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GI-targeted ROCK inhibitor

First-in-class programme designed to treat Crohn’s Disease-associated fibrosis

Fibrosis

Up to 50% of patients with Crohn’s disease can develop significant fibrosis and stricture formation within 10 years after diagnosis. The current management of fibrotic strictures of the gastrointestinal (GI) tract is primarily surgical as there are no drugs approved that target this fibrosis, and can progress despite intervention with anti-inflammatory therapies.

ROCK1 and ROCK2 are intracellular kinases with multiple functions, shown to be implicated at various points in pathways leading to fibrosis. However, systemic ROCK1/2 inhibitors (or pan-ROCK inhibitors) are known to induce hypotension and are therefore unlikely to be tolerated by patients. Our GI-targeted ROCK inhibitor is designed to only work at the site of action in the GI tract and to degrade quickly, once absorbed into the bloodstream, through enzyme-mediated metabolism.

Our GI-targeted ROCK inhibitor shows both prophylactic and therapeutic effects on fibrosis in multiple animal models. Our inhibitor is designed to reduce fibrosis, prevent disease progression and surgical intervention thereby improving patients’ lives.

Our GI-targeted ROCK programme aims to address this high unmet need in the treatment of Crohn’s disease-associated fibrosis

Figure 1: Reduction in collagen in a murine model of Crohn’s fibrosis. Increase of collagen staining shown in blue in the DSS-treated animals. GI-targeted ROCK inhibitor reduces production of collagen seen as a reduction in blue (trichrome) staining.