Date: 2011-11-05
Type of information:
phase: 2a
Announcement: results
Company: Santaris Pharma (Denmark)
Product: miravirsen
Action mechanism: Miravirsen is a microRNA-targeted drug. Developed using Santaris Pharma proprietary Locked Nucleic Acid (LNA) Drug Platform, miravirsen is an inhibitor of miR-122, a liver specific microRNA critical for Hepatitis C virus RNA accumulation in the liver. Miravirsen is designed to recognize and sequester miR-122, making it unavailable to the Hepatitis C virus. As a result, the level of Hepatitis C virus is profoundly reduced.
Disease: hepatitis C
Therapeutic area: Infectious diseases
Country:
Trial
details: The randomized, double-blind, placebo-controlled, ascending multiple-dose Phase 2a study assessed the safety and tolerability of miravirsen in treatment-naïve patients with chronic HCV genotype 1 infection. Patients with chronic HCV genotype 1 infection were enrolled sequentially to one of three cohorts (9 active: 3 placebo per cohort) at doses of 3, 5 and 7 mg/kg. Miravirsen was given as a total of 5 weekly subcutaneous injections over 29 days.
Latest
news: * On November 5, 2011, Santaris Pharma has presented new data from the Phase 2a trial showing that miravirsen given as a four-week monotherapy treatment provided robust dose-dependent anti-viral activity with a mean reduction of 2 to 3 logs from baseline in HCV RNA (log10 IU/mL) that was maintained for more than four weeks beyond the end of therapy. These new clinical data as well as the data in the abstract are being presented in a late-breaking oral presentation on November 7 at 4p.m., at The Liver Meeting® 2011, the 62nd annual meeting of the AASLD, in San Francisco, California. Table 1: Mean HCV RNA (log10 IU/mL) Change from Baseline in all 3 Cohorts Dose Group Mean HCV RNA decline p-value (t) Pooled placebo -0.01 (0.19) --- Miravirsen 3 mg/kg -0.57 (0.13) 0.034 Miravirsen 5 mg/kg -2.16 (0.58) 0.007 Miravirsen 7 mg/kg -2.73 (0.55) <0.001
New clinical data from the Phase 2a study demonstrate that four out of nine patients treated at the highest dose (7 mg/kg) with miravirsen became HCV RNA undetectable with just four weeks of dosing. These data provide clinical evidence that miravirsen’s unique mechanism-of-action offers high barrier to viral resistance and the potential for cure with monotherapy. Miravirsen was also well tolerated in patients with HCV, signaling a possible advantage over standard of care treatment.
Data from the Phase 2a study show that the mean change from baseline in HCV RNA (log10 IU/mL) at 10 weeks after initiation of therapy was -0.57, -2.16, -2.73 in the 3, 5 and 7 mg/kg miravirsen dose groups, respectively vs. -0.01 in the placebo group (Table 1).
IU/mL (SEM) at week 10
MIR vs. placebo
