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Publication of data detailing the development of our microRNA (miRNA)-based multiplex shRNA approach, which allows to down-regulate several genes simultaneously, in Molecular Therapy – Nucleic AcidsFive posters were presented at the 38th SITC Annual Meeting and two posters were presented at the 4th ICLE conference, with further developments in our multiplex shRNA platform and encouraging data from our NKG2D-based multi-specific CAR T-cell platformCelyad Oncology has received approximately EUR 9.8m in private placement commitments from historical shareholders MONT-SAINT-GUIBERT, Belgium, Nov. 09, 2023 (GLOBE NEWSWIRE) -- Celyad Oncology (Euronext: CYAD) (the “Company” or “Celyad Oncology”), a biotechnology company focused on innovative technologies for chimeric antigen receptor (CAR) T-cell therapies, today reports its financial results for the third quarter of 2023 and provides an update on recent business developments. “Celyad Oncology team is resolutely dedicated to harnessing our expertise, extensive know-how, and valuable intellectual property portfolio to address the existing challenges within CAR T-cell therapies. We are excited to report compelling data from our short hairpin RNA (shRNA)-based multiplexing platform, underscoring the remarkable versatility and adaptability of this technology. In addition, we are making significant progress with our multispecific CAR program, and we look forward to sharing an update at international conferences in the coming months. These achievements mark our commitment to advancing the frontiers of cellular immunotherapy and bringing innovative solutions to patients in need,” commented Georges Rawadi, Chief Executive Officer of the Company. Third quarter 2023 and recent corporate highlights: On August 24, 2023, the Company announced that it has obtained commitments from Fortress, Tolefi and other longstanding existing shareholders to subscribe to a capital increase of up to €9.8 million in 2 tranches: A first tranche of 2.0 million was disbursed in the context of authorized capital as of September 4, 2023; andA second tranche to be subscribed by Fortress is subject to the approval by the extraordinary shareholders’ meeting. Following this private placement, the Company believes that its existing cash and cash equivalents should be sufficient, based on the current scope of activities, to fund operating expenses and capital expenditure requirements into the second quarter of 2025. Celyad Oncology has relocated from September 25, 2023 into a new research facility which fits better its current needs after the strategic shift. The Company remains headquartered at the Axis Parc, Mont-Saint-Guibert, Belgium but with its new business location at Dumont 9. Operational highlights shRNA multiplexing platform: Data validating our microRNA (miRNA)-based multiplex shRNA approach, which allows to down-regulate several genes simultaneously, were presented at the 4th International Conference on Lymphocyte Engineering (ICLE) in Munich (September 12-14) and at the 38th Annual Meeting of the Society for Immunotherapy of Cancer (SITC) in San Diego (November 1-5) and posters are available on the company’s website, at https://celyad.com/our-science-technology/publications/;With our approach we proved the feasibility of the simultaneous knock-down of 4 co-inhibitory receptors (PD-1, LAG-3, TIM-3 and CD95) to decrease the expression of exhaustion markers at the surface of CAR T-cells and the feasibility of this approach to improve allogeneic CAR T-cell viability by allowing evasion from graft-versus-host disease (GvHD), host-versus-graft (HvG) reaction and CD95L-induced autophagy.The results detailing the technical aspects of the development of this platform and showcasing the easiness, efficiency, and tunability of this technology to knock-down up to four target genes simultaneously have been published in Molecular Therapy – Nucleic Acids as of September 20. NKG2D-based CAR T-cells: We have developed different CD19/NKG2DL, BCMA/NKG2DL and PSMA/NKG2DL multi-specific CAR T-cells, utilizing both tandem constructs – that encompass the extracellular domain of the natural NKG2D receptor fused to a scFv targeting CD19, BCMA or PSMA, or dual constructs – that co-express the NKG2D-based CAR with an anti-CD19, anti-BCMA or anti-PSMA CAR, respectively;Our data provides the proof-of-concept that NKG2DL are valuable targets in a multispecific CAR approach;Specifically, we showed that CD19/NKG2DL multispecific CAR T-cells, and in particular dual receptors, are highly effective in vitro against CD19+ and CD19- cell lines and against CD19+ primary B-cell acute lymphoblastic leukemia (B-ALL) cells. In vivo, CD19/NKG2DL tandem CAR T-cells outperforms dual CAR T-cells in controlling tumor growth in an aggressive B-ALL relapse model.In vitro data generated with BCMA/NKG2DL and PSMA/NKG2DL multispecific CAR T-cells further validate this approach and its application in other hematological and solid