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Romark Announces Data Presented at AASLD Meeting 2010
Date:11/1/2010

uesday, November 2, 7:00 am – 12:00 pm.

Dr. Korba reports an extensive series of studies designed to evaluate mechanisms of potential resistance of hepatitis C virus (HCV) to nitazoxanide.  These studies show that nitazoxanide does not induce mutations in HCV that confer resistance.  Importantly, these findings distinguish nitazoxanide from direct-acting antiviral drugs (e.g., protease and polymerase inhibitors) and other host-targeting anti-HCV agents, such as the cyclophilin inhibitors, where resistance appears to be primarily due to mutations in viral sequences.

2. Augmentation of Interferon Signaling Pathway by Nitazoxanide: A Novel Therapeutic Strategy for Relapsers to Peginterferon and Ribavirin Therapy. Crystal Wang(1), Ziaozhen Zhang(1), Anu Osinusi(1), Henry Masur(2), Dawn Fishbein(3), Shyam Kottilil(1); (1)LIR, NIAID, NIH, Bethesda, MD; (2)CCMD, CC, NIH, Bethesda, MD; (3)SAIC-Frederick, Inc., CMRP in support of CCMD, NIH, Frederick, MD. Poster session: Tuesday, November 2, 7:00 am – 12:00 pm.

This team of researchers from NIH reports that nitazoxanide has potent in vitro anti-HCV activity in the Huh7.5/JFH-1 HCV genotype 2a continuous cell culture system and that the activity is synergistic with interferon. In PBMCs collected from SVR and relapser patients co-infected with HCV and HIV, nitazoxanide significantly enhanced interferon-inducible gene expression.  The addition of nitazoxanide to interferon also significantly enhanced interferon-inducible gene expression compared to interferon alone. Importantly, these investigators also report, for the first time, the activity of new nitazoxanide-related compounds (thiazolides) against HCV.

3. Nitazoxanide for the Prevention of Recurrent Hepatitis C Virus Infection after Liver Transplantation: A Pilot Study.  Sumeet K. Asrani, Stacy Anderson, Jennie Wilnso, Laura J. Myhre, Julie Heimbach, Walter K. Kremers, Charles B. Rosen, Terry M. Ther
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SOURCE Romark Laboratories, L.C.
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