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    Sulindac (MK-231)
    Sulindac (MK-231)

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    This product is for research use only, not for human use. We do not sell to patients.
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    InvivoChem Cat #: V1042
    CAS #: 38194-50-2Purity ≥98%

    Description: Sulindac (Aflodac; Algocetil; MK231; MK 231; MK-231), belonging to the arylalkanoic acid class of non-steroidal antiinflammatory drugs (NSAIDs), is a non-steroidal COX inhibitor, which potently inhibits prostaglandin synthesis. It has been used in the treatment of acute or chronic inflammatory conditions. Sulindac is a prodrug, derived from sulfinylindene, that is converted in the body to the active NSAID, sulindac sulfide, a cyclooxgenase inhibitor that represses ras signaling, and sulindac sulfone, an antitumor agent, following oral administration in vivo.

    References: J Biol Chem. 1999 Sep 17;274(38):27307-14; Cancer Res. 1997 Oct 1;57(19):4267-73.

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    Molecular Weight (MW)356.41
    FormulaC20H17FO3S 
    CAS No.38194-50-2
    Storage-20℃ for 3 years in powder form
    -80℃ for 2 years in solvent
    Solubility (In vitro)DMSO: 71 mg/mL (199.2 mM)
    Water: <1 mg/mL
    Ethanol: 9 mg/mL (25.25 mM)
    Other info

    Chemical Name: (Z)-2-(5-fluoro-2-methyl-1-(4-(methylsulfinyl)benzylidene)-1H-inden-3-yl)acetic acid

    InChi Key: MLKXDPUZXIRXEP-MFOYZWKCSA-N

    InChi Code: InChI=1S/C20H17FO3S/c1-12-17(9-13-3-6-15(7-4-13)25(2)24)16-8-5-14(21)10-19(16)18(12)11-20(22)23/h3-10H,11H2,1-2H3,(H,22,23)/b17-9-

    SMILES Code: O=C(O)CC(C1=C/2C=CC(F)=C1)=C(C)C2=C\C3=CC=C(S(C)=O)C=C3

    SynonymsSulindac; Aflodac; MK231; MK 231; Algocetil; MK-231; 


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    In Vitro

    In vitro activity: Sulindac and its metabolites sulindac sulfide and sulindac sulfone can also inhibit the NF-kappaB pathway in both colon cancer and other cell lines, due to sulindac-mediated decreases in IKKbeta kinase activity. Sulindac sulfide significantly reduces cell number in both preconfluent and confluent cultures of HT-29 cells with the sulfide showing approximately 4-fold greater potency. Sulindac sulfide inhibits the growth of a variety of tumor cell lines derived from other tissues, as well as normal epithelial cells and fibroblasts. Sulindac sulphide abrogates beta-catenin/TCF-mediated transcription in the CRC cell lines DLD1 and SW480, and decreases the levels of nonphosphorylated beta-catenin.


    Cell Assay: Cells are treated with Sulindac (MK-231) and/or vitamin C at the indicated doses for 48 h, and cell viability is analyzed using a trypan blue exclusion assay. For the annexin V staining assay, cells are treated with 0.5 mM Sulindac (MK-231) and/or 0.5 mM vitamin C for 48 h. The cells are then trypsinized, washed with PBS, stained with propidium iodide (PI) and FITC-labeled annexin V for 30 min, and analyzed by flow cytometry using a fluorescence-activated cell sorter.

    In VivoSulindac not only inhibits tumor formation but decreases small bowel Cox-2 and prostaglandin E(2) to baseline and restored normal levels of apoptosis in a murine modelof familial adenomatous polyposis. Sulindac reduces the tumor number by 95% but does not alter the levels of PGE2 and LTB4 in intestinal tissues in mice. Sulindac reduces tumor number by 82%, whereas eicosanoid levels remained elevates in Min/+ mice. 
    Animal modelMice: Female C57BL16J-Min/+ (Min) mice at 5 weeks of age are used in the assay. Beginning at 5-6 weeks of age, 10 Min mice are fed a low-fat AIN-76A chow diet modified with 0.001% ethoxyquin and Sulindac (MK-231), 0.5 ± 0.1 mg/day (0.05 mg/kcal/day or approximately 160 ppm) in drinking water. As controls, 9 Min mice and 5 C57BL/6J-+/+ non-affected littermates (+/+) are fed AIN-76A diet without Sulindac. Animals are checked daily for signs of distress or anemia. Animals and their food are weighed twice weekly. During the course of the experiment, there is no difference in body weight or food consumption among the various study groups. No toxicity is observed in the Min/Sulindac group. At 110 days of age, all mice are euthanized by CO2 inhalation, and their intestinal tracts are removed from esophagus to distal rectum, opened, flushed with saline, and examined under ×3 magnification to obtain tumor counts. Tumors are counted by an individual blinded to the animal's genetic status and treatment. Multiple samples of grossly normal, full-thickness bowel are harvested from the mid small intestine and either frozen in liquid nitrogen or fixed in 10% formalin for histological examination. All samples used for the analyses in this study are taken from mid small intestine.
    Formulation & Dosage0.5 ± 0.1 mg/day (0.05 mg/kcal/day; in drinking water
    References

    J Biol Chem. 1999 Sep 17;274(38):27307-14; Cancer Res. 1996 Jun 1;56(11):2556-60; Cancer Res. 1997 Oct 1;57(19):4267-73.


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

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