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    InvivoChem Cat #: V0122
    CAS #: 677338-12-4Purity ≥98%

    Description: PIK-90 is a novel and potent PI3Kα/γ/δ inhibitor with potential anticancer activity. It inhibits PI3Kα/γ/δ with IC50s of 11 nM/18 nM/58 nM, respectively, and is less potent to PI3Kβ. PIK-90 also inhibits DNA-PK with IC50 of 13 nM. Studies demonstrated that PIK-90 induced increased levels of secreted IgE at 1 μmol/L, while it inhibited IgE production at doses of greater than 2 μmol/L. PIk-90 has been reported to block Akt phosphorylation. PIK-90 combined with the CDK2 inhibitor has been demonstrated to induce apoptosis in LN229 PTENWT cells. In addition, PIK-90 combined with siRNA against both CDK1 and CDK2 has shown to induce cell death, whereas PIK-90 combined with siRNA against CDK1 or CDK2 had no apoptotic effect.

    References: J Cell Biol. 2006 Jul 31;174(3):437-45; Proc Natl Acad Sci U S A. 2012 Jul 31;109(31):12722-7. 

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    Molecular Weight (MW)




    CAS No.



    -20℃ for 3 years in powder form

    -80℃ for 2 years in solvent

    Solubility (In vitro)

    DMSO: 0.28 mg/mL (0.79 mM)

    Water:<1 mg/mL

    Ethanol: <1 mg/mL

    Solubility (In vivo)

    1% DMSO+30% polyethylene glycol+1% Tween 80: 15 mg/mL

    Chemical Name

    N-(7,8-dimethoxy-2,3-dihydroimidazo[1,2-c]quinazolin-5-yl)pyridine-3-carboxamide;  PIK90; PIK90; PIK 90.

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    In Vitro

    Kinase Assay: IC50 values are measured using either a standard TLC assay for lipid kinase activity or a high-throughput membrane capture assay. Kinase reactions are performed by preparing a reaction mixture containing kinase, inhibitor (2% DMSO final concentration), buffer (25 mM HEPES, pH 7.4, 10 mM MgCl2), and freshly sonicated phosphatidylinositol (100 μg/mL). Reactions are initiated by the addition of ATP containing 10 μCi of γ-32P-ATP to a final concentration 10 μM or 100 μM, and allowed to proceed for 20 minutes at room temperature. For TLC analysis, reactions are then terminated by the addition of 105 μL 1N HCl followed by 160 μL CHCl3:MeOH (1:1). The biphasic mixture is vortexed, briefly centrifuged, and the organic phase transferred to a new tube using a gel loading pipette tip precoated with CHCl3. This extract is spotted on TLC plates and developed for 3-4 hours in a 65:35 solution of n-propanol:1M acetic acid. The TLC plates are then dried, exposed to a phosphorimager screen, and quantitated. For each compound, kinase activity is typically measured at 10-12 inhibitor concentrations representing two-fold dilutions from the highest concentration tested (100 μM). For compounds showing significant activity, IC50 determinations are repeated two to four times, and the reported value is the average of these independent measurements.


    Cell Assay: For viabilty, cells (87 MG, SF188, SF763, LN229, A1207 and LN-Z3 cells) are seeded in 12-well plates in the presence of PIK-90 for 3 days. Cell viability is determined using a WST-1 assay.

    PIK-90 shows distinct patterns of isoform selectivity to inhibit different subsets of four class I PI3K isoforms. In addition, PIK-90 completely inhibits the fMLP-stimulated phosphorylation of Akt and impairs polarity and chemotaxis in dHL60 cells. PIK-90 exhibits significantly antiproliferative activity by effectively blocking phosphorylation of Akt in six glioma cell lines varying in mutational status at PTEN or p53, including U87 MG, SF188, SF763, LN229, A1207 and LN-Z30 cells. Moreover, PIK-90 induces a modest G0G1 arrest at a concentration (0.5 μM) sufficient to inhibit phosphorylation of Akt substantially. In chronic lymphocytic leukemia (CLL) cells, PIK-90 inhibits chemotaxis to levels that are 57.8% of controls at 1 μM and 56.8% of controls at 10 μM. Consistently, PIK-90 inhibits pseudoemperipolesis to levels that are 74.2% PIK-90 of controls at 1 μM and 57.9% of controls at 10 μM. In addition, PIK-90 also leads to a significant reduction of CLL cell migration into the stromal cell layer and decreases CXCL12-induced actin polymerization.

    In Vivo

    Immediately following insulin treatment, PIK-90 (10 mg/kg) completely protects animals from this insulin-stimulated decline in blood glucose.

    Animal model

    FVB/N female mice are fasted at 9:00 a.m. and then given human insulin or vehicle (PBS) intravenously at noon

    Formulation & Dosage

     Dissolved in DMSO and then diluted in water; 10 mg/kg; i.p.


    [1] Van Keymeulen A, et al. J Cell Biol. 2006, 174(3), 437-445.[2] Knight ZA, et al. Cell. 2006, 125(4), 733-747.

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


    Knight ZA, et al. Cell. 2006, 125(4), 733-747.





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