Morphic Therapeutic announced the completion of targeted enrollment of 30 patients ahead of schedule for the main cohort of the EMERALD-1 phase 2a study of MORF-057 in patients with moderate to severe ulcerative colitis (UC). Based on the rapid enrollment and substantial demand accrued to enter EMERALD-1, there were a significant number of patients in screening at the time of the 30th patient's enrollment; these patients will be eligible to enter the study if the eligibility criteria are met. Enrollment in the exploratory cohort of up to ~10 patients who have previously failed treatment with vedolizumab is ongoing.

EMERALD-1 (MORF-057-201) is an open-label multi-center phase 2a trial designed to evaluate the efficacy, safety, and tolerability of MORF-057 in adults with moderate to severe ulcerative colitis. The EMERALD-1 study is planned to enroll up to 30 patients with moderate to severe ulcerative colitis who will be treated with 100 mg BID (twice daily) at sites in the United States and Europe and 5 patients who have previously failed on advanced UC therapies. The primary endpoint of the trial is the change in Robarts Histopathology Index (RHI), a validated instrument that measures histological disease activity in ulcerative colitis at 12 weeks compared to baseline.

Patients will then continue for an additional 40 weeks of maintenance therapy followed by a 52-week assessment. Secondary and additional outcome measures in the EMERALD-1 study include change in the modified Mayo clinic score, safety, pharmacokinetic parameters and key pharmacodynamic measures including a4ß7 receptor occupancy and lymphocyte subset trafficking. Morphic is developing MORF-057 as a selective, oral small molecule inhibitor of the a4ß7 integrin for patients with inflammatory bowel disease (IBD).

a4ß7 has been clinically validated as a target for the treatment of IBD by the success of the approved injectable antibody therapeutic vedolizumab. MORF-057, like vedolizumab, is designed to block the interactions between a4ß7 on the surface of lymphocytes and the mucosal endothelial cell ligand MAdCAM-1, substantially reducing lymphocyte migration from the bloodstream into intestinal mucosal tissues and avoiding inflammation that is associated with IBD.