FibroStatin scientists have discovered an extracellular kinase named GPBP that is a key regulator of an important biological process called the epithelial-to-mesenchymal transition or EMT.
EMT causes a tumor cell to transition into a drug-resistant and invasive phenotype.
EMT also leads to the production of cells that cause organ fibrosis.
GPBP regulates the composition and organization of a bioactive extracellular collagen IV network which stabilizes the mesenchymal phenotype resulting from EMT.
GPBP inhibition compromises collagen IV network formation and the viability of cells that cause advanced cancer and organ fibrosis.
GPBP inhibition targets the microenvironment and not the cell, and therefore it is not expected to induce drug resistance.
These treatments have been designed to specifically target an oligomeric form of GPBP that is exclusive of the pathogenic EMT process.
Consistent with their specificity, they have exhibited robust treatment effects and low toxicity in animal studies.
These treatments impact a critical underlying cause of tumor drug resistance and fibrosis in the lungs and likely in other organs.
Plasma levels of GPBP increase in disease thereby providing a means to identify patients who are more likely to respond to GPBP targeted therapies.