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    InvivoChem Cat #: V2655
    CAS #: 1821496-27-8Purity ≥98%

    Description: BDA-366 is a potent and selective small-molecule antagonist of the Bcl2-BH4 domain, it binds to BH4 with high affinity and selectivity. The BH4 domain of Bcl2 is required for its antiapoptotic function, thus constituting a promising anticancer target. BDA-366-Bcl2 binding induces conformational change in Bcl2 that abrogates its antiapoptotic function, converting it from a survival molecule to a cell death inducer. BDA-366 suppresses growth of lung cancer xenografts derived from cell lines and patient without significant normal tissue toxicity at effective doses. mTOR inhibition upregulates Bcl2 in lung cancer cells and tumor tissues from clinical trial patients. Combined BDA-366 and RAD001 treatment exhibits strong synergy against lung cancer in vivo. Development of this Bcl2-BH4 antagonist may provide a strategy to improve lung cancer outcome.

    ReferencesOncotarget. 2016 May 10;7(19):27753-63; Cancer Cell. 2015 Jun 8;27(6):852-63. 

    Related CAS#:1909226-00-1

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    Molecular Weight (MW)423.5 
    CAS No.1821496-27-8
    Storage-20℃ for 3 years in powder form
    -80℃ for 2 years in solvent
    Solubility (In vitro)DMSO: 84 mg/mL (198.3 mM)
    Water: <1 mg/mL
    Ethanol: 5 mg/mL (11.8 mM) 
    SMILES Code CCN(CC)C[[email protected]@H](O)CNC1=CC=C(NC[[email protected]@H]2OC2)C3=C1C(C4=C(C3=O)C=CC=C4)=O
    Synonyms BDA-366; BDA 366; BDA366.

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    In Vitro

    In vitro activity: BDA-366 induces robust apoptosis in MM(Multiple myeloma) cell lines and primary MM cells by inducing BCL2 conformational change. BDA-366 induces a conformational change in the BCL2 molecule that converts it to a death protein, and inhibits lung cancer growth in vitro and in vivo. BDA-366 did not bind to other Bcl2 family members, including Bcl-XL, Mcl-1, or Bfl-1/A1, indicating the specificity of its Bcl2 binding. BDA-366 induces apoptotic cell death in a Bax-dependent manner and induces calcium (Ca2+) release via inhibition of Bcl2/IP3R interaction.

    Kinase Assay: BDA-366 is a potent and selective small-molecule antagonist of the Bcl2-BH4 domain, it binds to BH4 with high affinity and selectivity. The BH4 domain of Bcl2 is required for its antiapoptotic function, thus constituting a promising anticancer target. BDA-366 induced conformational change of BCL2 that exposed the BH3 domain, resulting in abrogation of its prosurvival function and conversion of BCL2 to a prodeath protein. In non-small cell lung cancer (NSCLC) and small cell lung cancer (SCLC) cells, BDA-366 selectively bound to BCL2 with high affinity. BDA-366 induced apoptosis by BCL2-dependent BAX activation and cytochrome c release. In H460 cells, BDA-366 reduced Bcl2/IP3R binding, which then increased Ca2+ release. 

    Cell Assay: Human MM cell lines RPMI8226 and U266 were treated with BDA366 at increasing concentrations (0, 0.1, 0.25, 0.5μM) for 48hr. Cells were harvested, stained with Annexin V and propidium iodide (PI), and subjected to FACS analysis. Apoptotic cells were gated on the Annexin V positive population. Annexin V+PI− cells were early apoptotic cells, Annexin+PI+ cells were late apoptotic cells, and Annexin−PI+ cells were necrotic cells.

    In VivoDelivery of BDA-366 substantially suppressed the growth of human MM xenografts in NOD-scid/IL2Rγ null mice, without significant cytotoxic effects on normal hematopoietic cells or body weight. Also, BDA-366 suppresses lung cancer growth via induction of apoptosis in animal models. The BH4 antagonist BDA-366 exhibits potent efficacy against human lung cancer in vivo without platelet reduction. 
    Animal modelNSG mice 
    Formulation & DosageDissolved in DMSO, diluted in PBS; 10 mg/kg; i.p.
    ReferencesOncotarget. 2016 May 10;7(19):27753-63; Cancer Cell. 2015 Jun 8;27(6):852-63.  

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


    BDA-366 targets the BH4 domain of Bcl2 and potently suppresses lung cancer cell growth.  2015 Jun 8;27(6):852-63. 


    BDA-366 induces Bcl2 conformational change via exposure of its BH3 domain, leading to conversion of Bcl2 from a survival into a killer molecule.  2015 Jun 8;27(6):852-63. 


    BDA-366 potently represses lung cancer in vivo. 2015 Jun 8;27(6):852-63. 


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