IBD Program
TP-317: First-in-Class, Oral BLT1 Agonist for
Moderate-to-Severe Ulcerative Colitis and Crohn’s Disease
The Challenge in IBD
Despite use of advanced therapies—anti-TNFs, IL-23 inhibitors, JAK inhibitors, anti-integrins—the majority of patients fail to achieve durable remission.
Current drugs directly target inflammation but not the epithelial barrier dysfunction that drives disease progression.
All approved therapies rely on immunosuppression, carrying significant safety burdens for long-term maintenance of remission.
RvE1 Activates Two Layers of Resolution Biology through BLT1
Mechanisms Not Addressed by Immunosuppressive Therapies
The TP-317 Approach
Breaking the IBD vicious cycle through four therapeutic pillars
Multi-Modal Mechanism
TP-317 addresses four key aspects of IBD pathology — targeting not just inflammation, but epithelial damage, fibrosis, and visceral pain through activation of the BLT1 receptor — without immunosuppression.
