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Image Search Results
Journal: Inflammatory Bowel Diseases
Article Title: Research-Based Product Innovation to Address Critical Unmet Needs of Patients with Inflammatory Bowel Diseases
doi: 10.1093/ibd/izab230
Figure Lengend Snippet: New potential therapeutic targets for IBD with differentiated MoAs. The diversity of IBD pathological mechanisms represents an opportunity for novel treatment approaches. Examples of therapeutic candidates in preclinical development include LBPs, which restore eubiosis by decolonizing pathobionts and repopulating commensal microbiota. Supplementation of RvE1 and inhibition of PAI-1 induce enterocyte proliferation and mucosal healing. An inhibitor of MLCK prevents its trafficking to TJs, avoiding barrier junction damage. A neutralizing MAb against IgA-coated bacteria-derived toxins can also prevent barrier damage. Inhibitors of SPNS2 abrogate leukocyte trafficking to sites of inflammation. BRD4 and Fbxo3 antagonists inhibit proinflammatory mediators, and an inhibitor of GCPII may abrogate local neuroinflammatory signals. Opportunities for treatment of fibrotic complications include neutralizing anti-TL1A monoclonal antibodies and inhibitors of ROCK. Programmable biopolymers are in development to enable tissue reconstruction and healing of the fistula tract. Abbreviations: BRD4, bromodomain-containing protein 4; GCPII, glutamate carboxypeptidase II; IBD, inflammatory bowel diseases; IgA, immunoglobin A; LBP, live biotherapeutic product; MAb, monoclonal antibody; MLCK, myosin light chain kinase; MoA, mechanism of action; PAI-1, plasminogen activator inhibitor–1; ROCK, rho-associated coiled-coil-containing protein kinase; RvE1, resolvin E1; TJ, tight junction.
Article Snippet: 212 Rho-associated coiled-coil-containing protein kinases (ROCKs) are a key mediator of these processes, but systemic inhibition of these kinases is toxic, leading several groups, including
Techniques: Inhibition, Derivative Assay