Presentation Information
[IS-1]Evolution of Treatment Strategies in IBD: Past, Present, and Future
*Stefan Wolfgang Schreiber (1. Department Medicine I, University Hospital Schleswig-Holstein, Kiel University, Germany)
IBD therapy has evolved from broad immunosuppression to an expanding repertoire of targeted drug classes. Corticosteroids, azathioprine and anti-TNF antibodies established the first effective therapeutic era: steroids induced remission, thiopurines maintained disease control in selected patients, and anti-TNF therapy changed the natural history of Crohn’s disease and ulcerative colitis by reducing inflammation, complications and the need for surgery.
The current era is defined by pathway-selective intervention. α4β7-integrin blockade provides gut-selective anti-trafficking therapy. IL-12/23 and, more specifically, IL-23 p19 inhibition have become central cytokine-directed strategies, with ongoing refinement of anti-IL-23 positioning, sequencing and use in early disease. Oral targeted therapies have added speed and flexibility: JAK inhibitors act broadly and rapidly on cytokine signalling, whereas S1P receptor modulators reduce lymphocyte egress.
The next wave will add new mechanisms rather than only more agents within existing classes. TL1A blockade may target inflammation and fibrosis-relevant pathways. Obefazimod, an oral small-molecule upregulator of miR-124, introduces an RNA-modulating therapeutic principle. Further approaches include barrier-protective therapies, epithelial protective receptor pathways, immunometabolic interventions such as the tryptophan–NAD axis, cellular therapies, organoid-based repair and rational biologic combinations, including heterofunctional antibodies.
Precision medicine should guide these choices: who receives which therapy, who needs early switching, and who should receive combination therapy. The future strategy is mechanism-based selection, early reassessment and rational escalation before irreversible damage occurs.
The current era is defined by pathway-selective intervention. α4β7-integrin blockade provides gut-selective anti-trafficking therapy. IL-12/23 and, more specifically, IL-23 p19 inhibition have become central cytokine-directed strategies, with ongoing refinement of anti-IL-23 positioning, sequencing and use in early disease. Oral targeted therapies have added speed and flexibility: JAK inhibitors act broadly and rapidly on cytokine signalling, whereas S1P receptor modulators reduce lymphocyte egress.
The next wave will add new mechanisms rather than only more agents within existing classes. TL1A blockade may target inflammation and fibrosis-relevant pathways. Obefazimod, an oral small-molecule upregulator of miR-124, introduces an RNA-modulating therapeutic principle. Further approaches include barrier-protective therapies, epithelial protective receptor pathways, immunometabolic interventions such as the tryptophan–NAD axis, cellular therapies, organoid-based repair and rational biologic combinations, including heterofunctional antibodies.
Precision medicine should guide these choices: who receives which therapy, who needs early switching, and who should receive combination therapy. The future strategy is mechanism-based selection, early reassessment and rational escalation before irreversible damage occurs.
The current era is defined by pathway-selective intervention. α4β7-integrin blockade provides gut-selective anti-trafficking therapy. IL-12/23 and, more specifically, IL-23 p19 inhibition have become central cytokine-directed strategies, with ongoing refinement of anti-IL-23 positioning, sequencing and use in early disease. Oral targeted therapies have added speed and flexibility: JAK inhibitors act broadly and rapidly on cytokine signalling, whereas S1P receptor modulators reduce lymphocyte egress.
The next wave will add new mechanisms rather than only more agents within existing classes. TL1A blockade may target inflammation and fibrosis-relevant pathways. Obefazimod, an oral small-molecule upregulator of miR-124, introduces an RNA-modulating therapeutic principle. Further approaches include barrier-protective therapies, epithelial protective receptor pathways, immunometabolic interventions such as the tryptophan–NAD axis, cellular therapies, organoid-based repair and rational biologic combinations, including heterofunctional antibodies.
Precision medicine should guide these choices: who receives which therapy, who needs early switching, and who should receive combination therapy. The future strategy is mechanism-based selection, early reassessment and rational escalation before irreversible damage occurs.
The current era is defined by pathway-selective intervention. α4β7-integrin blockade provides gut-selective anti-trafficking therapy. IL-12/23 and, more specifically, IL-23 p19 inhibition have become central cytokine-directed strategies, with ongoing refinement of anti-IL-23 positioning, sequencing and use in early disease. Oral targeted therapies have added speed and flexibility: JAK inhibitors act broadly and rapidly on cytokine signalling, whereas S1P receptor modulators reduce lymphocyte egress.
The next wave will add new mechanisms rather than only more agents within existing classes. TL1A blockade may target inflammation and fibrosis-relevant pathways. Obefazimod, an oral small-molecule upregulator of miR-124, introduces an RNA-modulating therapeutic principle. Further approaches include barrier-protective therapies, epithelial protective receptor pathways, immunometabolic interventions such as the tryptophan–NAD axis, cellular therapies, organoid-based repair and rational biologic combinations, including heterofunctional antibodies.
Precision medicine should guide these choices: who receives which therapy, who needs early switching, and who should receive combination therapy. The future strategy is mechanism-based selection, early reassessment and rational escalation before irreversible damage occurs.