Research & Development

Research & Development

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“"The biology around SAP regulation of innate immune system control of fibrotic processes is very exciting. We are going to change the way people  think about impacting this disease process.”

– Mark Lupher, Ph D. 
 Vice President, 
 Drug Discovery

The Biology of Fibrosis

Fibrosis is the harmful build-up of scar tissue that leads to loss of tissue and organ function.  A pathology common to a number of serious and chronic diseases, fibrosis is a leading cause of morbidity and mortality and can affect virtually all tissues and organ systems.  Despite the high prevalence of fibrosis and its enormous impact on human health, there currently are no approved anti-fibrotic drug therapies in the US or Europe for any fibrotic disease.

Groundbreaking New Insights

Breakthrough research by Promedior and its collaborators has identified the cellular source and control mechanisms for the initiation and progression of fibrotic and inflammatory diseases.  In particular, a specific innate immune white blood cell population, called monocytes, has been shown to be the key regulator that promotes either resolution or progression of fibrotic disease.  Monocytes have been identified as the source and master controller of key points in the pathways of fibrotic diseases including: the source of profibrotic and pro-inflammatory fibrocyte and M2 macrophage cell populations as well as pro-resolution cytokines, such as interleukin-10.

Monocytes Control the Fibrotic Process

 

Monocytes Are The Master Controller:  Vital to the immune system’s response to chronic or acute injury, monocytes are the key source and master controller cells that initiate and drive the pathological progression of fibrosis.  During normal healing they also trigger signaling cytokines and chemokines that direct the immune response to resolve fibrosis or inflammation.

Many individual and redundant stimuli, including cytokines, growth factors and chemokines, activate monocytes and the downstream fibrocyte and profibrotic (M2) macrophage cell populations.  Although fibrosis has been an area of active research for many years, the inherent biological complexity underlying fibrosis has, in the past, created a significant challenge for drug development.  With a large number of individual and redundant stimuli attempting to “wall off” the injury through production of fibrotic scar tissue, it has been difficult to effectively reverse the process and stimulate resolution, until now.

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