CXCL10

British Medical Journal Open publishes paper detailing the results of the international Phase II human trial for LSALT peptide targeting acute lung and kidney inflammation in hospitalized patients infected with SARS-CoV-2 virusPhase II findings previously disclosed support dipeptidase-1 (DPEP-1) as a relevant therapeutic target for diseases of the lung, kidneys and liver where inflammation plays a major role. New biomarker data from the pandemic Phase II trial, provides further scientific rationale for Arch to bring LSALT peptide into larger trials to inhibit DPEP-1 mediated organ inflammation. Arch is currently performing a Phase II human trial to support LSALT peptide as a first ever treatment for preventing cardiac surgery-associated acute kidney injury. TORONTO, March 18, 2024 (GLOBE NEWSWIRE) -- Arch Biopartners Inc., (“Arch” or the “Company”) (TSX Venture: ARCH and OTCQB: ACHFF), announced today that it has published a peer reviewed paper in the British Medical Journal Open (BMJ Open) detailing the results of the international Phase II human trial for LSALT peptide targeting acute lung and kidney inflammation in hospitalized patients infected with SARS-CoV-2 virus. LSALT peptide is a DPEP-1 inhibitor and the Company’s lead drug candidate for preventing and treating inflammation injury in the kidneys, lungs, and liver. The paper in BMJ Open describes the clinical highlights, outcomes and biomarker results of the study. The Phase II trial was an international, multicenter, randomized, double-blind, placebo-controlled, proof of concept study of LSALT peptide for the prevention of organ inflammation such as acute respiratory distress syndrome (ARDS) and acute kidney injury (AKI) in patients infected with SARS-CoV-2. The exploratory, adaptive trial was initiated in the early stages of the global pandemic to identify clinical signals of efficacy for LSALT peptide in the treatment of acute lung and kidney inflammation. The results of the Phase II trial provided first-ever evidence validating DPEP-1 as a mediator of organ inflammation and therapeutic target in humans. In addition, LSALT peptide was well tolerated with no safety issues related to the drug. New biomarker data for LSALT peptide was disclosed for the first time in the BMJ Open publication. An analysis of serum inflammatory biomarkers was performed from blood samples collected from study participants. Biomarkers analyzed which relate to organ inflammation included cytokines and chemokines such as IL-6, CXCL8, CXCL10, IL-1β and CCL7. Collectively, a greater proportion of inflammatory biomarkers decreased in patients receiving LSALT peptide compared with placebo. In particular, the reduction of CXCL10 in the LSALT peptide group versus the placebo group was statistically significant at the end of treatment. CXCL10 plays a role in facilitating leukocyte recruitment to various vascular beds including the lungs and kidneys. The reduction of CXCL10 and the other inflammatory biomarkers during LSALT peptide treatment is consistent with LSALT peptide’s mechanism of action as an inhibitor of DPEP-1 mediated leukocyte recruitment to the lungs and kidneys. The new data provides more scientific rationale for Arch to advance LSALT peptide to prevent leukocyte recruitment and organ inflammation for other indications, including a larger Phase II trial targeting cardiac surgery-associated AKI, which recently began recruiting patients. More information on the current trial can be found below and at clinicaltrials.gov Details of the results from the Phase II trial are reported in the peer-reviewed journal BMJ Open. The publication, titled “Multicenter, Randomized, Double-Blind, Placebo-Controlled, Proof of Concept Study of LSALT Peptide as Prevention of Acute Respiratory Distress Syndrome and Acute Kidney Injury in Patients Infected with SARS-CoV-2 (COVID-19)” by Somayaji et. al. can be found at the BMJ Open website. Quote from Richard Muruve, CEO of Arch Biopartners Inc.: “When the pandemic started and hospitals were filling up with patients with respiratory distress caused by inflammation, we postponed our plans to do a CS-AKI trial to urgently perform a Phase II trial to treat hospitalized COVID patients and reduce acute organ inflammation. Now that we have published our biomarker and clinical data from the trial, we are more confident today that inhibiting DPEP-1 mediated leukocyte recruitment to the kidneys, lungs and liver is a valid path toward first-ever treatments to prevent acute injury in these organs.” About the Phase II trial for LSALT Peptide in Pandemic Patients