HepaRegeniX: €11m for liver disease treatment

In preclinical studies, HepaRegeniX’ MKK4 inhibitor had demonstrated efficacy in liver regeneration and experimental acute and chronic liver disease models. Now, the Tübingen-based biotech plans to take its drug candicate to the clinic. To that end, HepaRegenix has secured a Series B financing in excess of €11m from its existing investors, namely Boehringer Ingelheim Venture Fund GmbH (BIVF), Novo Holdings A/S, the High-Tech Gruenderfonds, Coparion and Ascenion.

MKK4 (Mitogen-Activated Protein (MAP) Kinase 4) is a key regulator of liver regeneration and suppression of MKK4 unlocks the regenerative capacity of hepatocytes even in severely diseased livers. Based on this concept, HepaRegeniX has identified several preclinical drug candidates. Results from experimental, clinically relevant disease models further validated the concept that MKK4-inhibition improves the regeneration capacity of hepatocytes in affected organs and provided strong evidence for successful clinical development.

“This is an exciting phase for HepaRegeniX to soon advance our first compound into the clinic based on compelling preclinical data for our proprietary MKK4 inhibitor” commented HepaRegeniX CEO Michael Lutz. On behalf of the investors, Johannes Zanzinger from BIVF, concluded: “HepaRegeniX with its unique therapeutic concept around acute and chronic liver diseases represents a company with significant potential. This Series B round together with the recent appointment of Michael Lutz as CEO will substantially help to clinically validate the underlying concept and deliver novel and proprietary orally available small molecule kinase inhibitors with significant potential in the field of liver regeneration.”

HepaRegeniX was founded in 2017, when it announced the completion of a €9 million Series A financing. The start-up develops a novel therapeutic concept for the treatment of liver diseases, which was discovered by Professor Lars Zender and his research group at the University Hospital Tubingen.