LONDON--(BUSINESS WIRE)--Engitix Ltd (?Engitix?), a biotechnology company developing a portfolio of programmes in fibrosis and solid tumours using its proprietary human extracellular matrix (ECM) platform, today entered into a licensing and collaboration agreement with Takeda Pharmaceutical Company Limited (?Takeda?) to discover and develop novel therapeutics for advanced fibrotic liver diseases, including non-alcoholic steatohepatitis (NASH). Under the terms of this agreement, Engitix and Takeda will collaborate in the confirmation and validation of targets and preclinical development of therapeutics in liver fibrosis using Engitix?s unique extracellular matrix (ECM) discovery platform. Takeda will have exclusive rights to develop and commercialise clinical candidates generated against validated targets derived from the collaboration. Engitix will receive an upfront payment, with additional near-term payments based on the confirmation and functional validation of selected targets. Engitix will be eligible to receive more than $500 million for the achievement of preclinical, development, regulatory and commercial milestones, as well as further royalty payments upon sales of commercialised products. Dr Giuseppe Mazza, Co-Founder and CEO of Engitix, commented:??Having Takeda, one of the world?s leading pharmaceutical companies with world-class drug development and commercialization capabilities, as a major collaborator, will accelerate the translation of novel ECM-derived targets into potential therapeutics for humans. We are excited to continue working with Takeda as this is the only partnership in the field of liver fibrosis currently using a human disease-specific ECM platform, paving the way for potential first-in class anti-fibrotic therapeutics?. By incorporating tissue- and disease-specific human ECM into?in vitro?models, Engitix?s platform preserves the natural cell microenvironment offering the unique capability of understanding the bioactive role of human ECM in modulating disease progression in fibrosis. By more accurately predicting disease drivers in human samples, the platform has the potential to accelerate discovery and reduce late-stage clinical failures. Dr Gareth Hicks, Head of the GI Drug Discovery Unit at Takeda, added:??There is a vital need for new treatments that will positively impact the lives of patients with advanced liver diseases. Engitix?s ECM platform offers a powerful tool for identifying and validating novel targets that will be valuable in the development of direct anti-fibrotic therapies. Our partnership with Engitix underscores our commitment to explore innovative approaches to treat late-stage liver disease.? Liver fibrosis, or scarring, and its life-threatening end stage of liver cirrhosis, is the common pathway of chronic liver diseases (CLDs), such as NASH, alcoholic liver disease, viral hepatitis and cholangiopathies such as primary biliary cirrhosis and primary sclerosing cholangitis. It is estimated that 844 million people have CLDs worldwide, resulting in a mortality rate of 2 million deaths per year. Despite the clear need for effective therapeutics, there are currently no approved medicines to treat CLDs. - ENDS - Notes to Editors: About Engitix Ltd Engitix is developing a portfolio of programmes in fibrosis and solid tumours using its pioneering human extracellular matrix (ECM) drug discovery platform. The use of more physiologically relevant human?in vitro?models is transforming our ability to identify new targets, to develop more advanced liver treatments and to enable a more accurate prediction of the efficacy of therapeutic candidates. Now a transatlantic biotechnology company, Engitix was founded in 2016 to commercialise cutting-edge research at the Institute for Liver and Digestive Health, Division of Medicine, University College London (UCL). The Company is headquartered at the world renowned Royal Free Hospital, London, UK with its wholly owned US subsidiary Engitix, Inc, based in Cambridge, MA, US. For more information, please visit?www.engitix.com?or connect with us on?LinkedIn.