The Phase II trial was an international, multicenter, randomized, double-blind, placebo-controlled, proof of concept study of LSALT peptide for the prevention of organ inflammation such as acute respiratory distress syndrome (ARDS) and acute kidney injury (AKI) in patients infected with SARS-CoV-2. Six clinical sites located in Canada, United States, and Turkey participated in the Phase II trial in 2021. The composite primary endpoint of the Phase II trial reflected the severe effects often experienced by hospitalized patients in the early months of the pandemic and deemed appropriate for LSALT peptide’s novel mechanism of action in blocking consequential inflammation in the lungs, kidneys, and other organs. The exploratory study was designed to detect a clinical signal of efficacy and was not powered for statistical significance. Previously disclosed in December 2021 and included in the BMJ Open publication, there were no significant differences in adverse events between LSALT peptide and placebo treated patients. The study population of the Phase II trial did not have enough incidence of ARDS or AKI to detect a conclusion on these two particular clinical outcomes. In a secondary evaluation of patients on ventilation, despite being older by an average of 5 years, subjects in the LSALT peptide group demonstrated 22.8 ventilation-free days compared to 20.9 days in the placebo group in the unadjusted analysis at 28 days. “Ventilation” was defined as a need for high flow oxygen therapy (≥ 6L/min), non-invasive ventilation, mechanical ventilation, or extracorporeal membrane oxygenation (ECMO). In a post-hoc analysis adjusting for age, body mass index (BMI), and PaO2/FiO2 ratio (a measure of lung disease severity), the difference in ventilation-free days was 6.7 days favoring the LSALT peptide group compared to the placebo group. About Phase II trial for LSALT Peptide targeting CS-AKI Arch Biopartners is currently sponsoring a Phase II trial for LSALT peptide targeting cardiac surgery-associated acute kidney injury (CS-AKI). CS-AKI is often caused by ischemia-reperfusion injury (IRI) that reduces blood flow (ischemia) and thus oxygen in the kidney causing kidney cell damage. Once blood flow is restored to normal (reperfusion), inflammation is triggered and injury to kidney cells is exacerbated. In the worst cases of AKI, kidneys fail, leading to kidney dialysis or kidney transplant. At present, there are no therapeutic treatments available to prevent or treat CS-AKI or IRI. The CS-AKI Phase II trial is an international multi-center, randomized, double-blind, placebo-controlled study of LSALT peptide. The recruitment target for the trial is 240 patients. The primary objective of the trial is to evaluate the percentage of subjects with AKI within seven days following on-pump (heart-lung machine) cardiac surgery, defined by the KDIGO (Kidney Disease: Improving Global Outcomes) criteria. Details of the Phase II trial, entitled “Phase 2 Global, Multicenter, Randomized, Double-Blind, Placebo-Controlled Study of LSALT peptide for the Prevention or Attenuation of Acute Kidney Injury (AKI) in Patients Undergoing On-Pump Cardiac Surgery” can be viewed at clinicaltrials.gov. Recruitment of patients in the CS-AKI trial has begun in three hospital sites in Turkey with a hospital in Canada (University of Calgary) joining the trial last week. Additional sites are expected to be added in Turkey and Canada in the next few weeks. About LSALT Peptide LSALT peptide is a novel peptide drug candidate and DPEP-1 inhibitor. In August 2019, a scientific team led by Arch scientists Dr. Donna Senger and Dr. Stephen Robbins published a paper in the journal Cell describing a novel mechanism of action for organ inflammation. In the publication, DPEP-1 was identified, for the first time, as a major leukocyte (white blood cell) adhesion receptor on the lung, liver and kidney endothelium. DPEP-1 was also identified as the target of LSALT peptide, differing from typical anti-inflammatory drugs by targeting this novel adhesion receptor rather than targeting individual cytokines, of which there are many. The Cell publication, titled “Dipeptidase-1 is an adhesion receptor for neutrophil recruitment in lungs and liver” by Choudhry et. Al. can be found at the Cell journal’s website. LSALT peptide has been shown by Arch scientists and their collaborators to prevent ischemia-reperfusion injury to the kidneys in pre-clinical models (Video Link to pre-clinical proof of concept). Details of their findings were published in a Science Advances publication, titled “Dipeptidase-1 