HOUSTON - 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+CD127low cells and a synergistic increase in the percentages of CD25+CD4+ Tregs that express CD39+, ICOS+ markers, and GITR+.

Michael Dixon, Ph.D., President and CEO of UNeMed, noted, 'This agreement with Coya can potentially bring new therapies to patients suffering from neurodegenerative conditions. Coya's foundation and progress in low-dose IL-2 research makes them an ideal company to leverage our findings to date.'

About UNeMed Corporation

UNeMed Corporation is the technology transfer and commercialization office for the University of Nebraska Medical Center. UNeMed serves all UNMC researchers, faculty, and staff who develop new biomedical technology and inventions and strives to help bring those innovations to the marketplace.

About COYA 302

COYA 302 is an investigational and proprietary biologic combination therapy with a dual immunomodulatory mechanism of action intended to enhance the anti-inflammatory function of regulatory T cells (Tregs) and suppress the inflammation produced by activated monocytes and macrophages. COYA 302 is comprised of proprietary low dose interleukin-2 (LD IL-2) and CTLA-4 Ig and is being developed for subcutaneous administration for the treatment of patients with ALS. These mechanisms may have additive or synergistic effects.

In February of 2023, Coya announced results from a proof-of-concept, open-label clinical study evaluating LD IL-2 and CTLA-4 Ig in a small cohort of patients with ALS conducted at the Houston Methodist Research Institute (Houston, Texas) by Stanley Appel, M.D., Jason Thonhoff, M.D., Ph.D., and David Beers, Ph.D. This study was the first-of-its-kind evaluating this dual-mechanism immunotherapy for the treatment of ALS. Patients in the study received investigational treatment for 48 consecutive weeks and were evaluated for safety and tolerability, Treg function, serum biomarkers of oxidative stress and inflammation, and clinical functioning as measured by the ALSFRS-R scale.

During the 48-week treatment period, the therapy was well tolerated. The most common adverse event was mild injection-site reactions. No patient discontinued the study, and no deaths or other serious adverse events were reported.

Patients' disease progression was measured using the ALSFRS-R scale, a validated rating tool for monitoring the progression of disability in patients with ALS. The mean (+/-SD) ALSFRS-R scores at week 24 (33.75 +/-3.3) and week 48 (32 +/-7.8) after initiation of treatment were not statistically different compared to the ALSFRS-R score at baseline (33.5 +/-5.9), suggesting significant amelioration in the progression of the disease over the 48-week treatment period.

Treg suppressive function, expressed as percentage of inhibition of proinflammatory T cell proliferation, showed a statistically significant increase over the course of the treatment period and was significantly reduced at the end of the 8-week washout post-treatment period. Treg suppressive function at 24 weeks (79.9 +/-9.6) and 48 weeks (89.5 +/-4.1) were significantly higher compared to baseline (62.1 +/-8.1) (p

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