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Odin Therapeutics

 

Odin Therapeutics is an international leading provider of tankyrase (TNKS) inhibitors building on 18 years of research and profound experience. Our company presents a preclinical stage portfolio of highly potent tankyrase inhibitors for the treatment of pulmonary fibrosis, a disease with an in particular high unmet need, and also disease indications showing dependency on WNT and YAP signaling such as osteoarthritis and cancer.

There are no existing viable treatment options for idiopathic lung fibrosis and osteoarthritis, - and no TNKS inhibitors available in clinic.

 

Strategy

 

The company has a two-fold lead program strategy for leveraging the advantages of the proprietary portfolio of tankyrase inhibitors:

Lead program: Novel treatment for lung fibrosis

Development of inhaled OM-247 for treatment of fibrotic lung disease, a highly potent compound with low systemic exposure to mitigate toxicity.

Lung fibrogenesis involves three central signaling pathways: TGFβ, WNT, and YAP. While most attempts to block lung fibrogenesis have focused on inhibiting components in TGFβ signaling pathway, they have often failed in clinical testing due to efficacy issues and toxicity concerns. TNKS inhibition represents a novel therapeutic approach targeting the WNT/YAP signaling pathways, offering efficacy while potentially avoiding serious side effects in patients.

For pulmonary fibrosis, our tool compound TNKS inhibitor shows robust activity in key established and proprietary pre-clinical assays and models:

1) In vitro activity in lung fibroblast assays

2) In vitro activity in “scar in a jar” 3D model

3) Ex vivo efficacy in lung tissue from IPF patients

4) In vitro additivity/synergy with SoC

5) In vivo efficacy in bleomycin-induced model

Current model for TNKS inhibitor anti-fibrotic mechanism of action

  • TNKS inhibition does not show an anti-inflammatory effect ex vivo and in vivo

  • Reduces WNT/β-catenin and/or YAP signaling in vitro, ex vivo and in vivo

  • Counteracts pro-fibrotic fibroblast-myofibroblast transition (FMT)

  • Blocks synthesis of extracellular matrix proteins

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