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    InvivoChem Cat #: V1693
    CAS #: 307510-92-5Purity ≥98%

    Description: CFTRinh-172 (also known as CFTR inhibitor 172) is a potent, voltage-independent, selective CFTR inhibitor with Ki of 300 nM, showing no effects on MDR1, ATP-sensitive K+ channels, or a series of other transporters. CFTRinh-172 could reversibly inhibit CFTR short-circuit current in less than 2 minutes in a voltage-independent manner. 

    References: J Clin Invest. 2002 Dec;110(11):1651-8; PLoS Negl Trop Dis. 2013 Jun 27;7(6):e2293.

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    Molecular Weight (MW)409.4
    CAS No.307510-92-5
    Storage-20℃ for 3 years in powder form
    -80℃ for 2 years in solvent
    Solubility (In vitro)DMSO: 82 mg/mL (200.3 mM)
    Water: <1 mg/mL
    Ethanol: <1 mg/mL
    Other info

    Chemical Name: 4-{[(5Z)-4-Oxo-2-sulfanylidene-3-[3-(trifluoromethyl)phenyl]-1,3-thiazolidin-5-ylidene]methyl}benzoic acid


    InChi Code: InChI=1S/C18H10F3NO3S2/c19-18(20,21)12-2-1-3-13(9-12)22-15(23)14(27-17(22)26)8-10-4-6-11(7-5-10)16(24)25/h1-9H,(H,24,25)/b14-8-

    SMILES Code: O=C(O)C1=CC=C(/C=C(SC(N2C3=CC=CC(C(F)(F)F)=C3)=S)/C2=O)C=C1

    SynonymsCFTR inhibitor 172; CFTR Inh-172; CFTR Inh 172; CFTR Inh172; CFTR(Inh)-172; CFTR(Inh)172; CFTR Inhibitor-172; CFTR Inhibitor172;

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    In Vitro

    In vitro activity: CFTRinh-172 dose- and time-dependently inhibits CFTR-mediated I- transportation, and effectively inhibits CFTR activation by multiple types of agonists or activators. CFTRinh-172, as a selective CFTR channel inhibitor, also completely abolishes the Cl− current in the rabbit acinar and duct cells of rabbit lacrimal gland. CFTRinh-172 also induces ROS production, mitochondrial failure, and activation of the NF-κB signaling pathway, independently of CFTR inhibition.

    Kinase Assay: Assays are done using a customized screening system consisting of a 3-meter robotic arm, CO2 incubator, plate washer, liquid-handling workstation, bar code reader, delidding station, and two FLUOstar fluorescence platereaders, each equipped with two syringe pumps and HQ500/20X (500 ± 10 nm) excitation and HQ535/30M (535 ± 15 nm) emission filters. The robotic system is integrated using SAMI version 3.3 software modified for two platereaders. Custom software is written in Microsoft VBA (Visual Basic for Applications) to compute base-line–subtracted, normalized fluorescence slopes (giving halide influx rates) from stored data files. The assay is set up by loading the incubator (37°C, 90% humidity, 5% CO2) with 40–60 96-well plates containing the FRT cells, and loading a carousel with 96-well plates containing test compounds and disposable plastic pipette tips. To initiate the assay, each well of a 96-well plate is washed three times in PBS (300 μl/wash), leaving 50 μL PBS. Ten microliters of a CFTR-activating cocktail (5 μM forskolin, 100 μM IBMX, 25 μM apigenin in PBS) is added, and after 5 minutes one test compound (0.5 μL of 1 mM DMSO solution) is added to each well to give 10 μM final concentration. After 10 minutes, 96-well plates are transferred to a platereader for fluorescence assay. Each well is assayed individually for CFTR-mediated I- transport by recording fluorescence continuously (200 ms per point) for 2 seconds (base line) and then for 12 seconds after rapid (<0.5 seconds) addition of 165 μL of isosmolar PBS in which 137 mM Cl– was replaced by I-.

    Cell Assay: Cell toxicity is assayed by the dihydrorhodamine method at 24 hours after cell [Fischer rat thyroid (FRT) cells] incubation with 0–1,000 μM inhibitor.

    In VivoCFTRinh-172 (20 µg/6 h) completely abolishes the V. cholerae-induced intestinal fluid secretion without affecting V. cholerae growth in vivo.
    Animal modelAn adult mouse model of Vibrio cholerae-induced diarrhea 
    Formulation & DosageDissolved in 20 µg/6 h; i.p. administration 

    J Clin Invest. 2002 Dec;110(11):1651-8; PLoS Negl Trop Dis. 2013 Jun 27;7(6):e2293.

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


    Identification of CFTR inhibitors by high-throughput screening. J Clin Invest. 2002 Dec;110(11):1651-8.


    Inhibition of intestinal fluid secretion. J Clin Invest. 2002 Dec;110(11):1651-8.


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