Reovirus for Treatment of Fibrosis

DATE

January 4, 2021

Reovirus reduced the expression levels of fibrotic markers (α-SMA, TIMP1) on liver fibrosis model mice

Key Word : Fibrosis, Cardiovascular System, Dermatology, Hepatology, Respiratory System, Gene therapy, DNA vaccine

Background / Context / Abstract:

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. This occurs when fibroblasts are activated by several mediators (i.e. transforming growth factor-β (TGF-β)), causing them to produce excessive amounts of ECM.
Reovirus has been administered to over 1000 patients in clinical trials (Phase III) as an anti-cancer drug, and its safety has been verified.

Technology Overview:

Inventors at Osaka University recently found that reovirus exhibits anti-fibrotic effects. They have demonstrated that liver fibrosis was resolved by reovirus. These anti-fibrotic effects do not depend on viral replication and the reovirus doesn’t largely reduce cell viabilities. Therefore, this effect is induced via a different mechanism from the anti-cancer effects.

Benefits:

Novel drug candidate for treatment of fibrosis.
The safety of reovirus have been demonstrated in clinical trials.
Reovirus is applicable for various fibrotic diseases.

Further Details:

Reovirus reduced 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 administration.
Reovirus reduced the expression levels of fibrotic markers (α-SMA, TIMP1) on liver fibrosis model mice. Decrease of collagen deposition was observed in liver sections.
UV-irradiated reovirus (inactivated reovirus) also reduced the expression levels of fibrotic markers (α-SMA, TIMP1) in a liver fibrosis mouse model.

Potential Applications / Potential Markets:

・Potential treatment for fibrosis

State of Development / Opportunity / Seeking:

・Available for exclusive and non-exclusive licensing
・Exclusive/non-exclusive evaluation for defined period (set up for options)
・Collaborative/supportive research

IP Status:

WO/2017/141942 (National phase EP, US, JP, CN, CA etc.)

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