Future drugs for the treatment of hepatitis C
| Future therapies | Characteristics |
|---|---|
| HCV, hepatitis C virus; PEG-IFN, pegylated interferon. | |
| Albuferon-alpha (Human Genome Science) phase III | Longer half life than PEG-IFN due to fusion of albumin to IFN (85.7 kDa). |
| Viramidine (Valeant) phase III | Prodrug of ribavirin with less anaemia. |
| HCV protease inhibitors, HCV polymerase inhibitors phase I/II (see table 5) | Direct antiviral action with fewer side effects than IFN. Direct inhibition of the HCV protease/HCV polymerase which are crucial for viral replication. |
| Other small molecules (eg ribozymes, siRNA, antisense molecules) phase I/II | Direct antiviral effect with potentially fewer side effects than IFN. Interference with the HCV genome or blocking translation leading to inhibition of viral replication. |
| Caspase inhibitors (eg IDN-6556, Pfizer) phase I/II | Antifibrogenic effect. Reduction of hepatocyte apoptosis and reduction of hepatic stellate cell activation. |
| Toll-like receptor agonists (CpG 10101-TLR-9 agonist, Coley; ANA-975 TLR-7 agonist; Anadys) phase I | Therapeutic stimulation of Toll-like receptor pathways to modulate (Th1 shift) immune responses and to stimulate innate immunity. |
| Therapeutic vaccination (E1y—protein vaccine, Innogenetics; IC-41—peptide vaccine, Intercell) phase I/II | Stimulation of the impaired HCV specific immune response in order to control viral replication or alter the natural course of the disease (regression of fibrosis). |