Abstract: The present invention derives from the unexpected finding that necroptosis is a novel biomarker and target for therapy in patients with liver failure such as acute liver failure (ALF) and acute-on-chronic liver failure (ACLF). RIPK1, MLKL or RIPK3 can be detected and quantified in serum or plasma, and used as a biomarker for outcome in ACLF and other diseases involving aberrant necroptosis. By antagonising RIPK1, MLKL or RIPK3 many of the unwanted consequences or symptoms of acute-on-chronic liver failure (ACLF) may be reduced. The present invention utilises these findings to identify and provide antagonists of RIPK1, MLKL and RIPK3 that may be used in the treatment or prevention of ACLF. The present invention utilises these findings to identify and provide antagonists of RIPK1, MLKL or RIPK3 that may be used in the treatment or prevention of aberrant necroptosis in the kidney, brain, liver or other organ of the body.

Abstract: The present invention derives from the unexpected finding that the combination of the stem cell mobilisers such as G-CSF and antagonists of TLR4 is beneficial to patients with liver failure, such as acute liver failure (ALF) or acute-on-chronic liver failure (ACLF). The present invention utilises these findings to provide stem cell mobilisers such as G-CSF and antagonists of TLR4 that may be used in the treatment or prevention of liver failure, such as ALF or ACLF. Also encompassed by the invention is the provision of a stem cell and an antagonist of TLR4 for use in the treatment or prevention of liver failure, such as ALF or ACLF.

Abstract: Disclosed herein are methods of preventing, treating, and delaying the onset or progression of diseases associated with hepatic stellate cells (HSCs), such as non-alcoholic fatty liver disease (NAFLD), fibrosis, and liver cancer, using ammonia-lowering therapies.

Abstract: The present invention derives from the unexpected finding that necroptosis is a novel biomarker and target for therapy in patients with liver failure such as acute liver failure (ALF) and acute-on-chronic liver failure (ACLF). RIPK1, MLKL or RIPK3 can be detected and quantified in serum or plasma, and used as a biomarker for outcome in ACLF and other diseases involving aberrant necroptosis. By antagonising RIPK1, MLKL or RIPK3 many of the unwanted consequences or symptoms of acute-on-chronic liver failure (ACLF) may be reduced. The present invention utilises these findings to identify and provide antagonists of RIPK1, MLKL and RIPK3 that may be used in the treatment or prevention of ACLF. The present invention utilises these findings to identify and provide antagonists of RIPK1, MLKL or RIPK3 that may be used in the treatment or prevention of aberrant necroptosis in the kidney, brain, liver or other organ of the body.

Abstract: Disclosed herein are methods of preventing, treating, and delaying the onset or progression of diseases associated with hepatic stellate cells (HSCs), such as non-alcoholic fatty liver disease (NAFLD), fibrosis, and liver cancer, using ammonia-lowering therapies.

Abstract: Disclosed herein are methods of preventing, treating, and delaying the onset or progression of diseases associated with hepatic stellate cells (HSCs), such as non-alcoholic fatty liver disease (NAFLD), fibrosis, and liver cancer, using ammonia-lowering therapies.

Abstract: Disclosed herein are methods of preventing, treating, and delaying the onset or progression of diseases associated with hepatic stellate cells (HSCs), such as non-alcoholic fatty liver disease (NAFLD), fibrosis, and liver cancer, using ammonia-lowering therapies.

Abstract: Disclosed herein are methods of preventing, treating, and delaying the onset or progression of diseases associated with hepatic stellate cells (HSCs), such as non-alcoholic fatty liver disease (NAFLD), fibrosis, and liver cancer, using ammonia-lowering therapies.

Abstract: Disclosed herein are methods of preventing, treating, and delaying the onset or progression of diseases associated with hepatic stellate cells (HSCs), such as non-alcoholic fatty liver disease (NAFLD), fibrosis, and liver cancer, using ammonia-lowering therapies.