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."
Source:
Sucampo Pharmaceuticals, Inc.
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