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Cat. No. M2143
MK-1775 Structure


Size Price Availability Quantity
Free Sample (0.5-1 mg)  USD 0 In stock
5mg USD 80 In stock
10mg USD 130 In stock
50mg USD 330 In stock
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Quality Control
Biological Activity

MK-1775 is a potent and novel Wee1 inhibitor. MK-1775 inhibited CDC2 Y15 phosphorylation in cells, abrogated DNA damaged checkpoints induced by 5-FU treatment, and caused premature entry of mitosis determined by induction of Histone H3 phosphorylation. MK-1775 enhanced the cytotoxic effects of 5-FU in p53-deficient human colon cancer cells. MK-1775 also significantly enhanced the antitumor efficacy of radiation in vivo as shown in tumor growth delay studies, again for p53-defective tumors. In vivo, MK-1775 potentiated the anti-tumor efficacy of 5-FU or its prodrug, capecitabine, at tolerable doses. In addition, MK-1775 also potentiated the cytotoxic effects of pemetrexed, doxorubicin, camptothecin, and mitomycin C in vitro. MK-1775 treatment led to the inhibition of Wee1 kinase and reduced inhibitory phosphorylation of its substrate Cdc2. MK-1775 is currently in Phase I clinical trial in combination with anti-cancer drugs.

Product Citations
Customer Product Validations & Biological Datas
Source Nature (2017). Figure 6. AZD1775 (Abmole Bioscience)
Method oral gavage
Cell Lines Athymic nude immunodeficient mice
Concentrations 60 mg/kg
Incubation Time 1–5 days
Results The mice treated with AZD1775 + VCR + IRN had a better response than those treated with VCR + IRN alone.
Source Nature (2017). Figure 4. AZD1775 (Abmole Bioscience)
Method oral gavage
Cell Lines Athymic nude immunodeficient mice
Concentrations 60 mg/kg
Incubation Time 1–5 days
Results Asterisk indicates those models that had a significant difference in tumour progression for the AZD1775 + IRN + VCR relative to IRN + VCR.
Cell Experiment
Cell lines WiDr and H1299 cells
Preparation method Cell Viability Assay.
Cells were seeded in 96-well plates and treated with gemcitabine for 24 h, then with MK-1775 for an additional 24 h. Cell viability was determined with a WST-8 kit using SpectraMax (Molecular Devices).
Concentrations 0, 30, 100 and 300 nM
Incubation time 24 h
Animal Experiment
Animal models nude rats bearing WiDr Subcutaneous xenograft tumors
Formulation 0.5% methylcellulose solution
Dosages 20mg/kg
Administration p.o.
Conversion of different model animals based on BSA (Value based on data from FDA Draft Guidelines)
Species Mouse Rat Rabbit Guinea pig Hamster Dog
Weight (kg) 0.02 0.15 1.8 0.4 0.08 10
Body Surface Area (m2) 0.007 0.025 0.15 0.05 0.02 0.5
Km factor 3 6 12 8 5 20
Animal A (mg/kg) = Animal B (mg/kg) multiplied by  Animal B Km
Animal A Km

For example, to modify the dose of resveratrol used for a mouse (22.4 mg/kg) to a dose based on the BSA for a rat, multiply 22.4 mg/kg by the Km factor for a mouse and then divide by the Km factor for a rat. This calculation results in a rat equivalent dose for resveratrol of 11.2 mg/kg.

Chemical Information
Molecular Weight 500.61
Formula C27H32N8O2
CAS Number 955365-80-7
Purity 99.89%
Solubility DMSO 80 mg/mL
Storage at -20°C

MK-1775, a novel Wee1 kinase inhibitor, radiosensitizes p53-defective human tumor cells.
Bridges KA, et al. Clin Cancer Res. 2011 Sep 1;17(17):5638-48. PMID: 21799033.

MK-1775, a potent Wee1 inhibitor, synergizes with gemcitabine to achieve tumor regressions, selectively in p53-deficient pancreatic cancer xenografts.
Rajeshkumar NV, et al. Clin Cancer Res. 2011 May 1;17(9):2799-806. PMID: 21389100.

MK-1775, a small molecule Wee1 inhibitor, enhances anti-tumor efficacy of various DNA-damaging agents, including 5-fluorouracil.
Hirai H, et al. Cancer Biol Ther. 2010 Apr 1;9(7):514-22. PMID: 20107315.

Small-molecule inhibition of Wee1 kinase by MK-1775 selectively sensitizes p53-deficient tumor cells to DNA-damaging agents.
Hirai H, et al. Mol Cancer Ther. 2009 Nov;8(11):2992-3000. PMID: 19887545.

Abmole Inhibitor Catalog 2017

Keywords: MK-1775, AZD1775 supplier, Wee1, inhibitors

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