Landos Biopharma has dosed the first cohort of subjects in a Phase l clinical study designed to investigate the safety and tolerability of BT-11 for the treatment of inflammatory bowel disease (IBD), including ulcerative colitis (UC) and Crohn’s disease (CD).
The randomised, double-blind, placebo-controlled, single and multiple-ascending dose trial is expected to enrol up to 70 healthy subjects.
Landos Biopharma chairman and CEO Dr Josep Bassaganya-Riera said: “We raised our Series A round in September 2017 to finance the completion of the IND-enabling studies and Phase l clinical testing.
“The FDA accepted Landos’ IND for BT-11 in June, and the dosing of the first subject cohort confirms that we have effectively executed that plan. Launching this trial marks a significant milestone for Landos and represents the next step in confirming the safety and effectiveness of BT-11, which has the potential to greatly impact the treatment options of millions of people afflicted by IBD around the world.
“Despite current treatments, there remains an unmet clinical need for chronic therapies for UC and CD with improved safety and tolerability.”
BT-11 is an investigational, orally active, small molecule drug that is designed to activate the Lanthionine Synthetase C-Like 2 (LANCL2) pathway, targeting the gastrointestinal tract.
How well do you really know your competitors?
Access the most comprehensive Company Profiles on the market, powered by GlobalData. Save hours of research. Gain competitive edge.
Your download email will arrive shortly
Not ready to buy yet? Download a free sample
We are confident about the unique quality of our Company Profiles. However, we want you to make the most beneficial decision for your business, so we offer a free sample that you can download by submitting the below formBy GlobalData
Several researchers suggest that LANCL2 plays a vital role in the immunoregulatory process.
Various preclinical and translational studies have shown that BT-11 activates the LANCL2 pathway and modulates interactions between immunological and metabolic signals in immune cells to create a favourable regulatory microenvironment in the gut, thereby decreasing the production of key inflammatory mediators and increasing anti-inflammatory molecules within the site of inflammation.