Mk 1775

Manufactured by MedChemExpress

Sourced in United States

MK-1775 is a small molecule inhibitor that targets the Wee1 kinase. Wee1 is a regulator of the G2/M cell cycle checkpoint and plays a role in DNA damage response. MK-1775 can be used in biochemical and cell-based assays to study the inhibition of Wee1 kinase activity.

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Lab products found in correlation

Azd7762, by MedChemExpress (2 mentions) Sch772984, by Selleck Chemicals (1 mentions) Ly2606368, by Selleck Chemicals (1 mentions) Nutlin 3a, by MedChemExpress (1 mentions) Panobinostat, by Selleck Chemicals (1 mentions) Nvp bgt226, by Selleck Chemicals (1 mentions) Prexasertib, by MedChemExpress (1 mentions) Pd0166285, by Selleck Chemicals (1 mentions) Ve 821, by Selleck Chemicals (1 mentions) Vx 970, by Selleck Chemicals (1 mentions) Incucyte s3, by Sartorius (1 mentions)

5 protocols using mk 1775

Immune Cell Proliferation Assay

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Poly-2-hydroxyethyl methacrylate (polyHEMA, P3932) and propidium iodide (PI, P4170) were purchased from Sigma-Aldrich. The ERK inhibitor SCH772984 was purchased from SelleckChem (S7101). CFSE dye was purchased from Tonbo Biosciences (10140–976 VWR). The Wee1 inhibitor MK-1775 (HY-10993) and CHK1 inhibitor AZD-7762 (HY-10992) were purchased from MedChem Express.

Neilsen B.K., Frodyma D.E., McCall J.L., Fisher K.W, & Lewis R.E. (2019). ERK-mediated TIMELESS expression suppresses G2/M arrest in colon cancer cells. PLoS ONE, 14(1), e0209224.

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Inhibitors for Cancer Research

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MK1775 (WEE1 inhibitor) was purchased from MedChemExpress. FTD/TPI (TAS‐102) was provided by Taiho Pharmaceutical Co., Ltd. PD0166285 was purchased from AdooQ BioScience. LY2606368 (CHK1 inhibitor) was purchased from Selleck Chemicals. Nutlin‐3a (MDM2 inhibitor) was purchased from MedChemExpress.

Nguyen Vu T.H., Kikuchi O., Ohashi S., Saito T., Ida T., Nakai Y., Cao Y., Yamamoto Y., Kondo Y., Mitani Y., Kataoka S., Kondo T., Katada C., Yamada A., Matsubara J, & Muto M. (2023). Combination therapy with WEE1 inhibition and trifluridine/tipiracil against esophageal squamous cell carcinoma. Cancer Science, 114(12), 4664-4676.

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Pevonedistat and MK-1775 combination therapy

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Pevonedistat was a kind gift from Millennium Pharmaceuticals, Inc. (now Takeda Pharmaceuticals, Cambridge, MA, USA). Pevonedistat was dissolved in DMSO to an initial concentration of 10 mM and stored at −80 °C. For each experiment, the drug was further diluted in phosphate-buffered saline (PBS) to reach the desired final concentration as shown in each figure. The WEE1 inhibitor MK-1775 (300 nm) (MedChemExpress, Monmouth Junction, NJ, USA) was added to cells in culture after 24 h of treatment with pevonedistat, and cells were cultured for an additional 24 h.

Foster J.H., Barbieri E., Zhang L., Scorsone K.A., Moreno-Smith M., Zage P, & Horton T.M. (2021). The Anti-Tumor Activity of the NEDD8 Inhibitor Pevonedistat in Neuroblastoma. International Journal of Molecular Sciences, 22(12), 6565.

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Evaluating Anti-Cancer Drug Combinations

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We adjusted the dosages and the administration schemes for the different compounds (Table S2), using athymic nude six-week-old male mice, in which no tumor was engrafted. Treatments lasted for three weeks and the mice body weight was daily measured to analyze potential toxicity. Carfilzomib and Doxorubicin were obtained from our hospital pharmacy. NVP-BGT226 (S2749), Torin 2 (S2817), and Panobinostat (S1030) were purchased from Selleckchem and MK-1775 (31 (link)) (Adavorsetib, HY-10993) from MedChemExpress.

Fernández-Rodríguez J., Creus-Bachiller E., Zhang X., Martínez-Iniesta M., Ortega-Bertran S., Guha R., Thomas C.J., Wallace M.R., Romagosa C., Salazar-Huayna L., Reilly K.M., Blakely J.O., Serra-Musach J., Pujana M.A., Serra E., Villanueva A., Ferrer M, & Lázaro C. (2022). A high-throughput screening platform identifies novel combination treatments for Malignant Peripheral Nerve Sheath Tumors. Molecular cancer therapeutics, 21(7), 1246-1258.

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High-throughput Screening of DNA Damage Response Inhibitors

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Cells were seeded in a 96-well plate at a density of 1,000 cells per well overnight. The next day, drugs including MK-1775, ceralasertib/AZD6738, CCT245737, AZD7762, prexasertib, CHIR-124 (all from MedChemExpress), Debio 0123, ZN-c3, VE-821, PD0166285, and VX-970 (all from Selleckchem) or DMSO was added. Cells were exposed to the drug for 10–15 days, and cell confluency or nuclei count was measured using an IncuCyte S3 (Sartorius).

Yang Y., Badura M.L., O’Leary P.C., Delavan H.M., Robinson T.M., Egusa E.A., Zhong X., Swinderman J.T., Li H., Zhang M., Kim M., Ashworth A., Feng F.Y., Chou J, & Yang L. (2024). Large tandem duplications in cancer result from transcription and DNA replication collisions. medRxiv.

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