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    Mesalamine (5ASA; 5-aminosalicylic acid; Asacol; mesalazine; 5-ASA)
    Mesalamine (5ASA; 5-aminosalicylic acid; Asacol; mesalazine; 5-ASA)

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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 #: V0762
    CAS #: 89-57-6Purity ≥98%

    Description: Mesalamine (also named as 5ASA;  Z-206; AJG-501; MAX-002; 5-aminosalicylic acid; Asacol; mesalazine; 5-ASA)  is a specific and orally bioavailable inhibitor of TNFα-induced IKK activity with potential anti-inflammatory activity. It isalso a PPARγ agonist and an inhibitor of p21-activated kinase 1 (PAK1) and NF-κB. It has been approved to treat inflammatory bowel disease, specifically, ulcerative colitis. 

    References: J Biol Chem. 1999 Sep 10;274(37):26448-53.

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    Molecular Weight (MW)153.14
    FormulaC7H7NO3
    CAS No.89-57-6
    Storage-20℃ for 3 years in powder form
    -80℃ for 2 years in solvent
    Solubility (In vitro)DMSO: 31 mg/mL (202.4 mM)
    Water: <1 mg/mL
    Ethanol: 31 mg/mL (202.4 mM)
    Other info
    Chemical Name: 5-amino-2-hydroxybenzoic acid
    InChi Key: KBOPZPXVLCULAV-UHFFFAOYSA-N
    InChi Code: InChI=1S/C7H7NO3/c8-4-1-2-6(9)5(3-4)7(10)11/h1-3,9H,8H2,(H,10,11)
    MILES Code: O=C(O)C1=CC(N)=CC=C1O 
    SynonymsMAX-002; Z 206; 5 ASA; AJG 501; MAX 002; Mesalamine; 5-ASA; Mesalazine; 5-Aminosalicylic acid; Asacol; Z-206; AJG-501; Z206; 5ASA; AJG501; MAX002


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    In Vitro

    In vitro activity: Mesalamine inhibits the enzyme 3-hydroxysteroid dehydrogenase, involved in the reversible conversion between DHP and THP, and therefore may affect the local actions of DHP and THP in the brain. Mesalamine, an anti-inflammatory aminosalicylate, dose-dependently inhibits IL-1-stimulated NF-kappaB-dependent transcription without preventing IkappaB degradation or nuclear translocation and DNA binding of the transcriptionally active NF-kappaB proteins, RelA, c-Rel, or RelB. Mesalamine is found to inhibit IL-1-stimulated RelA phosphorylation. Mesalamine increases cell adhesion which is measured by cell adhesion assay and transcellular-resistance measurement. Mesalamine treatment restores membranous expression of adhesion molecules E-cadherin and β-catenin. Mesalamine or sulfasalazine (2 mM), but not sulfapyridine, significantly reduces the expression of the TC22 transcript and significantly reduces the expression of TC22 protein in a dose-dependent and reversible manner.


    Kinase Assay: 5-Aminosalicylic acid (Mesalamine) acts as a specific PPARγ agonist and also inhibits p21-activated kinase 1 (PAK1) and NF-κB.


    Cell Assay: Cytostatic effects are measured by MTT assay. HT-29 colon carcinoma cells are detached with a 0.25% trypsin solution for 5 min. Subsequently, the cells are seeded onto 96-well plates (1×106 cells/well), supplemented with 10% FCS and allowed to attach for 24 h before the addition of test compounds (5-Aminosalicylic acid 10, 50, 100, 500, and 1000 μM; Nimesulide; and their combination). Test compounds are diluted in serum-free culture medium. Then the cells are incubated in a medium or at different concentrations of drugs for 48 h, 20 μL of MTT solution (5 g/L) in PBS is added. Four hours later, the medium in each well is removed, and 120 μL of 0.04 mM muriatic isopropanol is added, slightly concussed for 10 min. Dye uptake is measured at 490 nm with an ELISA reader. Five wells are used for each concentration or as a control group. On the other hand, the cells are seeded onto 96-well plates (1×106 cells/well) and allowed to attach for 24 h, then treated with test compounds (5-Aminosalicylic acid, Nimesulide, and their combination). The final concentration is 100 μM. The same medium is added into the control group and dye uptake is then measured. Five wells are used for each test compound or control group.

    In Vivo5-Aminosalicylic acid (5-ASA) has an antineoplastic effect in a xenograft tumor model. To evaluate the in vivo antineoplasic effect of 5-Aminosalicylic acid, SCID mice engrafted with HT-29 colon cancer cells are treated daily for 21 consecutive days with 5-Aminosalicylic acid at 50 mM. At the end of the treatment, a reduction of 80-86% of tumor weight and volume is observed in SCID mice receiving 5-Aminosalicylic acid compared with control mice or mice treated with GW9662 alone. The antineoplastic effect of 5-Aminosalicylic acid is already detectable after 10 days of 5-Aminosalicylic acid treatment. Similar results are obtained with mice treated with 5-Aminosalicylic acid at 5 mM. Antitumorigenic effect of 5-Aminosalicylic acid is completely abolished at 21 days by simultaneous intraperitoneal administration of GW9662. Thus, the observed antineoplastic effect of 5-Aminosalicylic acid is at least partially dependent on PPARγ
    Animal modelBALB/c SCID mice
    Formulation & DosageSix to seven weeks old pathogen-free BALB/c SCID mice are used. Human colon cancer cells (107 HT-29 cells) pretreated or not with GW9662 for 24 h are implanted subcutaneously in the flank of animals. Two days after cell inoculation, mice are treated with 5-Aminosalicylic acid (5 or 50 mM) administered daily by peritumoral injection for 10 or 21 days. The effect of PPARγ during 5-Aminosalicylic acid treatment is evaluated by daily intraperitoneal injection of GW9662 (1 mg/kg/day). The control group receives saline instead of 5-Aminosalicylic acid. Mice are checked three times a week for tumor development. After killing at 10 or 21 days, tumor size and volume are calculated. Tumors are weighted before paraffin embedding for histological examination.
    ReferencesJ Biol Chem. 1999 Sep 10;274(37):26448-53; World J Gastroenterol. 2007 May 28;13(20):2872-7.Carcinogenesis. 2013 Nov;34(11):2580-6.


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

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