governs renal inflammation during ischemia reperfusion injury” by Lau et. al. and can be found at the Science Advances website. About Arch Biopartners Arch Biopartners Inc. is a late-stage clinical trial company focused on preventing inflammation and acute organ injury. The Company is developing new drug candidates that inhibit inflammation in the lungs, kidneys, and liver via the dipeptidase-1 (DPEP-1) pathway and are relevant for common injuries and diseases where organ inflammation is an unmet problem. For more information on Arch Biopartners' science and technologies, please visit: www.archbiopartners.com/our-science For investor information and other public documents the company has also filed on SEDAR+, please visit www.archbiopartners.com/investor-hub The Company has 62,755,633 common shares outstanding. Forward-Looking Statements This press release contains forward-looking statements within the meaning of applicable Canadian securities laws regarding expectations of our future performance, liquidity and capital resources, as well as the ongoing clinical development of our drug candidates targeting the dipeptidase-1 (DPEP-1) pathway, including the outcome of our clinical trials relating to LSALT peptide (Metablok), the successful commercialization and marketing of our drug candidates, whether we will receive, and the timing and costs of obtaining, regulatory approvals in Canada, the United States, Europe and other countries, our ability to raise capital to fund our business plans, the efficacy of our drug candidates compared to the drug candidates developed by our competitors, our ability to retain and attract key management personnel, and the breadth of, and our ability to protect, our intellectual property portfolio. These statements are based on management’s current expectations and beliefs, including certain factors and assumptions, as described in our most recent annual audited financial statements and related management discussion and analysis under the heading “Business Risks and Uncertainties”. As a result of these risks and uncertainties, or other unknown risks and uncertainties, our actual results may differ materially from those contained in any forward-looking statements. The words “believe”, “may”, “plan”, “will”, “estimate”, “continue”, “anticipate”, “intend”, “expect” and similar expressions are intended to identify forward-looking statements, although not all forward-looking statements contain these identifying words. We undertake no obligation to update forward-looking statements, except as required by law. Additional information relating to Arch Biopartners Inc., including our most recent annual audited financial statements, is available by accessing the Canadian Securities Administrators’ System for Electronic Document Analysis and Retrieval (“SEDAR”) website at www.sedarplus.ca . The science and medical contents of this release have been approved by the Company’s Chief Science Officer Neither TSX Venture Exchange nor its Regulation Services Provider (as that term is defined in the policies of the TSX Venture Exchange) accepts responsibility for the adequacy or accuracy of this release

MB-101 was well-tolerated and 50% of patients achieved stable disease or better with two partial responses and two complete responses lasting 7.5 and 66+ months, respectively ~70% improvement in median overall survival compared to expected survival rate in cohort with dual intratumoral (ICT)/ intraventricular (ICV) delivery and an optimized manufacturing process This is the largest reported trial to date of CAR-T therapy for solid tumors WORCESTER, Mass., March 07, 2024 (GLOBE NEWSWIRE) -- Mustang Bio, Inc. (“Mustang”) (Nasdaq: MBIO), a clinical-stage biopharmaceutical company focused on translating today’s medical breakthroughs in cell and gene therapies into potential cures for difficult-to-treat cancers and rare genetic diseases, today announced Phase 1 clinical data were published in Nature Medicine that demonstrated the promising safety and clinical activity of Mustang’s MB-101 (IL13Ra2-targeted CAR T-cells) for the treatment of patients with recurrent and refractory malignant glioma, including glioblastoma. MB-101 was developed by City of Hope, one of the largest cancer research and treatment organizations in the United States, and exclusively licensed to Mustang. Highlights from the data include: Stable disease or better was achieved in 50% (29/58) of heavily pretreated patients for at least two months, with two partial responses, one complete response (CR), and a second CR after additional CAR-T cycles