Azd0156

Manufactured by MedChemExpress

AZD0156 is a lab equipment product offered by MedChemExpress. It is a chemical compound used for research purposes. The core function of AZD0156 is to serve as a research tool.

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Lab products found in correlation

Oxaliplatin, by Selleck Chemicals (2 mentions) Ceralasertib, by MedChemExpress (2 mentions) 5 fluorouracil, by Selleck Chemicals (2 mentions) Sn 38, by Selleck Chemicals (2 mentions) Adavosertib, by MedChemExpress (2 mentions) Berzosertib, by MedChemExpress (2 mentions) Rabusertib, by MedChemExpress (2 mentions) Nedisertib, by MedChemExpress (2 mentions) Olaparib, by Selleck Chemicals (2 mentions) Mg132, by Merck Group (2 mentions) Olaparib, by MedChemExpress (1 mentions) Ku55933, by ChemScene (1 mentions) Crystal violet methanol solution, by Merck Group (1 mentions)

5 protocols using azd0156

Evaluation of PRMT5 Inhibitor C220 in Vivo

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C220 is a derivative of a published PRMT5 inhibitor (46 ) and was synthesized by Wuxi Apptec. For in vitro assays, it was stored as a 10 mM solution in DMSO. For in vivo assays, C220 was dissolved in a 0.5% methylcellulose, 0.1% Tween-20 solution. C220 was administered as oral gavage once daily for 5 days a week, for a total of 4–6 weeks. AZD0156 and Olaparib were purchased from MedChemExpress and stored as 10 mM DMSO solution.

Pastore F., Bhagwat N., Pastore A., Radzisheuskaya A., Karzai A., Krishnan A., Li B., Bowman R.L., Xiao W., Viny A.D., Zouak A., Park Y.C., Cordner K.B., Braunstein S., Maag J.L., Grego A., Mehta J., Wang M., Lin H., Durham B.H., Koche R.P., Rampal R.K., Helin K., Scherle P., Vaddi K, & Levine R.L. (2020). PRMT5 inhibition modulates E2F1 methylation and gene regulatory networks leading to therapeutic efficacy in JAK2V617F mutant MPN. Cancer discovery, 10(11), 1742-1757.

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Induced Cataract Lens Culture and Atm Inhibitor Treatment

Cited 1 time

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Rats were euthanized by CO₂ asphyxiation and lenses were extracted. All lenses were cultured in 2 mL M199 medium containing 0.1% BSA and 30 mM galactose for 2–4 days using an incubator set at 5% CO₂ and 37°C to induce cataracts as described previously [13 (link)]. Once opacity was induced, lenses were photographed under a microscope and same medium was replaced. At this time, the Atm inhibitors AZD0156 (MedChemExpress) or KU55933 (ChemScene), were dissolved in 16 μL DMSO per lens for final concentrations of 2.5, 5, 10, 20, and 40 μM. For the untreated lenses, vehicle control (16 μL DMSO) was added. Subsequently, lenses were cultured 2–4 days and photographed under a microscope. Control samples without cataracts were incubated for 6 days in 2 mL of M199 medium containing 0.1% BSA and galactose vehicle control (sterile water).

Nagaya M., Kanada F., Takashima M., Takamura Y., Inatani M, & Oki M. (2022). Atm inhibition decreases lens opacity in a rat model of galactose-induced cataract. PLoS ONE, 17(9), e0274735.

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Drug Combination Treatment Protocol

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5-fluorouracil (5-FU; S1209), oxaliplatin (S1224), SN-38 (S4908), and olaparib (AZD2281, Ku-0059436, S1060) were purchased from Selleckchem. Berzosertib (ATRi; HY-13902), ceralasertib (ATRi; HY-19323), rabusertib [CHK1 inhibitor (CHKi); HY-14720], adavosertib [Wee1 inhibitor (Wee1i); HY-10993], AZD0156 [ATM inhibitor (ATMi); HY-100016], and nedisertib [DNA-PK inhibitor (DNA-PKi); HY-101570] were purchased from MedChemExpress, while MG-132 (474790) was purchased from Merck and hydroxyurea (HU; H8627) from Sigma.

Durinikova E., Reilly N.M., Buzo K., Mariella E., Chilà R., Lorenzato A., Dias J.M., Grasso G., Pisati F., Lamba S., Corti G., Degasperi A., Cancelliere C., Mauri G., Andrei P., Linnebacher M., Marsoni S., Siena S., Sartore-Bianchi A., Nik-Zainal S., Di Nicolantonio F., Bardelli A, & Arena S. (2022). Targeting the DNA Damage Response Pathways and Replication Stress in Colorectal Cancer. Clinical Cancer Research, 28(17), 3874-3889.

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Colibactin Sensitivity and Drug Proliferation Assays

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On day 0, cells were plated at different densities in 24-multiwell plates. For colibactin sensitivity assay, the following day cells were infected with colibactin-producing or empty-vector bacteria at indicated MOIs as described above. Following 4 h of infection, residual bacteria were removed and cells were incubated at 37°C 5% CO₂ for 7 days in their respective complete medium supplemented with 20μg/mL gentamicin. For drug proliferation assays, serial dilutions of each drug were added to the cells, which were then incubated at 37°C in 5% CO₂ for 7 days. Following incubation, cells were fixed with 4% paraformaldehyde and stained with 1% Crystal Violet-Methanol solution (Sigma-Aldrich). Crystal Violet was then solubilized with 10% acetic acid and absorbance was quantified at 595nm. Oxaliplatin (S1224), SN-38 (S4908), olaparib (AZD2281, Ku-0059436, S1060), and ATM inhibitor AZD0156 were purchased from MedChemExpress. The sensitivity profile to chemotherapeutic agents shown in Figure 6A was derived from ref. ³³ (link).

Sogari A., Rovera E., Grasso G., Mariella E., Reilly N.M., Lamba S., Mauri G., Durinikova E., Vitiello P.P., Lorenzato A., Avolio M., Piumatti E., Bonoldi E., Aquilano M.C., Arena S., Sartore-Bianchi A., Siena S., Trusolino L., Donalisio M., Russo M., Di Nicolantonio F., Lembo D, & Bardelli A. (2024). Tolerance to colibactin correlates with homologous recombination proficiency and resistance to irinotecan in colorectal cancer cells. Cell Reports Medicine, 5(2), 101376.

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Drug Combination Treatment Protocol

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