The inflammatory bowel disease (IBD) therapy market is large and rapidly expanding, with a global value projected to reach $25.3–27.45 billion in 2025 and up to $40.27–44.5 billion by 2030–2034, driven by increasing prevalence of Crohn’s disease and ulcerative colitis, improved diagnostics, and greater awareness. Despite the market growth and a broad array of treatments, there remain substantial unmet patient needs. Many IBD patients experience chronic symptoms, frequent relapses, diminished quality of life, and a significant risk of surgery due to loss of therapeutic response or side effects. Key needs include long-term remission, reduced side effects, more predictable treatment responses, and options for patients refractory to existing biologics or small molecules.
Current therapies primarily consist of:
- Conventional agents: aminosalicylates, corticosteroids, and immunomodulators.
- Biologics: targeting TNF-α (e.g., infliximab, adalimumab), integrins (vedolizumab, natalizumab), and interleukins (ustekinumab).
- Small molecules: JAK inhibitors (tofacitinib, upadacitinib) and S1P receptor modulators.
- Surgical interventions are used when pharmacological options fail, especially in severe cases.
However, primary and secondary loss of response, risk of infections, and limited long-term efficacy remain problematic, particularly in patients with severe or refractory disease.
OPM-101 Summary
- Compound class: Small-molecule, highly selective orally available RIPK2 inhibitor
- Mechanism: Selective NOD2/RIPK2 pathway inhibition
- Indication: Inflammatory Bowel Disease (IBD): Ulcerative Colitis, Crohn’s Disease
- Clinical Phase: Phase 1 complete in HV (SAD & MAD); Phase 1b/2a in planning
- PK profile: Rapid absorption, long half-life
- Safety: Excellent; no serious adverse events
- Target engagement: Robust, sustained TNF-α inhibition even at low doses
- Key differentiator: Immunomodulation, not broad immunosuppression
Potential application
RIPK2, a central kinase in the NOD2 pathway, is overexpressed in inflamed IBD tissue and drives production of pro-inflammatory cytokines, such as TNF-α and IL-12/23, key mediators of intestinal inflammation. Preclinical and early clinical studies demonstrate that RIPK2 inhibitors can effectively reduce intestinal inflammation and suppress pathogenic immune signaling in IBD models, potentially offering a more targeted approach with fewer systemic immune effects. Thus, RIPK2 inhibitors represent a promising new class of oral, mechanism-based IBD therapeutics, with the potential to address unmet needs for efficacy, tolerability, and durable remission, especially among patients unresponsive to current biologics or immunosuppressive regimens.
OPM-101 modulates hyperinflammation of deregulated NOD/RIPK2 axis with strong link to IBD
Development status: Phase 1: Highlights
- Healthy Volunteers: Single Ascending Dose (SAD) phase with dosing from 5 to 1,000mg (including dedicated food-effect and female cohorts). Multiple Ascending dose (MAD) phase with dosing from 75 to 300mg bid for 14 days.
- Randomized, placebo-controlled, exploring PK/PD, safety, and target engagement metrics.
- Results: OPM-101 shows rapid absorption, long half-life of 12h. Safety is excellent with no serious adverse events, up to the largest doses. Target engagement is robust, with sustained TNF-α inhibition even at low doses
IP status
- Differentiated chemical backbone from other RIPK2 inhibitors based on OPM’s Nanocyclix technology.
- Composition of Matter patent filed in 2016, granted in most countries, including 5MM. Selection invention with OPM-101 and analogs filed in 2021
Licensing Opportunity
OPM-101 is available for out-licensing both globally and for specific regional development, potential asset acquisition worldwide