Publications — Azuriya Pharma

Peer-reviewed evidence for
Ref-1 inhibition in IBD

A growing body of published work spans acute and chronic colitis, hematopoiesis, CHIP, and tumor immunology. Recent papers in Blood, Communications Biology, and Cancer Cell International extend the mechanistic rationale for Ref-1 inhibition in Inflammatory Bowel Disease.

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Ref-1 drives ulcerative colitis-induced systemic defects in hematopoietic cells

Stavely R, et al. Communications Biology. 2026.

Key finding: Our program reverses UC-driven aberrant hematopoiesis via the Ref-1 / HIF-1α / IL-1r1 signaling cascade, restoring hematopoietic stem cell function and intestinal integrity in a chronic DSS colitis model.

IBD-induced inflammation augments Clonal Hematopoiesis of Indeterminate Potential (CHIP) through Ref-1

Stavely R, et al. Blood. 2026.

Key finding: CHIP mutations increase IBD risk. Our program ameliorated CHIP-IBD driven by DNMT3A mutation in preclinical models — the first direct CHIP therapeutic signal in an IBD context.

Our program reverses the immunosuppressive tumor microenvironment during colorectal carcinogenesis

Caston RA, et al. Cancer Cell International. 2026.

Key finding: Using the AOM/DSS colitis-associated cancer model, our program modulates the inflammatory microenvironment — demonstrating that upstream Ref-1 inhibition reverses immunosuppressive polarization, with implications bridging IBD biology and CRC prevention.

Ref-1 as a Therapeutic Target for Inflammatory Bowel Disease

Stavely R, Bhave S, Kelley MR, Nurgali K. Biomolecules. 2023.

Key finding: Comprehensive overview of Ref-1 biology in intestinal inflammation and the therapeutic potential of redox inhibitors. Consolidates the mechanistic rationale for our program as an IBD therapy.

Ref-1 — One Target with Multiple Indications: Emerging Aspects and New Directions

Kelley MR, Fishel ML. Journal of Cellular Signaling. 2021.

Key finding: Positions IBD as a critical non-cancer application for our program. Synthesizes evidence across oncology, ophthalmology, and gastrointestinal inflammation and emphasizes upstream pathway regulation as the unifying mechanism.

Inhibition of Ref-1 Redox Signaling Alleviates Intestinal Dysfunction in a Chronic Colitis Model

Sahakian L, Filippone RT, Stavely R, Robinson AM, Yan XS, Abalo R, Eri R, Bornstein JC, Kelley MR, Nurgali K. Inflammatory Bowel Diseases. 2020.

Key finding: The foundational Winnie chronic-colitis paper. Our program improves disease severity, reduces immune cell infiltration, and — critically — provides neuroprotection in the enteric nervous system. First study to identify the neural dimension of Ref-1 inhibition in IBD.

The Ref-1 platform extends well beyond IBD

Ref-1 overactivation drives damage across gut, eye, peripheral nerves, and the blood-forming system. Published evidence supports future opportunities in cancer, diabetic retinopathy, neonatal NEC, and neurodegenerative disease.

Azuriya Pharma

A clinical-stage, first-in-class oral small molecule targeting Inflammatory Bowel Disease through upstream modulation of Ref-1.

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© 2026 Azuriya Pharma. All rights reserved. Our program is an investigational compound and has not been approved by any regulatory authority.