indications.Preliminary data were presented at the 4th ICLE conference in Munich (September 12-14) and at the 38th SITC meeting in San Diego (November 1-5) and posters are available on the company’s website, at https://celyad.com/our-science-technology/publications/. Financial highlights – Third quarter 2023 financial review As of September 30, 2023, the Company had cash and cash equivalents of €2.3 million. Net cash burn during the third quarter of 2023 amounted to €2.7 million, in line with expectations. The Company projects that its existing cash and cash equivalents should be sufficient to fund operating expenses and capital expenditure requirements into the first quarter of 2024. After due consideration of detailed budgets and estimated cash flow forecasts for the years 2023 and 2024, the Company continues to project that its existing cash and cash equivalents will not be sufficient to fund its estimated operating and capital expenditures over at least the next 12 months from the date that this release is issued. On August 24, 2023, the Company announced that it has obtained commitments from Fortress, Tolefi and other longstanding existing shareholders to subscribe to a capital increase of up to €9.8 million (whose €2.0 million related to the first tranche has been already proceeded as of September 4, 2023). Taking into account the Management’s assumptions regarding estimated cash-flows for the years 2023, 2024 and 2025, the Company believes that following the close of the second tranche subscribed by Fortress which is subject to approval by the extraordinary shareholders’ meeting, its existing cash and cash equivalents should be sufficient, based on the current scope of activities, to fund operating expenses and capital expenditure requirements into the second quarter of 2025. Upcoming Anticipated Milestones More data and evidence in the context of the multi-specific CAR platform and shRNA multiplexing approach will be shared in the first quarter of 2024, with the aim of a clinical evaluation of assets and initiation of clinical trials either by the Company and/or through strategic partnerships afterwards. Upcoming Conferences Celyad Oncology will attend the 7th CAR-TCR Europe summit in London, UK (February 27-29, 2024), the must-attend forum to brainstorm advanced in cell therapies and stay at the forefront of cell therapy innovations. About Celyad Oncology Celyad Oncology is a cutting-edge biotechnology company dedicated to pioneering the discovery and advancement of revolutionary technologies for chimeric antigen receptor (CAR) T-cells. Its primary objective is to unlock the potential of its proprietary technology platforms and intellectual property, enabling to be at the forefront of developing next-generation CAR T-cell therapies. By fully leveraging its innovative technology platforms, Celyad Oncology aims to maximize the transformative impact of its candidate CAR T-cell therapies and redefine the future of CAR T-cell treatments. Celyad Oncology is based in Mont-Saint-Guibert, Belgium. For more information, please visit www.celyad.com. Celyad Oncology Forward-Looking Statement This release may contain forward-looking statements, within the meaning of applicable securities laws, including the Private Securities Litigation Reform Act of 1995, as amended, including, without limitation, statements regarding beliefs about and expectations for the Company’s updated strategic business model, including associated potential benefits, transactions and partnerships, statements regarding the potential value of the Company’s IP, and statements regarding the continuation of the Company’s existence. The words “will,” “potential,” “continue,” “target,” “project,” “should” and similar expressions are intended to identify forward-looking statements, although not all forward-looking statements contain these identifying words. Any forward-looking statements in this release are based on management’s current expectations and beliefs and are subject to a number of known and unknown risks, uncertainties and important factors which might cause actual events, results, financial condition, performance or achievements of Celyad Oncology to differ materially from those expressed or implied by such forward-looking statements. Such risks and uncertainties include, without limitation, risks related to the material uncertainty about the Company’s ability to continue as a going concern; the Company’s ability to realize the expected benefits of its updated strategic business model; the Company’s ability to develop its IP assets and enter into partnerships with outside parties; the Company’s ability to enforce its patents and other IP rights; the possibility that the Company may infringe on the patents or IP rights of others and be required to defend against patent or other IP rights suits; the possibility that the Company may not successfully defend itself against claims of patent infringement or other IP rights suits, which could result in substantial claims for damages against the