under compassionate use. Patients with recurrent GBM treated in the final cohort with dual intratumoral (ICT)/ intraventricular (ICV) delivery and an optimized manufacturing process exhibited superior median overall survival of 10.2 months, compared to the expected survival rate of six months in patients with recurrent GBM. The median overall survival for all patients was eight months. Intermediate/high pre-treatment tumor T-cell levels that are indicative of a “hot” tumor microenvironment (TME) correlated with a significant survival benefit over negative/low pre-treatment tumor T-cell levels that are indicative of a “cold” TME. Overall, all routes of delivery (ICT, ICV and dual ICT + ICV) were well-tolerated at doses up to 200×106 CAR T-cells. Central nervous system (CNS) increases in inflammatory cytokines, including IFNγ, CXCL9, and CXCL10, were associated with CAR T-cell administration and bioactivity. Dr. Christine Brown, Heritage Provider Network Professor in Immunotherapy, deputy director of the T-Cell Therapeutics Research Laboratories at City of Hope, and lead author on the publication, said, “These Phase 1 clinical trial results represent a significant step forward in our understanding of the potential of MB-101 CAR T-cell therapy to treat recurrent GBM, an extremely aggressive tumor with very limited treatment options. One of the main challenges for treating brain cancer is that medications have difficulty crossing the blood-brain barrier. To overcome that barrier, the trial delivered CAR T-cells directly into the brain tumor and the cerebrospinal fluid, the fluid that protects and surrounds the brain and spinal cord. Repetitive locoregional administration of IL13Rα2-CAR T-cells was feasible and well-tolerated with no dose limiting toxicities, even at the highest dose level of 200 x 106 CAR T-cells per infusion. The safety and promising therapy-related bioactivity data pave the way for future studies of MB-101 and offer hope for a transformative treatment approach. We look forward to continuing our work with Mustang on this promising therapy.” Manuel Litchman, M.D., President and Chief Executive Officer of Mustang, said, “MB-101 has demonstrated compelling therapeutic potential, including delivering unprecedented complete responses in two high-grade glioma patients; the first patient who achieved a complete response was published in The New England Journal of Medicine. These two patients treated solely with MB-101 both had high levels of intratumoral CD3+ T-cells pre-therapy (i.e., “hot” tumors) and achieved complete responses lasting 7.5 and 66+ months, respectively. This trial has led to several other studies using MB-101, including supporting our upcoming novel combination clinical trial of MB-109 [MB-101 (IL-13Rα2 targeted CAR T-cell therapy) + MB-108 (HSV-1 oncolytic virus)] to improve treatment of recurrent GBM and high-grade astrocytoma. The combination leverages initial treatment with MB-108 to reshape the tumor microenvironment and make immunologically “cold” tumors “hot,” thereby potentially enabling the MB-101 CAR T-cell therapy to achieve efficacy equivalent to that seen in intrinsically “hot” tumors in this City of Hope Phase 1 trial.” The data reported on 65 patients with recurrent high-grade glioma, the majority being glioblastoma (GBM; 2 + recurrences); 58 patients were evaluable for disease response. Primary endpoints were safety and feasibility, with secondary endpoints measuring therapy-related cytokine dynamics, CAR T-cell persistence and clinical outcomes. Patients were treated at one of three dose schedules with three weekly infusions administered without prior lymphodepleting chemotherapy and were evaluated one week after the third cycle for dose limiting toxicities. Additional infusions were allowed, and patients were followed for toxicities, response, and survival until they progressed or required subsequent therapy. This study evaluated five treatment arms: Arm 1, intratumoral following biopsy (ICT Biopsy); Arm 2, intratumoral following maximal surgical resection (ICT Resection); Arm 3, intraventricular (ICV); and Arms 4 and 5, combined ICT and ICV delivery (Dual ICT + ICV). ICV delivery (Arm 3) was added after trial initiation based on clinical experience, in which IL13Rα2-CAR T-cells that were administered ICV mediated a complete response in a patient with multifocal recurrent GBM, and preclinical data suggested ICV was more effective against multifocal tumors. Subsequently, City of Hope transitioned to dual delivery combining both ICV and ICT (Arms 4–5) – rather than continuing with