- Novel drug candidate for treatment of fibrosis.
- The safety of reovirus have been demonstrated in clinical trials.
Background & Technology
Tissue fibrosis is often found in various organs, such as Liver, Kidney, Lung, Skin and Heart and leads to organ failure and severe diseases. However current treatments for fibrotic disease are insufficient and often cause side effects.
Fibrosis is attributed to excess deposition of extracellular matrix (ECM) including collagen. Fibroblasts activated by several mediators (i.e. transforming growth factor-β (TGF-β)) produce excessive amounts of ECM.
Reovirus is administered to over 1000 patients in clinical trials (Phase III) as an anti-cancer drug, and verified its safety.
Inventors newly found that reovirus exhibits anti-fibrotic effects. They have demonstrated that liver fibrosis was resolved by reovirus. Anti-fibrotic effects do not depend on viral replication and reovirus don’t largely reduce cell viabilities. Therefore, this effect is induced via a different mechanism from anti-cancer effects.
- Reovirus declined the expression levels of fibrotic markers (α-SMA, COL1A1) on several cell lines (liver stellate cells, lung fibroblasts, heart fibroblasts and dermal fibroblasts), which are activated by TGF-β. Although cell viabilities were not largely reduced by reovirus
- Reovirus declined the expression levels of fibrotic markers (α-SMA, TIMP1) on liver fibrosis model mice. Decrease of collagen deposition was observed in liver section.
- UV-irradiated reovirus (inactivated reovirus) also declined the expression levels of fibrotic markers (α-SMA, TIMP1) on liver fibrosis model mice.
- Reovirus declined the expression levels of various fibrotic markers on bleomycin-induced pulmonary fibrosis model mice.
Fuminori Sakurai, Ph.D. (Osaka University)
We are looking for companies interested in licensing or co-developing for treating fibrotic diseases.
The inventors have some data, which support hypotheses on the mechanism of anti-fibrotic effects.
These data can be disclosed under CDA.