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    N-deacetylated BMS-202
    N-deacetylated BMS-202

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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 #: V3255
    CAS #: 1675203-84-5 (BMS-202)Purity ≥98%

    Description: N-deacetylated BMS-202, the deacetylated product of BMS-202 (also known as PD1-PDL1 inhibitor 2, BMS 202, BMS202), is a inhibitor of the PD-1 (Programmed death- 1)/PD-Ll (Programmed death-ligand 1) protein/protein interaction with potential anticancer activities. BMS-202 inhibits PD-1/PD-Ll interaction, and may augment therapeutic immune response to various histologically distinct tumors. Blockade of the PD-1/PD-Ll ligation using antibodies to PD-Ll has been shown to restore and augment T cell activation in many system. Structural basis for blocking the PD-1/PD-L1 interaction by small molecules is illustrated with the compound BMS-202 that binds to and induces dimerization of PD-L1.

    References:  WO/2015034820 A1


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    Molecular Weight (MW)377.48
    FormulaC23H27N3O2
    CAS No.1675203-84-5 (BMS-202)
    Storage-20℃ for 3 years in powder form
    -80℃ for 2 years in solvent
    Solubility (In vitro)DMSO: >33 mg/mL  
    Water:  
    Ethanol:  
    SMILES CodeNCCNCC1=CC=C(OCC2=C(C)C(C3=CC=CC=C3)=CC=C2)N=C1OC
    Chemical NameN-(2-(((2-methoxy-6-((2-methyl-[1,1'-biphenyl]-3-yl)methoxy)pyridin-3-yl)methyl)amino)ethyl)acetamide (BMS-202)


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    In VitroIn Vitro activity: N-deacetylated BMS-202, the deacetylated product of BMS-202 (also known as PD1-PDL1 inhibitor 2, BMS 202, BMS202), is a inhibitor of the PD-1 (Programmed death- 1)/PD-Ll (Programmed death-ligand 1) protein/protein interaction with potential anticancer activities. BMS-202 inhibits PD-1/PD-Ll interaction, and may augment therapeutic immune response to various histologically distinct tumors. Blockade of the PD-1/PD-Ll ligation using antibodies to PD-Ll has been shown to restore and augment T cell activation in many system. 



    Kinase Assay: All binding studies are performed in an HTRF assay buffer consisting of dPBS supplemented with 0.1% (with v) bovine serum albumin and 0.05% (v/v) Tween-20. For the PD-l-Ig/PD-Ll-His binding assay, inhibitors are pre-incubated with PD-Ll-His (10 nM final) for 15 m in 4 μL of assay buffer, followed by addition of PD-l-Ig (20 nM final) in 1 μL of assay buffer and further incubation for 15 m. PD-L1 from either human, cyno, or mouse are used. HTRF detection is achieved using europium crypate-labeled anti- Ig (1 nM final) and allophycocyanin (APC) labeled anti-His (20 nM final). Antibodies are diluted in HTRF detection buffer and 5 μL is dispensed on top of binding reaction. The reaction mixture is allowed to equilibrate for 30 minutes and signal (665 nm/620 nm ratio) is obtained using an En Vision fluorometer. Additional binding assays are established between PD-1-Ig/PD-L2-His (20, 5 nM, respectively), CD80-His/PD-Ll-Ig (100, 10 nM, respectively) and CD80-His/CTLA4-Ig (10, 5 nM, respectively). 


    Cell Assay: The programmed death-1/programmed death-ligand 1 (PD-1/PD-L1) interaction plays a dominant role in the suppression of T cell responses, especially in a tumor microenvironment, protecting tumor cells from lysis. PD-1/PD-L1 inhibitor 2 is reported to prevent the interaction of PD-L1 with PD-1 with an IC50 value of 18 nM.

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    ReferencesNat Rev Cancer. 2012 Mar 22;12(4):252-64; WO 2015034820 A1


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

    N-deacetylated BMS-202

    Structural Biology of the Immune Checkpoint Receptor PD-1 and Its Ligands PD-L1/PD-L2.  2017 Aug 1;25(8):1163-1174.

     

    N-deacetylated BMS-202

    New Directions in Designing the Therapeutics Targeting the PD-1/PD-L1 Interaction.  2017 Aug 1;25(8):1163-1174.

     N-deacetylated BMS-202


    Structural Basis of the PD-1/PD-L1 (PD-L2) Interaction.  2017 Aug 1;25(8):1163-1174.

     N-deacetylated BMS-202


     2017 Jul 13;60(13):5857-5867.

     

    N-deacetylated BMS-202

     2017 Jul 13;60(13):5857-5867.

    N-deacetylated BMS-202

     2017 Jul 13;60(13):5857-5867. 


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