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    NVP-BHG712 (BHG712)
    NVP-BHG712 (BHG712)

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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 #: V1007
    CAS #: 940310-85-0 Purity ≥98%

    Description: NVP-BHG712 (NVP BHG-712; NVP BHG712; BHG-712) is a selective and orally bioavailable EphB4 inhibitor with potential anticancer activity. It inhibits EphB4 with an IC50 of 25 nM; also inhibits other kinases such as c-Raf, c-Src and c-Abl with IC50s of 0.40 μM, 1.27 μM and 1.67 μM, respectively. NVP-BHG712 inhibits EphB4 kinase activity in the low nanomolar range in cellular assays showed high selectivity for targeting the EphB4 kinase when profiled against other kinases in biochemical as well as in cell based assays. BHG-712 shows excellent pharmacokinetic properties and potently inhibits EphB4 autophosphorylation in tissues after oral administration.

    References: Angiogenesis. 2010 Sep;13(3):259-67.

    Related CAS#: 2245892-85-5 (a regioisomer of NVP-BHG712)

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    Molecular Weight (MW)503.48
    CAS No.940310-85-0(NVP-BHG712);
    Storage-20℃ for 3 years in powder form
    -80℃ for 2 years in solvent
    Solubility (In vitro)DMSO: 101 mg/mL (200.6 mM)
    Water: <1 mg/mL
    Ethanol: 3 mg/mL (5.95 mM)
    Solubility (In vivo)NMP+polyethylene glycol 300 (10/90, v/v): 30mg/mL
    SynonymsNVP-BHG712; NVP BHG-712; NVP BHG712; NVP BHG712; NVP BHG-712; NVP BHG 712

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    In Vitro

    In vitro activity: NVP-BHG712 treatment also dose dependently leads to the inhibition of RTK autophosphorylation in stable transfected A375 melanoma cells with EC50 of 25 nM and 4.2 μM for EphB4 and VEGFR2, respectively.

    Kinase Assay: NVP-BHG712 is a specific EphB4 inhibitor with ED50 of 25 nM that discriminates between VEGFR and EphB4 inhibition; also shows activity against c-Raf, c-Src and c-Abl with IC50 of 0.395 μM, 1.266 μM and 1.667 μM, respectively.

    Cell Assay: In Hek293 cells transfected different EphRs, NVP-BHG712 dose-dependently inhibited EphRs autophosphorylation. NVP-BHG712 showed inhibitory preference for EphB4 over EphB2, EphA2, EphB3 and EphA3.

    In VivoIn a growth factor-induced angiogenesis model, NVP-BHG712 (3 mg/kg, p.o) significantly suppresses VEGF stimulated tissue formation and vascularization by inhibiting EphB4 forward signaling. Furthermore, NVP-BHG712 (10 mg/kg/kg, p.o.) potently reverses VEGF enhanced tissue formation and vessel growth. NVP-BHG712 (3 mg/kg, p.o.) shows a long lasting exposure with concentrations around 10 μM in plasma as well as in lung and liver tissue for up to 8 hours, and thus results in a long lasting inhibition of EphB4 kinase activity in mice.
    Animal modelVEGF-mediated angiogenesis in vivo is induced in a growth factor implant model in mice
    Formulation & DosageDissolved in 1-Methyl-2-pyrrolidone (NMP) and then diluted with polyethylene glycol 300 (PEG300) to a final concentration of 10% v/v NMP and 90% v/v PEG300.; 30mg/kg;  Oral gavage

    Angiogenesis. 2010 Sep;13(3):259-67

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


    NVP-BHG712 inhibits multiple Eph receptor kinases in cell based assays. Angiogenesis. 2010 Sep;13(3):259-67. 


    NVP-BHG712 inhibits endogenous EphB4 autophosphorylation in lung tissue of mice and has micromolar exposure in plasma and tissues. Angiogenesis. 2010 Sep;13(3):259-67. 


    Soluble EphB4-Fc protein inhibits VEGF driven tissue growth and angiogenesis. Angiogenesis. 2010 Sep;13(3):259-67. 


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