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    Sapanisertib (INK 128; MLN 0128)
    Sapanisertib (INK 128; MLN 0128)

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    This product is for research use only, not for human use. We do not sell to patients.
    Number: - + Pieces(InventoryPieces)
    InvivoChem Cat #: V0185
    CAS #: 1224844-38-5Purity ≥98%

    Description: Sapanisertib (formerly known as INK-128 and MLN-0128) is a novel, potent, orally bioavailable and selective mTOR inhibitor with IC50 of 1 nM in cell-free assays; it displayed >200-fold less potent to class I PI3K isoforms, and is superior in blocking mTORC1/2 and sensitive to pro-invasion genes (vs Rapamycin). INK128 binds to and inhibits both TORC1 and TORC2 complexes of mTOR, which may result in tumor cell apoptosis and a decrease in tumor cell proliferation.

    References: Nature. 2012 Feb 22;485(7396):55-61; Drug Discov Today Ther Strateg. 2009; 6(2):47-55.

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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: 62 mg/mL (200.4 mM)

    Water: <1 mg/mL

    Ethanol: 2 mg/mL (6.5 mM)

    Solubility (In vivo)

    30% PEG400+0.5% Tween80+5% propylene glycol: 30mg/mL


    MLN-0128; Sapanisertib; TAK-228; TAK 228; TAK228; INK128; INK-128; INK 128; MLN0128; MLN 0128; MLN-0128 

    Chemical Name: 3-(2-amino-5-benzoxazolyl)-1-(1-methylethyl)-1H-pyrazolo[3,4-d]pyrimidin-4-amine


    InChi Code: InChI=1S/C15H15N7O/c1-7(2)22-14-11(13(16)18-6-19-14)12(21-22)8-3-4-10-9(5-8)20-15(17)23-10/h3-7H,1-2H3,(H2,17,20)(H2,16,18,19)

    SMILES Code: NC1=C2C(N(C(C)C)N=C2C3=CC=C(OC(N)=N4)C4=C3)=NC=N1

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    In Vitro

    Kinase Assay: Sapanisertib (INK-128) is a ATP-dependent mTOR1/2 inhibitor with an IC50 of 1 nM for mTOR kinase. Sapanisertib (INK-128) exhibits an enzymatic inhibition activity against mTOR and more than 100-fold selectivity to PI3K kinases.


    Cell Assay: INK 128 exhibits an enzymatic inhibition activity against mTOR and more than 100-fold selectivity to PI3K kinases. As TORC1/2 inhibitor, INK 128 inhibits both the phosphorylation of S6 and 4EBP1, the downstream substrates of TORC1, and selectively inhibits AKT phosphorylation at Ser473, the downstream substrate of TORC2. Furthermore, INK 128 also shows potent inhibition effects on cell lines resistant to rapamycin and pan-PI3K inhibitors.

    In Vivo

    In a ZR-75-1 breast cancer xenograft model, INK 128 shows tumor growth inhibition efficacy at a dose of 0.3 mg/kg/day. Daily, oral administration of INK 128 inhibits angiogenesis and tumor growth in multiplexenograft models.

    Animal model

    Nude Mice

    Formulation & Dosage

    Nude mice are inoculated subcutaneously in the right subscapular region with 5×106 MDA-MB-361 cells. After tumours reach a size of 150-200 mm3, mice are randomLy assigned into vehicle control or treatment groups. Sapanisertib (INK-128) is formulated in 5% polyvinylpropyline, 15% NMP, 80% water and administered by oral gavage at 0.3 mg/kg and 1 mg/kg daily.


    Nature. 2012 Feb 22;485(7396):55-61; Drug Discov Today Ther Strateg. 2009; 6(2):47-55.

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

    INK 128 (MLN0128)

    Ribosome profiling reveals mTOR-dependent specialized translational control of the prostate cancer genome.  2012 Feb 22;485(7396):55-61.

    INK 128 (MLN0128)

    mTOR promotes prostate cancer cell migration and invasion through a translationally regulated gene signature.

    INK 128 (MLN0128)

    TheThe 4EBP1–eIF4E axis controls the post-transcriptional expression of mTOR-sensitive invasion genes.  2012 Feb 22;485(7396):55-61

    INK 128 (MLN0128)

    mTOR hyperactivation augments translation of YB1, MTA1, CD44 and vimentin mRNAs in a subset of pre-invasive prostate cancer cells in vivo.  2012 Feb 22;485(7396):55-61. 

    INK 128 (MLN0128)

    Complete mTOR inhibition by INK128 treatment prevents prostate cancer invasion and metastasis in vivo.  2012 Feb 22;485(7396):55-61. 

    INK 128 (MLN0128)

    INK 128 (MLN0128)

    INK 128 (MLN0128)

    mTOR signal pathway.  2009 Summer;6(2):47-55.


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