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    InvivoChem Cat #: V0324
    CAS #: 1226895-15-3Purity ≥98%

    Description: FLLL32, a synthetic curcumin analog,  is a novel and potent Janus kinases-JAK2/STAT3 inhibitor with potential antitumor activity. It inhibits JAK2 with IC50 of<5 μM. FLLL-32 shows potent in vitro antiproliferative activity and high in vivo antitumor efficacy.

    References: Cancer Res. 2010;70(6):2445-54; Mol Cancer. 2010;9:217; Invest New Drugs. 2012 Jun;30(3):916-26.

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    Molecular Weight (MW)464.55
    CAS No.1226895-15-3
    Storage-20℃ for 3 years in powder form
    -80℃ for 2 years in solvent
    Solubility (In vitro)DMSO: 92 mg/mL (198.0 mM)
    Water: <1 mg/mL
    Ethanol: 25 mg/mL warmed (53.8 mM)
    Solubility (In vivo)

    Chemical Name: (2E,2'E)-1,1'-(cyclohexane-1,1-diyl)bis(3-(3,4-dimethoxyphenyl)prop-2-en-1-one)


    InChi Code: InChI=1S/C28H32O6/c1-31-22-12-8-20(18-24(22)33-3)10-14-26(29)28(16-6-5-7-17-28)27(30)15-11-21-9-13-23(32-2)25(19-21)34-4/h8-15,18-19H,5-7,16-17H2,1-4H3/b14-10+,15-11+

    SMILES Code: O=C(C1(C(/C=C/C2=CC=C(OC)C(OC)=C2)=O)CCCCC1)/C=C/C3=CC=C(OC)C(OC)=C3


    FLLL-32; FLLL32; FLLL 32

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    In Vitro

    In vitro activity: In MDA-MB-231 breast and PANC-1 pancreatic cancer cells, FLLL32 downregulates STAT3 phosphorylation and DNA-binding activity. In MDA-MB-231 cells, FLLL32 inhibit the formation of colonies and cell invasion. In human multiple myeloma, glioblastoma, liver cancer, and colorectal cancer cell lines, FLLL32 also leads to the inhibition of cell proliferation and the induction of caspase-3 and PARP cleavages.

    Kinase Assay: JAK2 kinase activity was assessed with the HTScan JAK2 Kinase Assay Kit per manufacturer's protocol. The possible effects of FLLL32 on the other 10 purified human protein kinases were determined by using a Kinase Profiler Assay.

    Cell Assay: Cells are seeded in 96-well plates (3,000 per well) in triplicate and then treated with 0.5 to 5 μM of FLLL31 or FLLL32 or with 0.5 to 30 μM of curcumin for 72 h. MTT (25 μL) is added to each sample and incubated for 3.5 h. Then, 100 μL of N,N-dimethylformamide solubilization solution are added to each well. The absorbance at 450 nm is read the following day. IC50 are determined using Sigma Plot 9.0 software.

    In VivoIn MDA-MB-231 xenografted mice, FLLL32 (50 mg/kg, i.p.) significantly reduces tumor burdens. In mouse xenografts with OS-33 osteosarcoma cells, FLLL32 (50 mg/kg, i.p.) also inhibits tumor growth by targeting STAT3.
    Animal modelMDA-MB-231 xenografted mice
    Formulation & DosageDissolved in DMSO; 50 mg daily; i.p. injection

    Cancer Res. 2010 Mar 15;70(6):2445-54; Mol Cancer. 2010 Aug 16;9:217; Invest New Drugs. 2012 Jun;30(3):916-26.

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


    FLLL31 and FLLL32 inhibit STAT3-dependent transcriptional activation.Cancer Res. 2010 Mar 15;70(6):2445-54. 


    FLLL31 and FLLL32 are potent inhibitors of STAT3 phosphorylation. Cancer Res. 2010 Mar 15;70(6):2445-54. 



    A. FLLL31 and FLLL32 reduce STAT3’s ability to bind DNA in nuclear extracts isolated from MDA-MB-231 breast cancer and PANC-1 pancreatic cancer cells. B. FLLL31-and FLLL32-mediated decreases in STAT3 DNA binding activity correlate with increases in STAT1 DNA binding activity in MDA-MB-231 cells. Cancer Res. 2010 Mar 15;70(6):2445-54. 


    A. Comparison of tumor volumes over time in mouse xenografts with MDA-MB-231 breast cancer cells. B. Effect of FLLL32 on vascularity and tumor growth in CAMs. The pictures show blood vessel density around xenografted tumors (t). C. Relative tumor sizes of CAM xenografts. D. Relative CAM blood vessel density. Cancer Res. 2010 Mar 15;70(6):2445-54. 


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