Murigen is developing novel Anti-apoptotic agents: Several lead compounds have beenidentified that may have a broad therapeutic potential, proof of principle has been demonstrated in murine models.
Researchers at WEHI have discovered that two specialised molecules act in opposition to each other to control platelet life span by regulating apoptosis. Pro-survival Bcl-xL constrains the pro-apoptotic activity of Bak to maintain platelet survival, but as Bcl-xL degrades, aged platelets are primed for cell death.
Genetic ablation or pharmacological inactivation of Bcl-xL reduces platelet half-life and causes thrombocytopenia in a dose-dependent manner. Deletion of Bak corrects these defects, and platelets from Bak-deficient mice live longer than normal. Although these ground-breaking findings were initially in platlets, they have implications in a wide variety of cell types and as a result are potential therapeutic targets for a broad range of indications.
Therapeutics treatment of cancers extended platelet lifespan for transfusion extended life span of cells in liver diseases, neurodegenerative diseases, cardiac ischemic reperfusion injury.
The IP is protected by several provisional patent applications. These applications cover claims defining Bcl-2 family proteins as a therapeutic target for anti-apoptosis therapies, and assay methods for high throughput cell-based screening. The structures of compounds under investigation have not been disclosed.