Three EASL Studies Show Nebokitug Lowers Fibrosis Scores and IBD Markers
CMMB•Chemomab presented three EASL 2026 studies showing nebokitug achieved dose-dependent reductions in key fibrosis markers and CCL24-mediated gene expression signatures in PSC patients. Proteomic analyses using an AI model identified composite improvements in ELF score, FibroScan stiffness and PRO-C3, while inflammatory and tissue-remodeling proteins linked to IBD were significantly modulated in 62% of PSC patients with ulcerative colitis or Crohn’s disease.
1. First Quarter Update and Partnership Discussions
Chemomab continued productive strategic partner negotiations for nebokitug and prepared three data abstracts for presentation at EASL 2026, underscoring progress in clinical and corporate development based on Phase 2 SPRING trial findings.
2. AI-Generated Proteomic Composite Fibrosis Analysis
Using Olink proteomic profiling and an AI/machine learning model, researchers identified patients who achieved combined improvement in ELF score, FibroScan liver stiffness and PRO-C3. Key liver-related proteins driving these distinctions included those involved in metabolism, protein breakdown and extracellular matrix remodeling, highlighting nebokitug’s breadth of treatment-associated improvements.
3. Reduction in PSC Gene Expression Programs
Proteomic analysis of SPRING trial serum samples showed dose-dependent reductions in four PSC-specific gene expression programs—extracellular matrix remodeling, macrophage activation, fibrosis/myofibroblast pathways and immune activation. These statistically significant declines support CCL24 blockade as a mechanism-based approach targeting core molecular drivers of PSC pathogenesis.
4. Inflammatory and Tissue-Remodeling Modulation in PSC-IBD
Among the 62% of SPRING trial patients with coexisting ulcerative colitis or Crohn’s disease, nebokitug treatment modulated inflammatory cytokines, chemokines and tissue-remodeling proteins associated with IBD activation. Significant reductions in mucosal immune recruitment markers and an elevation in MST-1 suggest potential benefits on shared gut–liver inflammatory circuits.
