Fibrosis is a process of pathological wound healing, when normal parenchymal tissue is replaced by connective tissue including collagen. Fibrosis thus induces tissue remodelling with the formation of a scar tissue, which interferes with or totally inhibits the normal architecture and function of the underlying organ or tissue.
The condition can affect any organ such as liver, kidney, lung or heart, among many others. Even though the fibrotic lesions tend to be focal on individual organs, the cascade that triggers fibroblast activity is fairly conserved across tissues. While fibrosis is a key driver of end stage organ damage and death in a variety of chronic diseases, no treatments to halt or reverse the lesions are currently available.
Sygnature Discovery’s integrated teams of medicinal chemists, bioscientists, DMPK and translational scientists have developed significant expertise in drug discovery in the fibrosis field, with a particular focus on kidney, liver and lung fibrosis.
As well as having access to a range of ready, validated in vitro assays for fibrosis using liver and kidney fibroblasts, our bioscientists are skilled in developing bespoke assays for individual projects that precisely meet the needs of clients’ drug discovery efforts, regardless of the target organ.
Additionally, we offer a range of translational models to evaluate novel therapeutics for the treatment of fibrosis, these include the adriamycin model of kidney fibrosis with associated readouts and the CD, H-FFC, ob/ob H-FFC, and H-FFC CCl4 mouse which develop liver fibrosis alongside NASH.
Rat Kidney Cell TGF-β Fibroblast to Myofibroblast Transdifferentiation (FMT) Assay (inhibition and reversal modes). High-content imaging and RT-qPCR readouts.
Primary Human Hepatic Stellate Cell TGF-β Fibroblast to Myofibroblast Transdifferentiation (FMT) Assay (inhibition and reversal modes). High-content imaging and RT-qPCR readouts.
In vivo models of kidney fibrosis. Adriamycin-induced model of focal segmental glomerulosclerosis (FSGS) and fibrosis
Dietary induced models of liver fibrosis and NASH. Choline deficient (CD) mouse, high-fat high-fructose high-cholesterol (H-FFC) mouse, ob/ob H-FFC and H-FFC CCl4.