Galapagos NV recently regained full rights to their GPR84 program, the GLPG1205 inhibitor, and to GLPG2196 (GLPG1205 back compound), as part of a new agreement with partner Janssen Pharmaceuticals.
Galapagos is working on creating and developing new modes-of-action in several areas of life science, including the inflammation process. The company was founded in 1999 when biotech companies Crucell and Tibotec joined forces. Since then, Galapagos’ development model combines internal discovery programs and service-related capabilities, utilizing technological platforms for their research projects based on adenoviruses that introduce very specific gene sequences in human cells so that proteins can be knocked-in or knocked-out.
GLPG1205 (‘1205) functions on GPR84, a novel mechanism of action to treat Inflammatory Bowel Diseases (IBD) that was developed by Galapagos. The company presented evidence that shows how GPR84 plays a makor role in IBD pathology. Furthermore, Galapagos researchers discovered that GLPG1205, a selective antagonist of GPR84, is effective in preclinical models for inflammatory bowel diseases, revealing “good safety, target engagement, and favorable drug-like properties in Phase 1 studies in healthy volunteers,” according to a company press release. Galapagos is now starting patient recruitment for a new Phase 2 trial that will begin enrollment before the end of the year.
The GPR84 is a G-coupled protein receptor, a free fatty acid protein that plays an important role in the regulation of neutrophils, monocytes and macrophages in the immune system. The company recognizes that GPR84 is extremely important in the inflammation process and that it is over-expressed in IBD patients. Through in vitro models, Galapagos confirmed that when GPR84 is inhibited it prevents macrophage and neutrophil chemotaxis and, through in vivo models, that ‘1205 prevents IBD from progressing. This ‘1205 becomes the first inhibitor of GPR84 ever tested in humans; results show that it not only works, but that it is safe as well.