The epithelial-mesenchymal transition (EMT) of lung epithelium has been shown in in vivo studies to contribute to fibrosis and pathology of IPF. Using a high throughput screen, investigators at the University of California, San Francisco, have identified a small molecule compound that inhibits EMT both ex vivo and in vivo. This compound is already approved for human use and can be delivered orally. Ex vivo, the compound blocks EMT in both primary lung epithelial cells and lung tumor cells. In an in vivo bleomycin-induced pulmonary fibrosis mouse model, the compound was also able to block fibrosis, as measured both histologically and biochemically.

The investigators are also currently working on structure-activity relationship (SAR) analyses and generating analogs of the compound with more specific and optimized properties for treating IPF, which could lead to new drug entities.

File Number: 22206 

Web site: http://techtransfer.universityofcalifornia.edu/...

Disease: Respiratory and Pulmonary System

Other Information:

Partnership Opportunities

The technology is available for licensing and the investigators welcome the opportunity to work with industry partners.

Advantages and Suggested Uses

• Could lead to the first effective treatment of idiopathic pulmonary fibrosis


• Lead compound is already approved for use in humans


• Small molecule can be delivered orally


• Generation of analogs of the lead compound could lead to new drug entities


• Compounds effective in treating IPF could become the standard of care