1. Cell Cycle/DNA Damage
  2. Wee1

MK-1775 (Synonyms: AZD-1775; AZD1775; AZD 1775)

Cat. No.: HY-10993 Purity: 98.96%
Handling Instructions

MK-1775 is a potent Wee1 inhibitor with IC50 of 5.2 nM.

For research use only. We do not sell to patients.
MK-1775 Chemical Structure

MK-1775 Chemical Structure

CAS No. : 955365-80-7

Size Price Stock Quantity
Free sample   Apply now  
10 mM * 1 mL in DMSO $77 In-stock
5 mg $70 In-stock
10 mg $90 In-stock
50 mg $250 In-stock
100 mg $450 In-stock
200 mg   Get quote  
500 mg   Get quote  

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  • Biological Activity

  • Protocol

  • Technical Information

  • Purity & Documentation

  • References


MK-1775 is a potent Wee1 inhibitor with IC50 of 5.2 nM.

IC50 & Target

IC50: 5.2 nM (Wee1)

In Vitro

MK-1775 enhances the cytotoxic effects of 5-FU in p53-deficient human colon cancer cells. MK-1775 inhibits CDC2 Y15 phosphorylation in cells, abrogates DNA damaged checkpoints induced by 5-FU treatment, and causes premature entry of mitosis determined by induction of Histone H3 phosphorylation[1]. MK-1775 abrogates the radiation-induced G₂ block in p53-defective cells but not in p53 wild-type lines[2]. The combination of gemcitabine with MK-1775 produces robust anti-tumor activity and remarkably enhances tumor regression response (4.01 fold) compared to gemcitabine treatment in p53-deficient tumors[3].

In Vivo

In vivo, MK-1775 potentiates the anti-tumor efficacy of 5-FU or its prodrug, capecitabine, at tolerable doses[1]. MK-1775 (60 mg/kg twice daily, p.o.) enhances H1299 xenograft tumor response to fractionated radiotherapy[2]. MK-1775 (30 mg/kg. p.o.) regresses tumor growth in PANC198, PANC215 and PANC185 as compared to GEM treated mice[3].

Clinical Trial
Sponsor Condition Start Date Phase
The University Health Network Metastatic head and neck cancer 2013-09-30 Phase 2
The University Health Network Squamous cell carcinoma 2013-09-30 Phase 2
National Cancer Institute Advanced solid tumor 2013-03-31 Phase 2
Netherlands Cancer Institute Ovary tumor 2010-07-31 Phase 2
Merck & Co Inc Ovary tumor 2011-07-31 Phase 2
Merck & Co Inc Uterine cervix tumor 2010-05-31 Phase 2
Preparing Stock Solutions
Concentration Volume (DMSO) Mass 1 mg 5 mg 10 mg
1 mM 1.9976 mL 9.9880 mL 19.9760 mL
5 mM 0.3995 mL 1.9976 mL 3.9952 mL
10 mM 0.1998 mL 0.9988 mL 1.9976 mL
Cell Assay

Total protein is extracted from the cell pellet using a lysis solution containing 50 mM HEPES (pH 7.9), 0.4 mol/L NaCl, and 1 mM EDTA and fortified with 10 µL/mL phosphatase inhibitor cocktail 1, 10 µL/mL phosphatase inhibitor cocktail 2, 10 µL/mL protease inhibitor, and 1% NP-40. Protein concentration of the lysates is determined by the Bio-Rad protein assay. Equal amounts of protein are separated by 12% SDS-PAGE and transferred to an Immobilon membrane. Nonspecific binding sites on the membrane are blocked in 5% nonfat dry milk in Tris (20 mM)-buffered saline (150 mM, pH 7.4) with 0.1% Tween (TBS-T). Protein signals are detected by incubating the membrane in primary antibody in 5% nonfat dry milk overnight at 4°C, followed by a 45-min incubation in the appropriate peroxidase-conjugated secondary antibody. The membrane is then developed by enhanced chemiluminescence with ECL plus Western Blotting Detection Reagents on a Typhoon 9400 scanner.

Animal Administration

Tumor xenografts are produced in the leg by im inoculation of 1×106 Calu-6 cells in 10 µL. Irradiation and MK-1775 treatment are started when tumors reach 8 mm diameter and continue for 5 days. Gamma-rays are delivered locally to the tumor-bearing legs of unanesthetized mice using a small-animal irradiator consisting of two parallel-opposed 137Cs sources, at a dose rate of 5 Gy/min. Tumors are irradiated twice daily separated by 6 h. MK-1775 is given by gavage in 0.1 mL volumes 1 h before and 2 h after the first daily radiation dose.







Powder -20°C 3 years
  4°C 2 years
In solvent -80°C 6 months
  -20°C 1 month

Room temperature in continental US; may vary elsewhere

Solvent & Solubility

10 mM in DMSO

Purity: 98.96%

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