Morphic Presents Positive Preclinical Data Supporting MORF-057 as an Oral Inhibitor of the α4β7 Integrin and Potential Treatment for Inflammatory Bowel Disease

Oral presentation at ECCO highlights MORF-057 as a potent, selective and orally available small molecule development candidate

Mechanism of action demonstrated in in vitro and in vivo models

WALTHAM, Mass., Feb. 14, 2020 (GLOBE NEWSWIRE) -- Morphic Therapeutic (NASDAQ: MORF), a biopharmaceutical company developing a new generation of oral integrin therapies for the treatment of serious chronic diseases, announced an oral presentation today highlighting Morphic’s product candidate MORF-057 at the 15^th Congress of the European Crohn’s and Colitis Organisation (ECCO). MORF-057 is in development as an oral inhibitor of the α₄β₇ integrin, a clinically proven target for the treatment of inflammatory bowel diseases (IBD).

“The approved antibody therapeutic vedolizumab has provided validation of α₄β₇ as an effective target for the treatment of inflammatory bowel disease. However, a significant opportunity remains to address IBD with an orally administered therapeutic,” commented Bruce Rogers, Ph.D., chief scientific officer of Morphic Therapeutic. “We are highly encouraged that the data presented at ECCO demonstrate MORF-057’s favorable in vitro pharmacodynamic characteristics and these results are reinforced by the positive outcomes in in vivo models using oral administration of MORF-057. These data further strengthen our conviction to move MORF-057 forward into clinical studies as planned.”

MORF-057 was specifically designed to inhibit α₄β₇-mediated migration of α₄β₇-expressing lymphocytes to the gut, which is a fundamental contributor to IBD. The data presented at ECCO support MORF-057 as a potent, selective and orally bioavailable small molecule inhibitor of the α₄β₇ integrin. In the studies presented, MORF-057 showed greater than 41,600-fold selectivity for α₄β₇ over α₄β_1.¹ High specificity for α₄β₇ over α₄β₁ is necessary to avoid inhibiting α₄β₁, which enables potentially pathological migration of lymphocytes to the central nervous system. Further, the data demonstrate that MORF-057 acts through its intended mechanism of action, by blocking the migration of α₄β₇-high-expressing lymphocytes. Notably, these results were replicated in both murine and primate models, with MORF-057 activity being equivalent to the murine equivalent of vedolizumab.