Odyssey Therapeutics Announces Publication Highlighting Differentiated Therapeutic Potential of TNFR2 Agonism
Globe Newswire•10/11/2026•08:00 ET
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Key Highlights
- ➤OD-003 IND-enabling studies expected to complete in Q1 2027
- ➤TNFR2 agonism tripled PD-1+BATF+ lung Tregs in mice, from 22% to 66%
- ➤TNFR2 agonism reduced disease severity in skin inflammation and encephalomyelitis models
- ➤Human Tregs maintained FOXP3 CNS2 demethylation, supporting lineage stability
- ➤Publication highlighted TNFR2 agonism’s tissue-directed differentiation versus IL-2 mutein
Expert Statements
Gary D. Glick, Founder and Chief Executive Officer of Odyssey Therapeutics
“A key challenge in harnessing Tregs therapeutically is directing their differentiation into stable populations capable of controlling inflammation in affected tissues. These findings demonstrate that TNFR2 agonism promotes the expansion of tissue-competent Tregs while preserving phenotype stability and enhancing immuno-suppressive ability. Together with evidence of reduced disease severity in preclinical models, this research strengthens the therapeutic rationale for OD-003, our TNFR2 agonist, as an investigational treatment for autoimmune and inflammatory diseases and supports the potential superiority of this approach to IL-2-based therapies.”
“Cutting Edge” article demonstrates that compared with IL-2, TNFR2 agonism promotes tissue-directed regulatory T-cell differentiation and lineage stability, as well as reduces autoimmune inflammation in preclinical models
Company’s investigational TNFR2 agonist, OD-003, expected to complete IND-enabling studies in the first quarter of 2027
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