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    InvivoChem Cat #: V0676
    CAS #: 260415-63-2Purity ≥98%

    Description: PD173955 (PD-173955), a src-selective tyrosine kinase inhibitor, is a novel and potent Bcr-Abl inhibitor with potential anticancer activity. It inhibits Bcr-Abl with an IC50 of 1-2 nM, it also inhibits Src activity with IC50 of 22 nM. 

    References: Cancer Res. 2002 Aug 1;62(15):4244-55; Cancer Res. 1999 Dec 15;59(24):6145-52.

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    Molecular Weight (MW)443.35
    CAS No.260415-63-2
    Storage-20℃ for 3 years in powder form
    -80℃ for 2 years in solvent
    Solubility (In vitro)DMSO: 15 mg/mL (33.8 mM)
    Water:<1 mg/mL
    Ethanol:<1 mg/mL
    Other infoChemical Name: 6-(2,6-dichlorophenyl)-8-methyl-2-((3-(methylthio)phenyl)amino)pyrido[2,3-d]pyrimidin-7(8H)-one
    InChi Code: InChI=1S/C21H16Cl2N4OS/c1-27-19-12(9-15(20(27)28)18-16(22)7-4-8-17(18)23)11-24-21(26-19)25-13-5-3-6-14(10-13)29-2/h3-11H,1-2H3,(H,24,25,26)
    SMILES Code: O=C1C(C2=C(Cl)C=CC=C2Cl)=CC3=CN=C(NC4=CC=CC(SC)=C4)N=C3N1C 
    SynonymsPD 173955; PD173955; PD-173955

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    In Vitro

    In vitro activity: PD173955 potently inhibits Bcr-Abl-dependent cell growth with IC50 of 2-35 nM in Bcr-Abl-positive cell lines, about 100- to 200-fold more sensitive than in Bcr-Abl-negative cell lines. PD173955 also inhibits kit ligand-dependent proliferation of M07e cells with IC50 of 40 nM, by inhibition of kit ligand-dependent c-kit autophosphorylation. In addition, PD173955, as a Src inhibitor, potently inhibits mitotic progression during early mitosis in cells of all types and induces varying degrees of apoptotic cell death.

    Kinase Assay: Bcr-Abl complexed to SHIP2 is immunoprecipitated from cell lysates of K562 cells maintained in log-phase culture conditions. Complexes are collected on protein A-Sepharose, and complexes are washed three times in lysis buffer and then washed twice in abl kinase buffer [50 mM Tris (pH 8.0), 10 mM MgCl2, 1 mM DTT, 2 mM p-nitrophenylphosphate, and 2 μM ATP; New England Biolabs Buffer and protocol]. Kinase assays are performed with 10 μM [γ-32P]ATP/sample for 15–60 min at 30°C in the presence or absence of the indicated concentrations of drug. The reaction is stopped by the addition of SDS-PAGE sample buffer and heated at 100°C for 10 min. Proteins are separated on 7.5% SDS-polyacrylamide gels, gels are dried under vacuum, and phosphorylation is visualized by autoradiography on X-ray film.

    Cell Assay: Cell growth is determined by two methods. For the [3H]thymidine assay, cells (104 cells/well, Bcr-Abl-positive cell lines (R10(+), R10(−), K562, and RWLeu4); Bcr-Abl-negative cell lines (HL-60, SK-N-ER, SK-N-MC, U138MG, and HS-16)) are cultured in 96-well, round-bottomed plates with diluted DMSO (control) or with varying concentrations of a specific compound that is resuspended in DMSO for 48 h at 37°C. [3H]Thymidine is added at a concentration of 1 μCi/well, and cells are incubated for an additional 18 h. Cells were harvested with the Unifilter system, scintillation fluid (25 μl/well) is added to each well, and [3H]thymidine incorporation is determined on a Packard Scintillation Counter. Data points for all assays are obtained in triplicate, and background incorporation from cell-free wells is determined and subtracted from all data points. For cell viability, control and drug-treated harvested cells are counted on a hemocytometer using the trypan blue dye exclusion method.

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    Cancer Res. 2002 Aug 1;62(15):4244-55; Cancer Res. 1999 Dec 15;59(24):6145-52.

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


    PD173955 inhibits Bcr-Abl-dependent substrate tyrosine phosphorylation in vivo. Cancer Res. 2002 Aug 1;62(15):4244-55.


    PD173955 induces strong accumulation in G1 phase of the cell cycle. Cancer Res. 2002 Aug 1;62(15):4244-55.


    PD173955 and PD166326 selectively inhibit the growth of primary CD34+ CML primitive progenitor cells from a patient with chronic phase CML. Cancer Res. 2002 Aug 1;62(15):4244-55.


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