On January 21, 2020 HepaRegeniX GmbH, a preclinical stage company developing a novel therapy for the treatment of acute and chronic liver diseases reported the closing of its Series B financing round in excess of € 11 Mio. with contribution from all its existing investors namely Boehringer Ingelheim Venture Fund GmbH (BIVF), Novo Holdings A/S, the High-Tech Gruenderfonds, Coparion and Ascenion.

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The proceeds will be used to advance the first MKK4 inhibitor for treatment of acute and chronic liver diseases to the clinics later in 2020. 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. Over the last 2,5 years, HepaRegeniX focused on discovery of new and proprietary MKK4 inhibitors which led to the identification of 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 Dr. Wolfgang Albrecht, Managing Director of HepaRegeniX. "In this regard, we are very proud to have been able to secure this Series B financing round from our current investor base within a very short time period".

Prof. Dr. Johannes Zanzinger from BIVF, concluded on behalf of all investors, "HepaRegeniX with its unique therapeutic concept around acute and chronic liver diseases represents a company with significant potential. This Series B round 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".

(Press release, HepaRegeniX, JAN 21, 2020, View Source [SID1234666460])