HOUSTON - Coya Therapeutics, Inc. (Nasdaq: COYA) ('Coya' or the 'Company'), a clinical-stage biotechnology company developing biologics intended to enhance Treg function, announces that it is expanding its pipeline in neurodegenerative conditions for COYA 302 beyond ALS to include frontotemporal dementia (FTD) and Parkinson's disease (PD).

FTD and PD share a similar disease pathogenesis to ALS that is associated with a heightened proinflammatory cascade involving dysfunctional Tregs and proinflammatory microglia and macrophages. The biological redundancies in molecular immune pathways in these complex diseases limit the efficacy of many single drug therapies, requiring the development of novel therapeutics that can address this pathophysiologic complexity.

Dr. Fred Grossman, Coya's President and Chief Medical Officer stated, 'ALS, FTD, and PD are driven by a similar, yet complex, proinflammatory environment that requires targeting more than a single pathway. COYA 302 has been designed to target multiple pathways, such as restoring dysfunctional Tregs and inhibiting proinflammatory microglia and macrophages, and may have disease modifying potential in these severe diseases with high unmet need.'

COYA 302 is a dual-mechanism investigational biologic combination immunotherapy comprised of proprietary low dose IL-2 and fusion protein CTLA-4 Ig. Low dose IL-2 enhances anti-inflammatory Treg function and numbers while the fusion protein CTLA-4 Ig suppress proinflammatory cell function, enabling potentially synergistic mechanisms in modulating inflammatory pathways and restoring immune balance. COYA 302 has the potential to be disease modifying by targeting multiple dysregulated immune pathways while restoring function in anti-inflammatory Treg function.

Coya intends to file an IND for COYA 302 for the treatment of ALS in the first half of 2024 and an IND for COYA 302 for the treatment of FTD before the end of 2024. In addition, studies in animal models of PD are planned in 2024, and based on those studies, a subsequent IND filing is anticipated for the treatment of PD.

Howard H. Berman, Ph.D., Coya's CEO stated: 'Our vision has always been to leverage the potential of Tregs in neurodegenerative diseases. With COYA 302, we have taken a page from the playbook of oncology and viral disease where combination therapies have been transformational. We believe that the complementary and possibly synergistic multi-mechanism mode of action of COYA 302 in targeting the complex immune environment will lead to promising clinical outcomes in patients with neurodegenerative diseases.'

The Company also announces its key milestones and catalysts anticipated in 2024, including: H1 2024

COYA 302 File IND and Initiate Phase 2 Trial in ALS Patients

COYA 302 Publication of Phase 1 Investigator Initiated Trial clinical data in ALS Patients

COYA 302 Publication of Longitudinal Biomarker study with correlation to patient survival in ALS Patients

COYA 302 Presentation on Longitudinal Biomarker Data in ALS Patients at Conference

COYA 301 Presentation of Phase 1 Investigator Initiated Trial data in AD Patients at 18th annual AD + PD Conference

H2 2024

COYA 302 First patient dosed in Phase 2 Trial in ALS Patients

COYA 302 File IND and Initiate Phase 2 Trial in FTD Patients

COYA 302 Animal data released in PD model

COYA 301 Proof of Concept combination data with Drug X in AD mouse model

COYA 301 Phase 2 Investigator Initiated Trial Topline AD data Presented

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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