During the conferencecall they dsaid they were going to release Phase IIb data in June after the full 12 week study. So during the EASL meeting what is the actual data that will be released? In thier PR it says "Valopicitabine (NM283), Alone or With Peg-Interferon, Compared to Peg-Interferon/Ribavirin (Peg-IFN/RBV) Retreatment in Patients With HCV-1 Infection and Prior Non-Response to Peg-IFN/RBV: One-Year Results" where will this info come from can someone with bio investing please help me?
24wk and 36wk data are posted in the EASL site. Another Abstract from EASL program 2007, which is I thought encouraging, is:
VALOPICITABINE (NM283) IS FULLY ACTIVE AGAINST KNOWN HCV PROTEASE RESISTANCE MUTATIONS IN VITRO
V. Bichko 1, L. Lallos 1, M. Soubasakos 1, M. LaColla 1, M.M. Tausek 1, J. Gillum 1, D.N. Standring 1 1 Idenix Pharmaceuticals, Cambridge, MA, USA
Background and aims: Valopicitabine (NM283), an inhibitor of the HCV NS5B polymerase, is an orally bioavailable prodrug of NM107 (2�-C-methylcytidine), and is in phase II clinical development for the treatment of chronic hepatitis C. Agents that target the NS3 serine protease are also in development for HCV. A number of NS3 mutations that confer resistance to protease inhibitors have been identified in vitro and have emerged rapidly in clinical trials. This suggests that development of resistance to these agents may limit clinical efficacy, and combinations of HCV antivirals with different resistance profiles may maintain viral suppression more consistently. To evaluate the potential for development of such combinations, the present study assesses the antiviral activity of NM107 against major mutations that confer resistance to protease inhibitors. Methods: Protease inhibitor resistance mutations, including R155Q, A156T, D168A, D168V, and D168Y, were introduced into the HCV replicon cDNA by site-directed mutagenesis. Following RNA electroporation and G418 selection, stable Huh7 cell lines harboring mutant replicons were generated. Alternatively, mutant HCV replicons were transiently transfected into Huh7 cells (that had been cured of the replicon) for drug susceptibility studies. Inhibition of viral replication was measured by quantitative real-time RT-PCR as well as western blot analyses for NS5A protein. To identify NM283/NM107 resistance mutations, a Huh7 cell line harboring NM107-resistant HCV subgenomic replicon was selected by passaging with increasing amounts of NM107. Results: All tested protease inhibitor resistance mutations were fully sensitive to NM107, with EC50 values similar to that of the wild type replicon. In separate experiments, sequencing of NM107-resistant HCV replicons identified a single mutation (S282T), in the highly conserved B domain of NS5B, that conferred a moderate degree of resistance to NM107 (<20-fold change in EC50 values).
CONCLUSIONS: These initial results suggest that valopicitabine and HCV protease inhibitors have complementary cross-resistance profiles, thus combination therapies with these agents could be an advantageous strategy to suppress the emergence of resistance and maintain effective viral suppression. Additional in vitro drug combination studies are underway.
The 12 week data you mention is the NM283 - Riba study. This study (data set)will not be released @ EASL. This Info will remain blinded until study is complete ... top line data will be relaesd in June... full data set in a scientific meeting thereafter Yes, The latest Peg - NM283 data will be @ EASL