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    InvivoChem Cat #: V0177
    CAS #: 1009298-09-2Purity ≥98%

    Description: AZD8055 is a novel, potent selective, and orally bioavailable ATP-competitive mTOR (mammalian target of rapamycin) inhibitor with potential anticancer activity. It inhibits mTOR with an IC50 of 0.8 nM in MDA-MB-468 cells and has excellent selectivity (∼1,000-fold) against PI3K isoforms and ATM/DNA-PK. As an mTOR inhibitor, AZD-8055 showed potent antineoplastic activity by inhibiting the serine/threonine kinase activity of mTOR, resulting in decreased expression of mRNAs necessary for cell cycle progression, which may induce cell cycle arrest and tumor cell apoptosis. mTOR phosphorylates transcription factors, such as S6K1 and 4E-BP1, which stimulate protein synthesis and regulate cell growth, proliferation, motility, and survival.

    References:  Cancer Res. 2010 Jan 1;70(1):288-98Br J Cancer. 2011 Mar 29;104(7):1116-25. 

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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: 50 mg/mL (107.4 mM)

    Water: <1 mg/mL

    Ethanol: 3 mg/mL (6.4 mM)

    Solubility (In vivo)

    4% DMSO+30% PEG 300+ddH2O: 5 mg/mL


    AZD8055; AZD-8055; AZD 8055; (5-(2,4-bis((3S)-3-methylmorpholin-4-yl)pyrido(2,3-d)pyrimidin-7-yl)-2-methoxyphenyl)methanol.

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    In Vitro

    Kinase Assay: A high-throughput screening cell-based assay is developed using MDA-MB-468 cells to detect mTORC1 and mTORC2 activity. Cells are exposed for 2 hours to increasing concentrations of AZD8055. At the end of the incubation period, cells are fixed, washed, and probed with antibodies against S473 pAkt or against S235/236 phosphorylated S6 (pS6). Levels of phosphorylation are assessed using an Acumen laser scanning cytometer.


    Cell Assay: Cells (U87MG, A549 and H838 cells) are exposed to AZD8055 for 72 to 96 hours and stained for cell nuclei (0.03 mg/mL Hoechst 33342) and acidic vesicles (1 μg/mL acridine orange). Images are captured at 450 and 536 nm on an ArrayScan II platform, and the percentage of acidic vesicles and the number of cells are quantified. For LC3 assessment, cells are exposed to e64d/pepstatin (10 μg/mL) for 30 to 90 min before incubation with AZD8055. Cells are lysed on ice and analyzed by immunoblotting.

    AZD8055 shows low activity (∼1,000-fold) against all PI3K isoforms (α, β, γ, δ) and other members of the PI3K-like kinase family (ATM and DNA-PK). AZD8055 inhibits the phosphorylation of mTORC1 (p70S6K and 4E-BP1) as well as phosphorylation of the mTORC2 (Akt) and downstream proteins. The rapamycin-resistant T37/46 phosphorylation sites on 4E-BP1 can be fully inhibited by AZD8055, resulting in significant inhibition of cap-dependent translation. AZD8055 potently inhibits proliferation in U87MG, A549 and H838 cells with IC50 of 53, 50 and 20 nM, respectively. AZD8055 also induces autophagy and increased LC3-II levels in H838 and A549 cells. AZD8055 decreases AML blast cell proliferation and cell cycle progression, reduces the clonogenic growth of leukemic progenitors and induces caspase-dependent apoptosis in leukemic cells but not in normal immature CD34+ cells. AZD8055 indicates inhibitory against the pediatric preclinical testing program (PPTP) cell lines with IC50 of 24.7 nM and induces significant differences in EFS distribution.

    In Vivo

    AZD8055 inhibits the pS6 and pAkt in U87MG and A549 xenografts at 2.5/10 mg/kg, which leads to tumor growth inhibition. AZD8055 shows significant antitumor activity in many xenografts, including U87MG, BT474c, A549, Calu-3, LoVo, SW620, PC3 and MES-SA at a dose of 10/20 mg/kg. AZD8055 induces ~40% reduction in tumour volume, accompanied by ablation of phosphorylation of Akt, S6K and SGK protein kinases. Administration of AZD8055 (5mg/kg, Bid) and SAHA (100 mg/kg/d) results in complete tumor growth inhibition in PTEN+/−LKB1+/hypo xenografts without side effects on mice by inhibition of mTORC1 and mTORC2 signaling.

    Animal model

    U87MG, BT474c, A549, Calu-3, LoVo, SW620, PC3 and MES-SA U87-MG and A549 are established in pathogen-free, female nude mice (nu/nu:Alpk).

    Formulation & Dosage

    Dissolved in captisol (CyDex, pH 3.0) and diluted to a final captisol concentration of 30% (w/v); 2.5-20 mg/kg; Oral gavage BID


    Cancer Res. 2010 Jan 1;70(1):288-98;  Br J Cancer. 2011 Mar 29;104(7):1116-25. 

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




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