Elevated Poster Presentation International Celiac Disease Symposium 2026

EVQ-001, a NanoDisc Antigen-Specific Immune Tolerance Therapy for Celiac Disease (141223)

Weston L Daniel 1 , Melinda Y Hardy 2 3 , Amy Russell 2 3 , Linda Fothergill 2 3 , Jason A Tye-Din 2 3 4 , James J Moon 5 6 , Cheng Xu 5 6 , Yue He 5 6 , Scott Mix 1
  1. EVOQ Therapeutics, Ann Arbor, Michigan, United States
  2. The Walter and Eliza Hall Institute, Parkville, Victoria, Australia
  3. The University of Melbourne, Parkville, V, Australia
  4. The Royal Melbourne Hospital, Parkville, Victoria, Australia
  5. Department of Pharmaceutical Sciences, University of Michigan, Ann Arbor, Michigan, United States
  6. Biointerfaces Institute, University of Michigan, Ann Arbor, Michigan, United States

Background: Celiac disease is an autoimmune disorder in which dietary gluten activates gluten-specific CD4+ T cells, leading to gastrointestinal symptoms and enteropathy. The only established treatment is lifelong adherence to a gluten-free diet, and no drug therapy is approved. EVQ-001 is an investigational subcutaneous NanoDisc therapy incorporating three gluten-derived peptides that contain five immunodominant HLA-DQ2.5-restricted T-cell epitopes. EVQ-001 is designed to treat celiac disease by promoting tolerogenic antigen presentation and antigen-specific immune regulation.

Methods: EVQ-001 was evaluated in complementary translational systems. Human whole blood and peripheral blood mononuclear cells from 20 adult HLA-DQ2.5+ celiac disease patients were assessed before and after gluten challenge for cytokine release, T-cell proliferation, and antigen-specific T-cell phenotypes. In vivo pharmacology was evaluated using an EVQ-001 surrogate in transgenic mice. A first-in-human clinical study was designed to evaluate safety, tolerability, and pharmacodynamic activity in celiac disease patients.

Results: In patient whole blood, EVQ-001 elicited IL-2 release consistent with engagement of gluten-reactive T cells and an emerging IL-10 signal consistent with regulatory immune activity. In PBMC culture, EVQ-001 induced gluten-specific CD4+ T-cell proliferation and increased antigen-responsive CD4+ T cells expressing activation/inhibitory receptors, including PD-1 and TIM-3, as well as Tr1-like CD49b+LAG3+ phenotypes. In transgenic mice, repeated subcutaneous administration of an EVQ-001 surrogate produced dose-dependent suppression of antigen-specific splenocyte recall responses, reducing IFN-γ and IL-2 toward background levels. The planned first-in-human study is a two-part single- and multiple-ascending-dose study in HLA-DQ2.5+ celiac disease patients on a gluten-free diet, incorporating blood-based cytokine and immune-cell profiling pharmacodynamic endpoints and gluten challenge in the multiple-dose portion.

Conclusions: EVQ-001 demonstrates antigen-specific immune engagement and induction of regulatory/inhibitor phenotypes in human ex vivo assays, with concordant suppression of antigen-specific recall responses in vivo. These data support clinical evaluation of EVQ-001 as a disease-targeted immune tolerance therapy for celiac disease.