Anti IL25 for Type 2 Inflammatory Disease

LNR 125.38

(aka ABM125)

Taking on the Whole Disease

Allergic and Non-allergic Induced Type 2 Inflammation in One Proprietary, First-in-class Medicine

  • Moderate-to-severe asthma
  • Atopic dermatitis
  • Chronic rhinosinusitis with nasal polyps
  • Eosinophilic esophagitis
  • Food allergies

Type 2 Inflammation Treatment Market

To Reach USD 26.01 Billion by 2027

Blocking Upstream Epithelial Cytokines

Like IL25 Rather Than Proximal Type 2 Cytokines (IL4, IL5, IL13) is a New Approach for Treatment of Exacerbations in Uncontrolled Asthma Patients Caused by Both Allergens and RV

Target epithelial expressed cytokines

  • Bronchial epithelial cells (BECs) release IL25 in response to viral infection and allergens
  • Single target – upstream of other TH2 cytokines
  • Possibility of reducing or eliminating the effects of all downstream cytokines simultaneously
  • Potential for directly treating airways

Target proximal TH2 cytokines (IL-4, IL-5 and IL-13)

  • Current approach pursued by multiple companies
  • Cannot target all cytokines simultaneously
  • Mixed clinical results (disease phenotype dependent)
  • Not clear if preventing viral exacerbations


Substantial Body of Research

Validates IL25 as a Target in Asthma

  • Fort et al, 2001: Repeated intraperitoneal treatment with recombinant IL25 caused splenomegaly and gut inflammation driven by serum IgE production, eosinophilia, and upregulation of the type-2 cytokines; IL-4, IL-5, and IL-13
  • Kim et al, 2002: Transgenic mice overexpressing human IL25 develop eosinophilia, splenomegaly, and increased IL4 and IL5 production
  • Wang et al, 2007: IL25 and IL25 receptor are upregulated in human asthmatic lung
  • Ballantyne et al, 2007: Neutralization of IL25 bioactivity, during both the sensitization and challenge phase in acute OVA-induced experimental lung allergy, using an anti-IL25 monoclonal antibody, resulted in complete suppression of airways hyper-reactivity and a significant reduction in type-2 cytokine production, lung cell infiltration, and airways mucus production.
  • Kouzaki et al, 2013: IL25 is stored intracellularly in airway epithelial cells, and is released upon exposure to many allergens. IL25 transcription is also increased.
  • Yao et al, 2015: IL25 induces proliferation and expression of collagen I and III and smooth muscle α-actin in primary human lung fibroblasts
  • Corrigan et al, 2011: IL25 is elevated in asthma and contributes to angiogenesis, at least partly by increasing endothelial cell VEGF/VEGF receptor expression
  • Yao et al, 2015: Administration of IL25 to lungs is sufficient to cause functionally relevant airway remodeling
  • Jung et al, 2009: IL17RB gene polymorphism and lower receptor expression genetically associated with asthma protection
  • Chairakaki et al, 2017: Plasmacytoid dendritic cells drive acute exacerbation of asthma

LNR 125.38

Significantly Reduces Type 2 Cytokines and Inflammatory Cells Increased in Allergic Mice and in Mice with RV-induced Asthma Exacerbations

LNR 125.38