Cobiprostone shows promise against NSAID-induced gastric mucosal injury

May 21 2012

Sucampo Pharmaceuticals, Inc. (NASDAQ: SCMP) today 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.

"NSAIDs are commonly prescribed drugs for pain, fever and inflammation, but are not ideal for long-term use because of the risk of ulcer formation," said Anthony Blikslager, DVM, Ph.D., DACVS, NC State University, College of Veterinary Medicine. "In this study, we demonstrated that cobiprostone exerts a protective effect against epithelial barrier dysfunction in the presence of an NSAID in human gastric epithelial cells. Based on these data, we believe that cobiprostone could serve as a treatment option in patients taking NSAIDs."