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    InvivoChem Cat #: V0521
    CAS #: 1433953-83-3Purity ≥98%

    Description: SAR131675 (SAR-131675) is a novel, potent and selective VEGFR3 inhibitor with potential antineoplastic activity. It inhibits VEGFR3 with IC50/Ki of 23 nM/12 nM in cell-free assays, it is about 50- and 10-fold more selective for VEGFR3 than VEGFR1/2, and has little activity against Akt1, CDKs, PLK1, EGFR, IGF-1R, c-Met, Flt2 etc. SAR131675 dose dependently inhibited the proliferation of primary human lymphatic cells, induced by the VEGFR-3 ligands VEGFC and VEGFD, with an IC(50) of about 20 nmol/L. SAR131675 is the first highly specific VEGFR-3-TK inhibitor described to date, displaying significant antitumoral and antimetastatic activities in vivo through inhibition of lymphangiogenesis and TAM invasion. 

    References: Mol Cancer Ther. 2012 Aug;11(8):1637-49.

    Related CAS: 1092539-44-0 

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    Molecular Weight (MW)358.39
    CAS No.1433953-83-3;
    Storage-20℃ for 3 years in powder form
    -80℃ for 2 years in solvent
    Solubility (In vitro)DMSO: 30 mg/mL (83.7 mM)
    Water: <1 mg/mL
    Ethanol:<1 mg/mL
    Solubility (In vivo)0.5% CMC+0.25% Tween 80: 20 mg/mL
    SynonymsSAR-131675; SAR131675; SAR 131675;  

    Chemical Name: 2-amino-1-ethyl-7-(3-hydroxy-4-methoxy-3-methylbut-1-yn-1-yl)-N-methyl-4-oxo-1,4-dihydro-1,8-naphthyridine-3-carboxamide


    InChi Code: InChI=1S/C18H22N4O4/c1-5-22-15(19)13(17(24)20-3)14(23)12-7-6-11(21-16(12)22)8-9-18(2,25)10-26-4/h6-7,25H,5,10,19H2,1-4H3,(H,20,24)

    SMILES Code: O=C(C(C(NC)=O)=C(N)N1CC)C2=C1N=C(C#CC(O)(COC)C)C=C2

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    In Vitro

    In vitro activity: SAR131675 dose dependently inhibits the proliferation of primary human lymphatic cells, induced by the VEGFR-3 ligands VEGFC and VEGFD, with an IC50 of about 20 nM. SAR131675 dose dependently inhibits rh-VEGFR-3–TK activity with an IC50 of 23 nM. SAR131675 inhibits VEGR-3–TK activity with a Ki of about 12 nM. SAR131675 inhibits VEGFR-1–TK activity with an IC50 of > 3 μM and VEGFR-2–TK activity with an IC50 of 235 nM. SAR131675 inhibits VEGFR-1 autophosphorylation with an IC50 of about 1 μM and VEGFR-2 with an IC50 of about 280 nM. SAR131675 moderately inhibits VEGFR-2 and has very little effect on VEGFR-1, showing a good selectivity for VEGFR-3. SAR131675 inhibits VEGFA-induced VEGFR-2 phosphorylation in a dose-dependent manner, with an IC50 of 239 nM. SAR131675 potently inhibits lymphatic cell survival induced by VEGFC and VEGFD with IC50 of 14 nM and 17 nM, respectively. SAR131675 inhibits VEGFA-induced survival with an IC50 of 664 nM. SAR131675, significantly and dose dependently inhibits VEGFC-induced Erk phosphorylation, with an IC50 of about 30 nM.

    Kinase Assay: Multiwell plates are precoated with a synthetic polymer substrate poly-Glu-Tyr (polyGT 4:1). The reaction is carried out in the presence of kinase buffer (10×: 50 mM HEPES buffer, pH 7.4, 20 mM MgCl2, 0.1 mM MnCl2, and 0.2 mM Na3VO4) supplemented with ATP and dimethyl sulfoxide (DMSO) for the positive control (C+) or SAR131675 (ranging from 3-1,000 nM). ATP is used at 30 μM for VEGFR-1 and VEGFR-3 and at 15 μM for VEGFR-2. The phosphorylated poly-GT is probed with a phosphotyrosine specific monoclonal antibody (mAb) conjugated to horseradish peroxidase and developed in the dark with the HRP chromogenic substrate (OPD). The reaction is then stopped by the addition of 100 μL 1.25 mol/L H2SO4, and absorbance is determined using an Envision spectrophotometer at 492 nm.

    Cell Assay: HLMVECs are seeded in 96-well plates coated with 0.3% gelatin (5000 cells per well). Cells are incubated in RPMI 0.1% FCS with VEGFA (10 ng/mL) VEGFC (300 ng/mL), VEGFD (300 ng/mL), or FGF2 (10 ng/mL) in the absence or presence of SAR131675. Five days later, viable cells are quantified with the cell Titer-glo luminescent cell viability assay.

    In VivoIn embryonic angiogenesis using the zebrafish model, SAR131675 efficiently impaires embryonic vasculogenesis. SAR131675 at 100 mg/kg/d has significantly reduced the levels of VEGFR-3 and hemoglobin content by about 50%. SAR131675 efficiently abrogates lymphangiogenesis and angiogenesis induced in vivo by FGF2. SAR131675 at a dose of 300 mg/kg is able to inhibit both VEGFR-2 and VEGFR-3 signaling. In the prevention study, 5 weeks treatment with SAR131675 is well tolerated and the number of angiogenic islets in the pancreas of SAR131675-treated mice is significantly decreased by 42%, compared with the vehicle-treated group. In the intervention study, daily oral administration of SAR131675 from week 10 to week 12.5 causes a significant decrease in tumor burden by 62%. Treatment with SAR131675 significantly reduces the tumor volume 24% and 50% at 30 mg/kg/d and 100 mg/kg/d, respectively.
    Animal model BALB/c mice with 4T1 cells
    Formulation & DosageDissolved in a 0.6% methylcellulose/0.5% Tween 80 solution;  30, 100, 300 mg/kg/d; oral administration
    ReferencesMol Cancer Ther. 2012 Aug;11(8):1637-49.

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


    Effect of SAR131675 on VEGFR tyrosine kinases.  2012 Aug;11(8):1637-49.


    Effect of SAR131675 on human primary lymphatic cells.  2012 Aug;11(8):1637-49.


    In vivo effect of SAR131675 on embryonic and adult angiogenesis and lymphangiogenesis.  2012 Aug;11(8):1637-49.


    Effect of SAR131675 on spontaneous multistage tumor model (RIP1.Tag2; A) studies designed to target discrete stages of tumoral growth in the RIP1. 2012 Aug;11(8):1637-49.


    Antitumoral effect of SAR131675 treatment on a murine mammary carcinoma model. A, tumor volume monitoring in Balb/c mice in control or mice treated with SAR131675 at 30 and 100 mg/kg/d. B, murine VEGFR3 levels were quantified by ELISA in the tumor lysates of each treated group at the end of the experiment (day 21).  2012 Aug;11(8):1637-49.


    Antimetastatic effect of SAR131675 after 4T1 tumor resection. A, experiment schedule: SAR131675 treatment at 100 mg/kg/d started 5 days after 4T1 cell implantation in mammary fat pads;   2012 Aug;11(8):1637-49.


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