ICV alone – as preclinical data also suggested that intratumoral delivery was more effective for defined unifocal tumors in comparison to ICV-only delivery. Weekly ICT and/or ICV administration of IL13Rα2-CAR T-cells was well-tolerated, with clinically manageable adverse events. No high-grade cytokine release syndrome or immune effector cell-mediated neurotoxicity adverse events were observed, and no dose limiting toxicities (DLTs) were noted during the 28-day dose limiting toxicity period. The most common toxicities with possible or higher attribution to CAR T-cells were fatigue, headache, and hypertension. Grade 3 and above toxicities with possible or higher attribution to CAR T-cells were seen in 35% of patients, including two incidences of transient grade 4 cerebral edema with possible attribution to CAR T-cells and one grade 3 encephalopathy and one grade 3 ataxia with probable attribution to CAR T-cells. A link to the Nature Medicine publication can be found here. Dr. Brown has a financial interest in Mustang and has previously been a paid consultant for the company. Additional information on the Phase 1 study can be found on using identifier NCT02208362. About Mustang Bio Mustang Bio, Inc. is a clinical-stage biopharmaceutical company focused on translating today’s medical breakthroughs in cell and gene therapies into potential cures for difficult-to-treat cancers and rare genetic diseases. Mustang aims to acquire rights to these technologies by licensing or otherwise acquiring an ownership interest, to fund research and development, and to outlicense or bring the technologies to market. Mustang has partnered with top medical institutions to advance the development of CAR-T therapies across multiple cancers, as well as lentiviral gene therapies for severe combined immunodeficiency. Mustang’s common stock is registered under the Securities Exchange Act of 1934, as amended, and Mustang files periodic reports with the U.S. Securities and Exchange Commission (“SEC”). Mustang was founded by Fortress Biotech, Inc. (Nasdaq: FBIO). For more information, visit . Forward‐Looking Statements This press release contains “forward-looking statements” within the meaning of Section 27A of the Securities Act of 1933 and Section 21E of the Securities Exchange Act of 1934, each as amended. Such statements, which are often indicated by terms such as “anticipate,” “believe,” “could,” “estimate,” “expect,” “goal,” “intend,” “look forward to,” “may,” “plan,” “potential,” “predict,” “project,” “should,” “will,” “would” and similar expressions. The Company’s forward-looking statements, include, but are not limited to, any statements relating to our growth strategy and product development programs, including the timing of and our ability to make regulatory filings such as INDs and other applications and to obtain regulatory approvals for our product candidates, statements concerning the potential of therapies and product candidates and any other statements that are not historical facts. Actual events or results may differ materially from those described in this press release due to a number of risks and uncertainties. Risks and uncertainties include, among other things, risks related to the satisfaction of the conditions necessary to transfer the lease of the Company’s manufacturing facility and receive the contingent payment in connection with the Company’s sale of its manufacturing facility in the anticipated timeframe or at all; whether the purchaser of the Company’s manufacturing facility is able to successfully perform its obligation to produce the Company’s products under the manufacturing services agreement on a timely basis and to acceptable standards; disruption from the sale of the Company’s manufacturing facility making it more difficult to maintain business and operational relationships; negative effects of the announcement or the consummation of the transaction on the market price of the Company’s common stock; significant transaction costs; the development stage of the Company’s primary product candidates, our ability to obtain, perform under, and maintain financing and strategic agreements and relationships; risks relating to the results of research and development activities; risks relating to the timing of starting and completing clinical trials; uncertainties relating to preclinical and clinical testing; our dependence on third-party suppliers; our ability to attract, integrate and retain key personnel; the early stage of products under development; our need for substantial additional funds; government regulation; patent and