Inflabloc Pharmaceuticals, Inc, of Salt Lake City, Utah, has announced the closing of $6 million in Series C financing, co-led by Friedli Corporate Finance and vSpring Capital, as well as a merger with MantiCore Pharmaceuticals, Inc. Inflabloc's lead product is a proprietary oral  dehydroepiandrosterone (DHEA, a weak adrenal steroid) combination product, IP-1001, for the treatment of chronic and subchronic inflammatory diseases.

A dose-response phase II clinical trial is currently nearing completion to evaluate the efficacy and safety of IP-1001 in treating the symptoms of Crohn's disease. In an independent pilot study, six out of seven Crohn's disease patients as well as eight out of 13 colitis patients responded to 8 weeks of treatment with 200 mg of micronized DHEA. Ulcerative colitis patients from this study also showed higher DHEAS levels, which correlated with lower disease activity. In phase I studies, IP-1001 was found to be safe, well-tolerated, and more bioavailable than micronized DHEA.

IP-1003 is also a proprietary fixed combination drug, with DHEA as a primary active ingredient, and has been shown to reduce colonic lesions and inflammatory markers (TNF-alpha and IL-6) in inflammatory bowel disease animal model studies. According to Inflabloc, the improvements of the DHEA combination product are greater than those observed in treatments with Remicadeâ„¢. Inflabloc is continuing development of this fixed-combination drug, with clinical studies planned to begin in 2006. IP-1005 is another proprietary fixed combination drug with DHEA as a primary active ingredient that reduces inflammatory markers and may reduce C-reactive protein.

Inflabloc Pharmaceuticals has demonstrated that DHEA suppresses immune cell activation and the subsequent recruitment of inflammatory cells, interrupts multiple pathways that can lead to proinflammatory cytokines such as TNF-alpha, IL-8, and IFN-gamma at the posttranscriptional and transcriptional level of expression, and disrupts the inflammatory signal transduction pathway by affecting the action of specific MAP kinases.

—A. Techman