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> Insights > World Inflammatory Bowel Disease Day | ACRO Stands with You in Safeguarding Intestinal Health 
Every year on May 19th, the global medical community turns its focus to those battling inflammatory bowel disease (IBD). Behind this observance lie 10 million patients enduring relentless abdominal pain, bloody stools, and malnutrition, alongside countless families trapped in the vicious cycle of chronic diarrhea, intestinal obstruction, and cancer progression. Clinical evidence reveals a sobering reality: untreated IBD patients face a 70% risk of requiring intestinal resection within a decade, while early therapeutic intervention enables mucosal healing in 75% of cases. As the medical war against immune system dysregulation intensifies, precision-targeted therapies are emerging as breakthrough strategies to dismantle this invisible biological siege.
Factors influencing the development of IBD
ACROBiosystems has developed a comprehensive product portfolio for IBD research including highly active recombinant proteins, stable cell lines, and inhibitor screening kits. Our solutions span the entire drug development continuum – from target discovery and validation, candidate drug screening and development to CMC manufacturing and quality control – accelerating the efficient translation of IBD innovative therapies from foundational research to clinical implementation.
Free download: ACRO's autoimmune disease drug development solutions!
IBD encompasses chronic inflammatory bowel disorders driven by immune dysregulation, primarily comprising Crohn’s Disease (CD) and Ulcerative Colitis (UC). The pathogenesis involves a complex interplay where genetic predisposition converges with environmental triggers—such as dietary patterns and infections—to disrupt intestinal barrier integrity. This breakdown manifests as epithelial tight junction disruption, compromised mucus layer thickness, and gut microbiota dysbiosis, collectively permitting luminal antigen leakage into the submucosa. Such breaches trigger hyperactivation of the innate immune system, initiating a self-perpetuating inflammatory cascade.
The cytokines of immunological pathogenesis of IBD
Following activation of the innate immune system, macrophages and neutrophils aberrantly release pro-inflammatory cytokines such as TNF-α and IL-23, recruiting additional immune cells to trigger the "initial inflammatory surge." Subsequently, the adaptive immune system becomes dysregulated, characterized by hyperactivation of Th1/Th17 cells and impaired regulatory T cell function, leading to autoantibody production and chronic inflammatory cycling. Concurrently, the equilibrium between pro-inflammatory cytokines (e.g., TNF-α, IL-6) and anti-inflammatory mediators (e.g., IL-10) collapses. This imbalance amplifies the "cytokine storm" through NF-κB and JAK-STAT signaling pathways, enabling indiscriminate inflammation propagation. Such immune hyperactivation accelerates intestinal epithelial apoptosis, degrades tight junction proteins, and ultimately establishes refractory intestinal ulceration.
Among leading global pharmaceutical companies, a significant number have prioritized the IBD therapeutic area. In 2023, clinical pipeline projects in this field increased by 25% year-over-year, with target innovation demonstrating a tripartite competitive landscape.
Within the cytokine domain, TNF-α inhibitors remain market dominants, exemplified by adalimumab achieving over $20 billion in annual sales. The IL-23 target has emerged as a new focal point, with Johnson & Johnson’s ustekinumab surpassing $10 billion in annual sales. AbbVie’s risankizumab demonstrated 60% clinical response at 14 weeks in Phase III trials, directly challenging ustekinumab's market position.
The JAK-STAT pathway has witnessed safety-driven innovation: AbbVie’s upadacitinib achieved 26% mucosal healing rate with 1.2% serious infection incidence, driving 45% annual growth for JAK1-selective inhibitors. Bristol Myers Squibb’s TYK2 inhibitor deucravacitinib demonstrated 40% remission rate with zero thrombotic events, potentially reshaping treatment paradigms.
In gut-specific targets, Takeda’s vedolizumab maintains leadership in α4β7 integrin inhibition with 45% 5-year sustained remission. The oral MAdCAM-1 inhibitor AJM300 achieved 63% Phase II response rate, targeting a billion-dollar market. Emerging target TL1A has emerged as the standout contender: Merck’s TEV-48574 demonstrated superior Phase II results (62% clinical remission + 42% fibrosis reversal), prompting intensified investments from Pfizer, Roche, and others. The TL1A inhibitor market is projected to exceed $5 billion by 2030.
Approved originator biologics for IBD (Source: Pharmacodia)
Advances in understanding IBD pathogenesis are driving systemic innovation in therapeutic paradigms: A multidimensional coordinated framework integrates dual defense mechanisms through targeted synergy between immunomodulators and biologics (e.g., azathioprine combined with anti-TNF-α/integrin agents), establishes multi-pathway inhibitory networks via small-molecule agents (JAK inhibitors/S1P modulators), and implements activity-adapted dynamic treatment protocols. Precision medicine implementation leverages genotype-guided interventions (e.g., IL-17A/TNF-α dual blockade for NOD2-mutated IBD), microbiota-targeted modulation (fecal microbiota transplantation/probiotic combinations), and biomarker-stratified therapeutic algorithms. Innovative modalities feature bifunctional biologics (ustekinumab targeting IL-12/IL-23), tissue-selective agents (α4β7 integrin inhibitors/oral MAdCAM-1 antagonists), and emerging targets like TL1A inhibitors. Notably, intestinal organoids and organs-on-chips enable revolutionary three-dimensional simulation of the "epithelial-immune-microbiota" interaction system, accelerating target validation and drug discovery. This evolution positions IBD therapy at the threshold of a new era defined by multi-omics-guided dynamic precision medicine.
Intestinal organoids as models for IBD research
The accelerated clinical translation of targeted biologics, combined with breakthroughs in microbiome-based therapies and AI-driven personalized therapeutics, is propelling IBD therapeutics toward a paradigm-shifting transition—from symptom management to disease-modifying reversal. We have developed a comprehensive product portfolio for IBD research including highly active recombinant proteins, stable cell lines, and inhibitor screening kits. Our solutions span the entire drug development continuum – from target discovery and validation, candidate drug screening and development to CMC manufacturing and quality control – accelerating the efficient translation of IBD innovative therapies from foundational research to clinical implementation.
Free download: ACRO's autoimmune disease drug development solutions!
Hot IBD Target Recommendations
Ready-to-use intestinal organoids and differentiation kits are available to support IBD research.
• The cell composition and arrangement of intestinal organoids closely resemble the structure of intestinal epithelium, enabling the maintenance of crypt characteristics even after prolonged culture.
• Due to their short culture cycle, intestinal organoids can be easily frozen and passaged.
• The apical membrane, positioned on the outer layer, provides an optimal interface for absorption testing.
Immunostaining of intestinal organoid shows the marker expression of goblet cells (mucus-producing, MUC2), brush borders (Villin), enterochromaffin cells (CHGA) and endothelial cells (CD31.)
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1. Ekstedt, Natalia, Dominika Jamioł-Milc, and Joanna Pieczyńska. "Importance of gut microbiota in patients with inflammatory bowel disease." Nutrients 16.13 (2024): 2092.
2. Dunleavy, Katie A., Laura E. Raffals, and Michael Camilleri. "Intestinal barrier dysfunction in inflammatory bowel disease: underpinning pathogenesis and therapeutics." Digestive diseases and sciences 68.12 (2023): 4306-4320.
3. Lu, Quan, et al. "Immunology of inflammatory bowel disease: molecular mechanisms and therapeutics." Journal of inflammation research (2022): 1825-1844.
4. Tian, Cheng-mei, et al. "Stem cell-derived intestinal organoids: a novel modality for IBD." Cell Death Discovery 9.1 (2023): 255.
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