intellectual property matters; competition; as well as other risks described in Part I, Item 1A, “Risk Factors,” in our Annual Report on Form 10-K filed on March 30, 2023, subsequent Reports on Form 10-Q, and our other filings we make with the SEC. We expressly disclaim any obligation or undertaking to release publicly any updates or revisions to any forward-looking statements contained herein to reflect any change in our expectations or any changes in events, conditions or circumstances on which any such statement is based, except as required by law, and we claim the protection of the safe harbor for forward-looking statements contained in the Private Securities Litigation Reform Act of 1995. Company Contacts: Jaclyn Jaffe and Nicole McCloskey Mustang Bio, Inc. (781) 652-4500 ir@mustangbio.com

Regulatory T cell (Treg) immunomodulatory function significantly compromised and inflammatory cytokines and chemokines significantly increased in FTD patients COYA 302, Coya’s lead investigational product, is believed to restore Treg immunomodulatory function and target the inflammatory milieu observed in neurodegenerative diseases like FTD HOUSTON--(BUSINESS WIRE)-- Coya Therapeutics, Inc. (“Coya” or the “Company”), a clinical-stage biotechnology company developing biologics primarily focused on the restoration of regulatory T cell (Treg) immunomodulatory function, announces the presentation of data demonstrating the role of the peripheral immune system in the pathophysiology of Frontotemporal Dementia (FTD) from a biomarker study conducted at the Houston Methodist Hospital by Dr. Stanley Appel and Dr. Alireza Faridar and funded by the Houston Methodist Clinical Scholar Award Program. The poster presentation was shared for the first time today at the AD/PD 2024 Conference in Lisbon, Portugal and can be found here. The poster is titled, “Deciphering the Role of the Peripheral Immune System in the Pathology of Frontotemporal Dementia.” “The data from this biomarker study clearly depicts a compromised peripheral immune environment present in patients with FTD that, we believe, contributes to the pathophysiology of the disease process. Further, we believe that targeting systemic inflammation with COYA 302 may lower both peripheral and central nervous system inflammatory cell types while enhancing Treg function and may be a meaningful approach for FTD. We intend to Investigational New Drug (IND) application with the FDA for COYA 302 in FTD later this year and initiate a Ph. 2 trial in FTD patients shortly thereafter,” stated Fred Grossman, Chief Medical Officer at Coya Therapeutics. Summary of Study Results The study was designed to evaluate Treg immunosuppressive function, monocyte mRNA expression, levels of inflammatory cytokines and chemokines, and immune cell markers in peripheral blood mononuclear cells (PBMCs) in blood samples of 22 FTD patients and 11 age-matched healthy individuals as a control group. Treg Function Compromised: Treg suppressive function was significantly reduced in FTD, compared to controls (p<0.01), demonstrating that Treg immunomodulatory function is negatively impacted in FTD. Pro-Inflammatory Systemic Immune Activity: Plasma levels of inflammatory chemokines and cytokines, including C-X-C motif chemokine ligand 9 (CXCL9), CXCL10, CXCL11, CXCL12, tumor necrosis factor alpha (TNFα), chemokine (C-C motif) ligand 3 (CCL3), CCL7, and colony stimulating factor 1 (CSF-1) were consistently and significantly increased in FTD patients (p<0.05). In addition, several inflammation transcripts in monocyte genes known to be involved in neuroinflammatory signaling pathways were dysregulated in FTD, compared to controls. Results of the study demonstrate that FTD patients exhibit a compromised immunosuppressive function of Tregs, along with increased peripheral levels of inflammatory cytokines and chemokines, dysregulation of peripheral monocyte’s inflammation transcriptome and systemic activation of the inflammatory cascade, supporting the critical role of the immune system in the pathophysiology of FTD. The data in FTD is consistent the Treg dysfunction and increased levels of inflammatory cytokines and chemokines previously reported by Coya in other serious and progressive neurodegenerative diseases and support the multi-pathway combination approach of COYA 302 to target numerous components of the dysfunctional immune system. 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, FTD, and PD. 