S7178), and SRA737 (CCT245737, #S8253) were purchased from Selleck Chemicals. olaparib (100 μM) and 10 μM prexasertib and SRA737 were prepared as stocks in dimethyl sulfoxide (DMSO; #S-002-M, Sigma-Aldrich). All drugs were stored in aliquots at −80°C until use. For in vivo studies, prexasertib mesylate hydrate (prexasertib; #1234015–57-6, InvivoChem LLC) was prepared in 20% CAPTISOL (CyDex Pharmaceuticals Inc.,), whereas olaparib (#V300, InvivoChem LLC) was formulated in phosphate-buffered saline (PBS) containing 10% DMSO and 10% (w/v) 2-hydroxy-propyl-β-cyclodextrin as described previously (18 (link), 58 (link)).

Gupta N., Huang T.T., Nair J.R., An D., Zurcher G., Lampert E.J., McCoy A., Cimino-Mathews A., Swisher E.M., Radke M.R., Lockwood C.M., Reichel J.B., Chiang C.Y., Wilson K.M., Chih-Chien Cheng K., Nousome D, & Lee J.M. (2023). BLM overexpression as a predictive biomarker for CHK1 inhibitor response in PARP inhibitor–resistant BRCA-mutant ovarian cancer. Science translational medicine, 15(701), eadd7872.

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