Coya Therapeutics Licenses Intellectual Property Rights for Use of Next Generation Immune Modulatory Biologics in Combination with COYA 301 to Enhance Regulatory T Cells (Tregs) in Inflammatory Diseases

Coya Therapeutics, Inc. (NASDAQ: COYA) (“Coya” or the “Company”), a clinical-stage biotechnology company developing multiple therapeutic programs intended to enhance regulatory T cell (Treg) function, has expanded and strengthened its patent estate beyond COYA 302, which is a combination of COYA 301 with CTLA-4 Ig. This license with UNeMed Corporation (UNeMed), the Technology Transfer Office of University of Nebraska Medical Center, covers the combination of COYA 301 with GM-CSF and additional immune analogues and provides a next generation approach with a novel combination to synergistically modulate and reduce inflammation. UNeMed will receive payments upon achievement of certain milestones and will be eligible to receive tiered low single-digit royalty on net sales.

“We believe that COYA 301 is ideally situated to serve as a backbone drug in combination with other biologics that synergistically modulate the immune system and represent next generation approaches to treating inflammatory disorders, which are driven by complex and multi-factorial pathways. Enhancing Treg activity with COYA 301 in combination with GM-CSF and additional immune analogues creates yet another novel biologic combination in addition to Coya’s lead asset, COYA 302 and expands optionality and potential partnerships,” stated Arun Swaminathan Ph.D., Chief Business Officer.

GM-CSF is a potent immune modulator known to promote Treg activities and dampen pro-inflammatory T effector responses, and ld IL-2 is a cytokine that enhances Treg function and numbers. Preclinical data (here) generated by the Gendelman laboratory at UNeMed demonstrated that the combination of ld IL-2 + GM-CSF generated a synergistic increase in Tregs in mice tissue, including in peripheral blood, spleen, and lymphoid cells. This included a 4-to-6-fold higher expression of Tregs in mice treated with the combination compared to treatments with either cytokine alone. Other markers that indicate a suppressive Treg phenotype were dramatically increased as well, including a 4-fold increase in CD25⁺CD127^low cells and a synergistic increase in the percentages of CD25⁺CD4⁺ Tregs that express CD39⁺, ICOS⁺ markers, and GITR⁺.