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    Adavosertib (AZD-1775; MK-1775)
    Adavosertib (AZD-1775; MK-1775)

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    This product is for research use only, not for human use. We do not sell to patients.
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    InvivoChem Cat #: V1588
    CAS #: 955365-80-7Purity ≥98%

    Description: Adavosertib (formerly known as AZD-1775; MK-1775; AZD1775; MK1775) is a novel potent and selective small molecule Wee1 tyrosine kinase inhibitor with potential anticancer activity. It inhibits Wee1 with an IC50 of 5.2 nM in a cell-free assay; Adavosertib hinders G2 DNA damage checkpoint. MK-1775 is a small molecule inhibitor of the tyrosine kinase WEE1 with potential antineoplastic sensitizing activity. MK-1775 selectively targets and inhibits WEE1, a tyrosine kinase that phosphorylates cyclin-dependent kinase 1 (CDC2) to inactivate the CDC2/cyclin B complex.  In vivo, MK-1775 potentiated the anti-tumor efficacy of 5-FU or its prodrug, capecitabine, at tolerable doses. These enhancements were well correlated with inhibition of CDC2 phosphorylation and induction of Histone H3 phosphorylation in tumors. In addition, MK-1775 also potentiated the cytotoxic effects of pemetrexed, doxorubicin, camptothecin, and mitomycin C in vitro. These studies support the rationale for testing the combination of MK-1775 with various DNA-damaging agents in cancer patients.

    References: Mol Cancer Ther. 2009 Nov;8(11):2992-3000;  2010 Apr 1;9(7):514-22. 

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    Molecular Weight (MW)500.6
    CAS No.955365-80-7
    Storage-20℃ for 3 years in powder form
    -80℃ for 2 years in solvent
    Solubility (In vitro)DMSO: 80 mg/mL (159.8 mM)
    Water: <1 mg/mL
    Ethanol: <1 mg/mL
    Solubility (In vivo)2% DMSO+30% PEG 300+5% Tween+ddH2O: 5 mg/mL  
    SynonymsAZD-1775; MK-1775; AZD1775; MK1775; AZD-1775; AZD 1775; MK 1775; adavosertib.

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    In Vitro

    In vitro activity: MK-1775 inhibits Wee1 kinase in an ATP-competitive manner. Compared to Wee1, MK-1775 displays 2- to 3-fold less potency against Yes with IC50 of 14 nM, 10-fold less potency against seven other kinases with >80% inhibition at 1 μM, and >100-fold selectivity over human Myt 1, another kinase that inhibits cyclin-dependent kinase 1 (CDC2) by phosphorylation at an alternative site (Thr14). By abrogating the DNA damage checkpoint via blockade of Wee1 activity in WiDr cells bearing mutated p53, MK-1775 treatment inhibits the basal phosphorylation of CDC2 at Tyr15 (CDC2Y15) with EC50 of 49 nM, and suppresses gemcitabine-, carboplatin- or cisplatin-induced phosphorylation of CDC2 and cell cycle arrest in a dose-dependent manner, with EC50 of 82 nM and 81 nM, 180 nM and 163 nM, as well as 159 nM and 160 nM, respectively. MK-1775 treatment alone at 30-100 nM has no significant antiproliferative effect in WiDr and H1299 cells, whereas MK-1775 at 300 nM, sufficient to inhibit Wee1 by >80%, displays moderate but significant antiproliferative effects by 34.1% in WiDr cells and 28.4% in H1299 cells.

    Kinase Assay: Recombinant human Wee1 is used. Kinase reaction is conducted with 10 μM ATP, 1.0 μCi of [γ-33P]ATP, and 2.5 μg of poly(Lys, Tyr) as a substrate in the presence of increasing concentrations of MK-1775 at 30°C for 30 minutes. Radioactivity incorporated into the substrate is trapped on MultiScreen-PH plates and is counted on a liquid scintillation counter.  

    Cell Assay: Cells (WiDr, NCI-H1299, TOV21G, and HeLa) are treated with or without gemcitabine for 24 hours, then with MK-1775 for an additional 24 hours. Cell viability is determined with a WST-8 kit using SpectraMax. Cellular caspase-3/7 activities are determined with a Caspase-3/7 Glo kit.

    In VivoMK-1775 treatment alone at ~20 mg/kg displays minimal antitumor effects against WiDr xenografts in rats with T/C of 69% at day 3. Antitumor efficacy by MK-1775 alone in the nude rat HeLa-luc and TOV21G-shp53 xenograft models is also moderate.
    Animal modelImmunodeficient nude rats (F344/NJcl-rnu) bearing WiDr, HeLa-luc, or TOV21G-shp53 tumors 
    Formulation & DosageDissolved in a vehicle of 0.5% methylcellulose solution; 20 mg/kg/day; oral gavage

    Mol Cancer Ther. 2009 Nov;8(11):2992-3000.

    These protocols are for reference only. InvivoChem does not independently validate these methods.







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