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 commercially available 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<0.01), suggesting enhanced and durable Treg suppressive function over the course of treatment. In contrast, Treg suppressive function (mean ±SD) was significantly decreased at the end of the 8-week washout period compared to end-of-treatment at week 48 (70.3 ±8.1 vs. 89.5 ±4.1, p <0.05). The study also evaluated serum biomarkers of inflammation, oxidative stress, and lipid peroxides. The available data up to 16 weeks after initiation of treatment suggest a decrease in these biomarker levels, which is consistent with the observed enhancement of Treg function. The evaluation of the full biomarker data is ongoing. COYA 302 is an investigational product not yet approved by the FDA or any other regulatory agency. About Amyotrophic Lateral Sclerosis Amyotrophic lateral sclerosis (ALS), also known as Lou Gehrig's Disease, is a rare neurological disease that affects motor neurons, the nerve cells in the brain and spinal cord that control voluntary muscle movement. About 20,000 people live with ALS in the United States and approximately 5,000 new cases are diagnosed every year. The disease is progressive, meaning the symptoms get worse over time. The functional status of ALS patients declines about 1 point per month on average, as measured by the Revised ALS Function Rating Scale1, or ALSFRS-R, a validated tool to monitor the progression of the disease. ALS has no cure, and the currently approved drug treatments provide limited benefit to patients. ALS is a type of motor neuron disease. As motor neurons degenerate and die, they stop sending messages to the muscles, which causes the muscles to weaken, start to twitch (fasciculations), and waste away (atrophy). Eventually, the brain loses its ability to initiate and control voluntary movements. Most people with ALS die from respiratory failure, usually within three to five years from when the symptoms first appear.2 About Frontotemporal Dementia Frontotemporal dementia (FTD) is the result of damage to neurons in the frontal and temporal lobes of the brain. Many possible symptoms can result, including unusual behaviors, emotional problems, trouble communicating, difficulty with work, or difficulty with walking. FTD is rare and tends to occur at a younger age than other forms of dementia. About 60% of people with FTD are 45 to 64 years old. FTD is progressive, meaning symptoms get worse over time. In the early stages, people may have just one symptom. As the disease progresses, other symptoms appear as more parts of the brain are affected. It is difficult to predict how long someone with FTD will live. Some people live more than 10 years after diagnosis, while others live less than two years after they are diagnosed. There is no cure for FTD, and no treatments slow or stop the progression of the disease.3 References Atassi N, et al. The PRO-ACT database: design, initial analyses, and predictive features. Neurology, 2014;83:1719–1725. doi: 10.1212/WNL.0000000000000951. National Institutes of Health (NIH) Website ( ), accessed on January 8, 2024. National Institutes of Health (NIH) Website ( ), accessed on January 8, 2024. About Coya Therapeutics, Inc. Headquartered in Houston, TX, Coya Therapeutics, Inc. (Nasdaq: COYA) is a clinical-stage biotechnology company developing proprietary treatments focused on the biology and potential therapeutic advantages of regulatory T cells (“Tregs”) to target systemic inflammation and neuroinflammation. Dysfunctional Tregs underlie numerous conditions, including neurodegenerative, metabolic, and autoimmune diseases, and this cellular dysfunction may lead to sustained inflammation and oxidative stress resulting in lack of homeostasis of the immune system. Coya’s investigational product candidate pipeline leverages multiple therapeutic modalities aimed at restoring the anti-inflammatory and immunomodulatory functions of Tregs. Coya’s therapeutic platforms include Treg-enhancing biologics, Treg-derived exosomes, and autologous Treg cell therapy. COYA 302 – the Company’s lead biologic investigational product or “Pipeline in a Product”– is a proprietary combination of COYA 301 (Coya’s proprietary LD IL-2) and CTLA4-Ig for subcutaneous administration with a unique dual mechanism of action that is now being developed for the treatment of Amyotrophic Lateral Sclerosis, Frontotemporal Dementia, Parkinson’s Disease, and Alzheimer’s Disease. Its multi-targeted approach enhances the number and anti-inflammatory function of Tregs and simultaneously lowers the expression of activated microglia and the secretion of pro-inflammatory mediators. This synergistic mechanism