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    SC66
    SC66

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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 #: V0074
    CAS #: 871361-88-5Purity ≥98%

    Description: SC66 is a novel, potent and allosteric inhibitor of AKT with potential anticancer activity, it reduces cell viability in a dose- and time-dependent manner, inhibits colony formation and induces apoptosis in hepatocellular carcinoma (HCC) cells. SC66 exhibits a dual-inhibitory function toward AKT activity with IC50 values of 0.77, 2.85 and 0.47 μg/ml in HepG2, Huh7 and Hep3B cells, respectively. SC66 reduces cell viability in a dose- and time-dependent manner, it also inhibits colony formation and induces apoptosis in hepatocellular carcinoma (HCC) cells.  SC66 treatment led to a reduction in total and phospho-AKT levels. SC66 induced the production of reactive oxygen species (ROS) and DNA damage. SC66 significantly potentiated the effects of both conventional chemotherapeutic and targeted agents, doxorubicin and everolimus, respectively. In vivo, SC66 inhibited tumor growth of Hep3B cells in xenograft models, with a similar mechanism observed in the in vitro model. SC66 had antitumor effects on HCC cells.

    References:  2015 Jan 30;6(3):1707-22.


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    Molecular Weight (MW) 276.33
    Formula C18H16N2O 
    CAS No. 871361-88-5 
    Storage-20℃ for 3 years in powder form
    -80℃ for 2 years in solvent
    Solubility (In vitro)DMSO: >30 mg/mL
    Water: N/A
    Ethanol: N/A
    Chemical Name (2E,6E)-2,6-bis(pyridin-4-ylmethylene)cyclohexanone
    Synonyms SC-66, SC66, SC 66
    SMILES Code O=C1/C(CCC/C1=C\C2=CC=NC=C2)=C/C3=CC=NC=C3


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    In Vitro

    In vitro activity: SC66 is a novel, potent and allosteric inhibitor of AKT, it displays a dual-inhibitory function toward AKT activity with IC50 values of 0.77, 2.85 and 0.47 μg/ml in HepG2, Huh7 and Hep3B cells, respectively. SC66 reduces cell viability in a dose- and time-dependent manner, it also inhibits colony formation and induces apoptosis in hepatocellular carcinoma (HCC) cells.  SC66 treatment led to a reduction in total and phospho-AKT levels. SC66 induced the production of reactive oxygen species (ROS) and DNA damage. SC66 significantly potentiated the effects of both conventional chemotherapeutic and targeted agents, doxorubicin and everolimus, respectively. In vivo, SC66 inhibited tumor growth of Hep3B cells in xenograft models, with a similar mechanism observed in the in vitro model. SC66 had antitumor effects on HCC cells.

      

    Cell Assay: Cells  are seeded into each well (5 ×103/well) of 96-well microtiter plates and then incubated overnight. At time 0, the medium is replaced with fresh complete medium and different doses of SC66 are added. Cells are cultured for 24, 48 and 72 hours. At the end of treatment, MTS assays are performed using the CellTiter Aqueous OneSolution kit. Cell viability is expressed as a percentage of the absorbance measured in the control cells. Values are expressed as means±SD of three separate experiments, each performed in triplicate

    In Vivo

    Male nude athymic mice (Fox1 nu/nu) aged 4 weeks were obtained from Harlan and allowed to acclimatize for 1 week. Suspensions of 10 × 106 Hep3B cells in 0.2 ml of PBS were inoculated into the right flank of the animal. When tumors became palpable (around 150 mm3), the mice were randomly divided into three groups of 6 animals each, with the various tumor volumes equally distributed among the three groups. Two groups of mice were treated twice a week with 15 and 25 mg/Kg SC66 suspended in DMSO, further diluted in a solution of 25% ethanol and administered via i.p. injection. The control group received the vehicle alone. Tumor volumes were determined twice a week using calipers. Primary tumor volumes were calculated with the formula: v = length × (width)2/2. Mice were euthanized by cervical dislocation when the tumor burden exceeded 10% of animal body weight, or when tumor ulcerated or other conditions of morbidity were ascertained, in conformity with institutional guidelines which are in compliance with national (D.L., 116 G.U., Suppl.40; 18 February 1992) and international laws and policies (ECC Council Directive 86/609, OJ L358.1, 12 December 1987). This study was authorized by the Italian Ministry of Health (D.M. n. 39/2014-B).

    Animal model

    Male nude athymic mice

    Formulation & Dosage

    15 and 25 mg/Kg SC66 suspended in DMSO; i.p.

    References

      2015 Jan 30;6(3):1707-22.


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

    SC66

    SC66 is cytotoxic to HCC cell lines.  2015 Jan 30;6(3):1707-22.


    SC66

    SC66 induces apoptosis in HCC cell lines.  2015 Jan 30;6(3):1707-22.

    SC66

    Effects of SC66 on the phosphorylation status of critical components of the cellular signaling pathway.  2015 Jan 30;6(3):1707-22.

    SC66

    SC66 induces anoikis.  2015 Jan 30;6(3):1707-22.

    SC66

    SC66 induces ROS production.  2015 Jan 30;6(3):1707-22.

    SC66

    The antioxidant NAC reverts SC66-induced anoikis, cell growth and AKT signaling inhibition.  2015 Jan 30;6(3):1707-22.

    SC66

    SC66 significantly reduced cell viability in combination with doxorubicin and everolimus in Hep3B cells.  2015 Jan 30;6(3):1707-22.



    SC66

    The effect of SC66 on xenograft models of Hep3B cells.  2015 Jan 30;6(3):1707-22.



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