On behalf of the entire Genkyotex team, I would like to thank you for the trust you have placed in our project. I am thrilled to welcome you to our new website and introduce our Group that is now listed, following the strategic operation with Genticel, which you supported.
Our unique therapeutic approach is based on the selective inhibition of NOX enzymes and covers a broad range of disease processes, including fibrosis, inflammatory pain, cancer growth, and neurodegeneration. These diseases are responsible for almost 45% of all deaths in the developed world*.
We have developed a platform capable of identifying orally available small-molecules that selectively inhibit specific NOX enzymes. Our portfolio of drug candidates enables one or multiple NOX enzymes to be targeted. Our lead product candidate, GKT831, a NOX1 and NOX4 inhibitor, is expected to be tested in a phase II clinical trial in primary biliary cholangitis (PBC, an orphan fibrotic disease) during the first half of 2017. This product candidate may also be active in other fibrotic indications. Our second drug candidate, GKT771, a NOX1 inhibitor targeting multiple pathways in pain processing, and inflammation, should go through a clinical trial in the second half of 2017.
Our recent strategic operation with Genticel was a major milestone for Genkyotex. It turned our company into a listed Group, with a stronger financial structure. Our improved cash position will allow us to perform a clinical trial with GKT831, start early clinical development with GKT771, and continue our discovery activities in other therapeutic fields. The licensing agreement signed between Genticel and Serum Institute of India Ltd., in 2015, could also generate substantial additional revenue in the longer term.
We are delighted to have you onboard as we achieve another milestone in Genkyotex’s development. We will continue to work hard to develop our first-in-class drugs with substantial therapeutic potential for application such as fibrosis and inflammatory pain.
Chief Executive Officer
* The Journal of Clinical Investigation; Common and unique mechanisms regulate fibrosis in various fibroproliferative diseases; March 2007