Tribune Therapeutics AB, a biotechnology company dedicated to treating the root causes of fibrotic diseases, has raised EUR 37 million in seed and Series A funding to advance a portfolio of therapies targeting central drivers of scar tissue formation. The funding includes a EUR 23 million Series A led by new investor LifeArc Ventures and joined by seed investors Innovestor’s Life Science Fund, Novo Holdings, HealthCap, and Inven2 as well as new Series A investors Industrifonden and Investinor.
“Tribune was founded on groundbreaking discoveries about the underlying drivers of fibrosis. From the beginning, it was clear that these discoveries had far-reaching therapeutic implications,” said Georg Vo Beiske, PharmD, Tribune Chief Executive Officer and HealthCap Venture Partner. “Advancing our programs towards the clinic with the backing of such a strong and prestigious investor group further increases our confidence in our innovative approach to treat fibrotic diseases, many of which are fatal.”
Current standard-of-care for the millions of patients with fibrotic diseases of the lung, kidney, liver and other tissue types is limited to managing symptoms or moderately slowing disease progression by targeting inflammatory mediators or growth factors. To create broadly applicable disease-modifying therapies, Tribune is instead targeting downstream, tissue-agnostic gatekeepers of scar formation and tissue remodeling, including the CCN family of proteins.
The company’s lead program, TRX-44, is currently in development for the treatment of fibrotic conditions including idiopathic pulmonary fibrosis (IPF), a chronic fibrotic lung disease that leads to respiratory failure and death within three to five years of diagnosis. The Series A financing will prepare TRX-44 to begin clinical trials and will advance additional programs targeting the CCN protein family.
TRX-44 prevents scar formation by mimicking the structure and function of CCN5. CCN5 is an endogenous protein that naturally blocks the pro-fibrotic effects of other CCN family members, including CTGF/CCN2 and WISP1/CCN4, on multiple cell types contributing to the fibrotic pathology. This approach is an evolution from blocking individual CCN proteins and their upstream activator, TGF-beta, and has the potential to combat a broader set of fibrotic diseases while avoiding the toxic side effects that have hampered the development of less targeted approaches.
Read more about the company here.
***
Additional information:
Milla Koistinaho, Partner, Innovestor Life Science
milla.koistinaho@innovestor.fi
+358 44 590 0603
