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    InvivoChem Cat #: V0513
    CAS #: 219580-11-7Purity ≥98%

    Description: PD173074 (PD-173074) is a novel, potent, cell permeable and selective FGFR1 inhibitor with potential antineoplastic activity. It inhibits FGFR1 with an IC50 of ~25 nM, also inhibits VEGFR2 with IC50 of 100-200 nM in cell-free assays, and shows ~1000-fold selectivity for FGFR1 over PDGFR and c-Src. PD173074 shows potent anti-proliferative activity in vitro against various cancer cell lines such as UM-UC-14 and MGHU3, which expressed mutated FGFR3 protein. 

    References: EMBO J. 1998;17(20):5896-904; Blood. 2004;103(9):3521-8; Cancer Res. 2009;69(22):8645-51.

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    Molecular Weight (MW)523.67
    CAS No.219580-11-7
    Storage-20℃ for 3 years in powder form
    -80℃ for 2 years in solvent
    Solubility (In vitro)DMSO: 100 mg/mL (191.0 mM)
    Water: <1 mg/mL
    Ethanol: 100 mg/mL (191.0 mM)
    Solubility (In vivo)5% DMSO+corn oil: 15mg/mL
    SynonymsPD 173074; PD-173074; PD173074 

    Chemical Name: 1-(tert-butyl)-3-(2-((4-(diethylamino)butyl)amino)-6-(3,5-dimethoxyphenyl)pyrido[2,3-d]pyrimidin-7-yl)urea


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    In Vitro

    In vitro activity: PD173074 is an ATP-competitive inhibitor of FGFR1 with Ki of ~40 nM. PD173074 is also an effective inhibitor of VEGFR2. Compared to FGFR1, PD173074 weakly inhibits the activities of Src, InsR, EGFR, PDGFR, MEK, and PKC with 1000-fold or greater IC50 values. PD173074 inhibits autophosphorylation of FGFR1 and VEGFR2 in a dose-dependent manner with IC50 of 1-5 nM and 100-200 nM, respectively. PD173074 inhibits FGF-2 promotion of granule neuron survival in a dose-dependent manner with IC50 of 12 nM, exhibiting 1,000-fold greater potency than that of SU 5402. PD173074 specifically inhibits FGF-2-mediated effects on proliferation, differentiation, and MAPK activation in oligodendrocyte (OL) lineage cells. PD173074 is active against the WT receptor and FGFR3 mutations in multiple myeloma (MM) cell lines. PD173074 also potently inhibits autophosphorylation of FGFR3 in a dose-dependent manner with IC50 of ~5 nM. PD173074 treatment potently reduces viability of FGFR3-expressing KMS11 and KMS18 cells with IC50 of<20 nM. Inhibition of aFGF-stimulated MM cell growth by PD173074 is highly correlated with the expression of FGFR3. PD173074 treatment completely abolishes NIH 3T3 transformation mediated by Y373C FGFR3 but not by Ras V12, demonstrating that PD173074 specifically targets FGFR3-mediated cell transformation and lacks nonspecific cytotoxic effect. PD173074 also induces functional maturation of KMS11 and KMS18 cells.

    Kinase Assay: Assays using the full-length FGFR-1 kinase are performed in a total volume of 100 μL containing 25 mM HEPES buffer (pH 7.4), 150 mM NaCl, 10 mM MnCl2, 0.2 mM sodium orthovanadate, 750 μg/mL concentration of a random copolymer of glutamic acid and tyrosine (4:1), various concentrations of PD173074 and 60 to 75 ng of enzyme. The reaction is initiated by the addition of [γ-32P]ATP (5 μM ATP containing 0.4 μCi of [γ-32P]ATP per incubation), and samples are incubated at 25°C for 10 minutes. The reaction is terminated by the addition of 30% trichloroacetic acid and the precipitation of material onto glass-fiber filter mats. Filters are washed three times with 15% trichloroacetic acid, and the incorporation of [32P] into the glutamate tyrosine polymer substrate is determined by counting the radioactivity retained on the filters in a Wallac 1250 betaplate reader. Nonspecific activity is defined as radioactivity retained on the filters following incubation of samples without enzyme. Specific activity is determined as total activity (enzyme plus buffer) minus nonspecific activity. The concentration of PD173074 that inhibits FGFR-1 enzymatic activity by 50% (IC50) is determined graphically.

    Cell Assay: PD 173074 dose-dependently inhibited autophosphorylation of FGFR1, with an IC50 value in the range of 1 ~ 5 nM. In addition, PD 173074 inhibited autophosphorylation of VEGFR2 with an IC50 value of 100 ~ 200 nM. Cells (KMS11 and KMS18) are incubated with increasing concentrations of PD173074 in the presence of aFGF/heparin for 48 hours. The percentage of viable cells is determined by MTT.

    In VivoAdministration of PD173074 at 1 mg/kg/day or 2 mg/ka/day in mice can effectively block angiogenesis induced by either FGF or VEGF in a dose-dependent manner with no apparent toxicity. PD173074 inhibits in vivo growth of mutant FGFR3-transfected NIH 3T3 cells in nude mice. Inhibition of FGFR3 by PD173074 delays tumor growth and increases survival of mice in a KMS11 xenograft myeloma model. In the H-510 xenograft, oral aministration of PD173074 blocks tumor growth similar to that seen with single-agent cisplatin administration, increasing median survival compared with control sham-treated animals. In H-69 xenografts, PD173074 induces complete responses lasting >6 months in 50% of mice. These effects are correlated with increased apoptosis in excised tumors, but not a consequence of disrupted tumor vasculature.
    Animal modelSwiss Webster mice with induced corneal angiogenesis
    Formulation & Dosage2 mg/kg; i.p.

    EMBO J. 1998 Oct 15;17(20):5896-904; Blood. 2004 May 1;103(9):3521-8; Cancer Res. 2009 Nov 15;69(22):8645-51.

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


    The expression of MYC and FGFR3 was analyzed by Western blotting in lysates from MGH‐U3 and RT112 cells transfected for 72 h with MYC siRNAs.


    The MYC accumulation induced by activated FGFR3 confers sensitivity to BET bromodomain inhibitors in FGFR3‐dependent bladder cancer cells in vitro and in vivo.  2018 Apr;10(4). pii: e8163.


    MGH‐U3 and RT112 cells were treated with control DMSO, PD [PD173074 (FGFR inhibitor)], SB [SB203580 (p38 inhibitor)] or LY [LY294002 (PI3 kinase inhibitor)] for 72 h and cell viability was then assessed by measuring MTT incorporation.


    Venn diagram showing the number of upstream regulators (transcription factors) significantly predicted by Ingenuity Pathway Analysis to be involved in the regulation of gene expression observed after FGFR3 knockdown in RT112 and MGH‐U3 cells (left panel). 2018 Apr;10(4). pii: e8163.




    The MYC accumulation induced by activated FGFR3 is dependent on the activation of p38 and AKT. 


    MYC and FGFR3 are involved in a positive feedback loop in bladder cancer cell lines expressing an activated form of FGFR3.  2018 Apr;10(4). pii: e8163.


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