may lead to the re-establishment of immune balance and amelioration of inflammation in a sustained and durable manner that may not be achieved by either low-dose IL-2 or CTLA4-Ig alone. For more information about Coya, please visit Forward-Looking Statements This press release contains “forward-looking” statements that are based on our management’s beliefs and assumptions and on information currently available to management. Forward-looking statements include all statements other than statements of historical fact contained in this presentation, including information concerning our current and future financial performance, business plans and objectives, current and future clinical and preclinical development activities, timing and success of our ongoing and planned clinical trials and related data, the timing of announcements, updates and results of our clinical trials and related data, our ability to obtain and maintain regulatory approval, the potential therapeutic benefits and economic value of our product candidates, competitive position, industry environment and potential market opportunities. The words “believe,” “may,” “will,” “estimate,” “continue,” “anticipate,” “intend,” “expect,” and similar expressions are intended to identify forward-looking statements. Forward-looking statements are subject to known and unknown risks, uncertainties, assumptions and other factors including, but not limited to, those related to risks associated with the impact of COVID-19; the success, cost and timing of our product candidate development activities and ongoing and planned clinical trials; our plans to develop and commercialize targeted therapeutics; the progress of patient enrollment and dosing in our preclinical or clinical trials; the ability of our product candidates to achieve applicable endpoints in the clinical trials; the safety pro our product candidates; the potential for data from our clinical trials to support a marketing application, as well as the timing of these events; our ability to obtain funding for our operations; development and commercialization of our product candidates; the timing of and our ability to obtain and maintain regulatory approvals; the rate and degree of market acceptance and clinical utility of our product candidates; the size and growth potential of the markets for our product candidates, and our ability to serve those markets; our commercialization, marketing and manufacturing capabilities and strategy; future agreements with third parties in connection with the commercialization of our product candidates; our expectations regarding our ability to obtain and maintain intellectual property protection; our dependence on third party manufacturers; the success of competing therapies or products that are or may become available; our ability to attract and retain key scientific or management personnel; our ability to identify additional product candidates with significant commercial potential consistent with our commercial objectives; and our estimates regarding expenses, future revenue, capital requirements and needs for additional financing. We have based these forward-looking statements largely on our current expectations and projections about future events and trends that we believe may affect our financial condition, results of operations, business strategy, short-term and long-term business operations and objectives, and financial needs. Moreover, we operate in a very competitive and rapidly changing environment, and new risks may emerge from time to time. It is not possible for our management to predict all risks, nor can we assess the impact of all factors on our business or the extent to which any factor, or combination of factors, may cause actual results to differ materially from those contained in any forward-looking statements we may make. In light of these risks, uncertainties and assumptions, the forward-looking events and circumstances discussed herein may not occur and actual results could differ materially and adversely from those anticipated or implied in the forward-looking statements. Although our management believes that the expectations reflected in our forward-looking statements are reasonable, we cannot guarantee that the future results, levels of activity, performance or events and circumstances described in the forward-looking statements will be achieved or occur. We undertake no obligation to publicly update any forward-looking statements, whether written or oral, that may be made from time to time, whether as a result of new information, future developments or otherwise.