Sucampo Pharma (SCMP) Updates on Protective Effect of SPI-8811 in NSAID-Induced GMI
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Sucampo Pharmaceuticals, Inc. (Nasdaq: SCMP) announced the presentation of preclinical data at Digestive Disease Week 2012, in San Diego, which demonstrates the protective effect of cobiprostone (also known as SPI-8811) against epithelial barrier dysfunction in models of non-steroidal anti-inflammatory drug (NSAID)-induced gastric mucosal injury.
The poster entitled, “The Protective Effect of ClC-2 Agonist SPI-8811 on Indomethacin-induced Epithelial Barrier Dysfunction in Human Gastric Epithelial Cells,” was authored by Meghali Nighot and Anthony Blikslager, of NC State University College of Veterinary Medicine, and Ryuji Ueno, of Sucampo.
In the study presented, treatment with the NSAID indomethacin resulted in increased permeability due to dysregulation of occludin co-localization. The results of this in vitro study show that cobiprostone, via ClC-2 activation, can counter act such adverse effects of NSAID on tight junction proteins. Additionally, cobiprostone was shown to prevent indomethacin-induced cell death.
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The poster entitled, “The Protective Effect of ClC-2 Agonist SPI-8811 on Indomethacin-induced Epithelial Barrier Dysfunction in Human Gastric Epithelial Cells,” was authored by Meghali Nighot and Anthony Blikslager, of NC State University College of Veterinary Medicine, and Ryuji Ueno, of Sucampo.
In the study presented, treatment with the NSAID indomethacin resulted in increased permeability due to dysregulation of occludin co-localization. The results of this in vitro study show that cobiprostone, via ClC-2 activation, can counter act such adverse effects of NSAID on tight junction proteins. Additionally, cobiprostone was shown to prevent indomethacin-induced cell death.
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