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    Tyrphostin AG 1296
    Tyrphostin AG 1296

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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 #: V0574
    CAS #: 146535-11-7Purity ≥98%

    Description: Tyrphostin AG 1296 (AG-1296) is a novel, potent, selective and ATP-competitive inhibitor of PDGFR with potential antitumor activity. It inhibits PDGFR with IC50 of 0.3-0.5 μM, it has no activity against EGFR. Tyrphostin AG 1296 acts by binding to PDGFR, which causes a conformational change at the ATP-binding site. In an in vitro assay, it potently inhibits the ligand-induced autophosphorylation of PDGF receptor in Swiss 3T3 cell membranes. Tyrphostin AG 1296 does not affect the EGF receptor when the concentration is up to 100μM. Tyrphostin AG 1296 also inhibits the mitogenesis induced by PDGF but not EGF or insulin. It reversibly inhibits PDGF-induced DNA synthesis with a mean IC50 value of 1.5μM. 

    References: Cancer Res. 1994 Dec 1;54(23):6106-14; Biochemistry. 1997 May 27;36(21):6260-9.

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    Molecular Weight (MW)266.29
    CAS No.146535-11-7
    Storage-20℃ for 3 years in powder form
    -80℃ for 2 years in solvent
    Solubility (In vitro)DMSO: 6 mg/mL (22.5 mM)
    Water: <1 mg/mL
    Ethanol: <1 mg/mL
    Solubility (In vivo)

    Chemical Name: 2-Phenyl-6,7-dimethoxyquinoxaline ; 6,7-Dimethoxy-2-phenylquinoxaline


    InChi Code: InChI=1S/C16H14N2O2/c1-19-15-8-12-13(9-16(15)20-2)18-14(10-17-12)11-6-4-3-5-7-11/h3-10H,1-2H3

    SMILES Code: COC1=C(OC)C=C2N=CC(C3=CC=CC=C3)=NC2=C1

    SynonymsAG 1296; AG1296; AG-1296; tyrphostin AG1296.

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    In Vitro

    In vitro activity: AG 1296 inhibits selectively the PDGF receptor kinase and the PDGF dependent DNA synthesis in Swiss 3T3 cells and in porcine aorta endothellal cells with 50% inhibitory concentrations below 5 and 1μM, respectively. AG1296 inhibits FGFR and c-Kit with IC50 of 12.3 μM and 1.8 μM in Swiss 3T3 cells. AG1296 potently inhibits signaling of human PDGF -α and -β receptors but has no effect on autophosphorylation of the VEGFR KDR or on DNA synthesis induced by VEGF in porcine aortlc endothelial cells. Treatment by AG1296 reverses the transformed phenotype of sis-transfected NIH 3T3 cells but has no effect on src-transformed NIH3T3 cells. AG1296 is an ATP-competitive inhibitor. AG1296 interferes neither with PDGF binding nor with PDGF receptor dimerization while it abolishes PDGF receptor autophosphorylation. Thus, AG1296 is a pure inhibitor of the catalytic activity of the receptor tyrosine kinase.

    Kinase Assay: Membranes are prepared from confluent cultures of Swiss 3T3 cells as described. For measuring receptor autophosphorylation, 10μg membrane protein per assay are incubated for 20 min on ice in the presence of 1.2μg/mL EGF or 2μg/mL PDGF, or both; 50 mM Hepes (pH 7.5); and 3 mM MnCl2 in a volume of 45μl. In order to test the effects of tyrphostins, these are added in a volume of 0.5 μl (in DMSO; final concentration, 0.5%) 15 min before addition of the growth factors. Phosphorylation is initiated by addition of [γ-32P]ATP and terminated after 2 min by addition of 10μL of a solution containing 6% SDS, 30%β-mercatoethanol, 40% glycerol, and 0.5 mg/mL bromophenol blue. The samples are heated for 5 min at 95 ℃ and subjected to SDS-PAGE using 10% acrylamide gels. The gels are stained and dried and subjected to autoradiographic analysis.

    Cell Assay: Swiss 3T3 Cells are seeded in 24-well plates (5000 cells/well) in DMEM/10% FCS. On the next day the medium is changed to DMEM/2% FcS with or without growth factors and tyrphostins are added as indicated. Three days later the cells are counted in a hemocytometer

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    Cancer Res. 1994 Dec 1;54(23):6106-14; Biochemistry. 1997 May 27;36(21):6260-9.

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

    Tyrphostin AG 1296


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