| 包装 | 价格(元) |
| 10mM (in 1mL Water) | 电议 |
| 1mg | 电议 |
| 5mg | 电议 |
| 25mg | 电议 |
Cell lines | Caco-2 and IEC6 cells |
Preparation Method | Treatment solutions containing LY with or without AT-1002 and different concentrations of larazotide acetate in HBSS were added to the apical compartment of each monolayer and incubated at 37 ℃, 50 rpm for 180 min. |
Reaction Conditions | 0-15mM larazotide acetate at 37 ℃ for 60 min or 180 min, |
Applications | In Lucifer yellow (LY) permeability assays, AT-1002 caused a substantial increase in LY passage, which was inhibited by larazotide acetate in a dose-dependent manner. Larazotide acetate at 15 and 12.5 mM significantly inhibited the AT-1002-induced increase in LY passage by 71 and 38%, respectively. |
Animal models | HLA-HCD4/DQ8 mice |
Preparation Method | Mice were gavaged with gliadin (2 mg/mouse), +/ treatment, 2 /week for 7 weeks. Group 1 received larazotide acetate (250 μg/mouse) and gliadin. |
Dosage form | 250 μg larazotide acetate /mouse, twice a week for 7 weeks |
Applications | In vivo in gliadin-sensitized HLA-HCD4/DQ8 double transgenic mice, larazotide acetate inhibited gliadin-induced macrophage accumulation in the intestine and preserved normal TJ structure. |
| 产品描述 | Larazotide acetate (formerly AT-001) is a highly polar octapeptide, derived from a prokaryotic zonula occludens protein secreted by Vibrio cholera[6]. In vitro studies have shown larazotide acetate can prevent the opening of tight junctions, induced by cytokines, bacterial agents and gluten fragments[7,8]. In Lucifer yellow (LY) permeability assays, AT-1002 induces TJ barrier dysfunction in human-derived Caco-2 cells[2], AT-1002 caused a substantial increase in LY passage, which was inhibited by larazotide acetate in a dose-dependent manner. Larazotide acetate at 15 and 12.5 mM significantly inhibited the AT-1002-induced increase in LY passage by 71 and 38%, respectively[1]. Larazotide acetate inhibits gliadin-induced cytoskeletal reorganization in IEC-6 cells[3]. In vivo in gliadin-sensitized HLA-HCD4/DQ8 double transgenic mice, Gliolidin-induced barrier function and macrophage recruitment were altered, larazotide acetate inhibited gliadin-induced macrophage accumulation in the intestine and preserved normal TJ structure[1]. larazotide acetate inhibited transport of gliadin peptides even at 0.1 mM. In animal experiments using BB Wor rats[4]and IL-10 / mice[5], the effective in vivo dose of larazotide acetate is on the order of 0.2-100 μM. Lupus-derived RG strains induced high levels of intestinal permeability that was significantly greater in female than male mice, Strikingly, gut permeability was completely reversed by oral treatment with larazotide acetate[9]. References: |
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