Company; the possibility that the Company may become involved in lawsuits to protect or enforce its patents, which could be expensive, time-consuming, and unsuccessful; the Company’s ability to protect its IP rights throughout the world; the potential for patents held by the Company to be found invalid or unenforceable; and other risks identified in Celyad Oncology’s U.S. Securities and Exchange Commission (SEC) filings and reports, including in the latest Annual Report on Form 20-F filed with the SEC and subsequent filings and reports by Celyad Oncology. These forward-looking statements speak only as of the date of publication of this document and Celyad Oncology’s actual results may differ materially from those expressed or implied by these forward-looking statements. Celyad Oncology expressly disclaims any obligation to update any such forward-looking statements in this document to reflect any change in its expectations with regard thereto or any change in events, conditions or circumstances on which any such statement is based, unless required by law or regulation. Celyad Oncology Contacts: Investor Contact:Media Contact:David Georgesinvestors@celyad.comcommunications@celyad.com Source: Celyad Oncology SA

A research team has identified a crucial mechanism on a specific cell receptor that can cause cells to self-destruct. Being able to activate the receptor -- Fas -- and trigger cell death could open the door for improved cancer treatments. Modulating Fas may also extend the benefits of chimeric antigen receptor (CAR) T-cell therapy to solid tumors. A research team from the UC Davis Comprehensive Cancer Center has identified a crucial epitope (a protein section that can activate the larger protein) on the CD95 receptor that can cause cells to die. This new ability to trigger programmed cell death could open the door for improved cancer treatments. The findings were published Oct. 14 in the Nature journal Cell Death & Differentiation. CD95 receptors, also known as Fas, are called death receptors. These protein receptors reside on cell membranes. When activated, they release a signal that causes the cells to self-destruct. Modulating Fas may also extend the benefits of chimeric antigen receptor (CAR) T-cell therapy to solid tumors like ovarian cancer. "We have found the most critical epitope for cytotoxic Fas signaling, as well as CAR T-cell bystander anti-tumor function," said Jogender Tushir-Singh, an associate professor in the Department of Medical Microbiology and Immunology and senior author of the study. "Previous efforts to target this receptor have been unsuccessful. But now that we've identified this epitope, there could be a therapeutic path forward to target Fas in tumors," Tushir-Singh said. Finding better cancer therapies Cancer is generally managed with surgery, chemotherapy and radiotherapy. These treatments may work initially, but in some cases, therapy-resistant cancers often return. Immunotherapies, such as CAR T-cell-based immune therapies and immune checkpoint receptor molecule activating antibodies, have shown tremendous promise to break this cycle. But they only help an extremely small number of patients, especially in solid tumors such as ovarian, triple-negative breast cancer, lung and pancreas. T cells are a type of immune cells. CAR T-cell therapies involve engineering patient T cells by grafting them with a specific tumor-targeting antibody to attack tumors. These engineered T cells have shown efficacy in leukemia and other blood cancers but have failed repeatedly to provide success against solid tumors. The reason is that tumor microenvironments are good at keeping T cells and other immune cells at bay. "These are often called cold tumors because immune cells simply cannot penetrate the microenvironments to provide a therapeutic effect," said Tushir-Singh. "It doesn't matter how well we engineer the immune receptor activating antibodies and T cells if they cannot get close to the tumor cells. Hence, we need to create spaces so T cells can infiltrate." Death receptors do precisely what their name implies -- when targeted, they trigger programmed cell death of tumor cells. They offer a potential workaround that could simultaneously kill tumor cells and pave the way for more effective immunotherapies and CAR T-cell therapy. Developing drugs that boost death receptor activity could provide an important weapon against tumors. However, though drug companies have had some success targeting the Death Receptor-5, no Fas agonists have made it into clinical trials. These findings could potentially change that. The right target While Fas plays an essential role in regulating immune cells, Tushir-Singh and his colleagues knew they might be able to target cancer cells selectively if they found the right epitope. Having identified this specific epitope, he and other researchers can now design a new class of antibodies to selectively bind to and activate Fas to potentially destroy tumor cells specifically. Other research in animal models and human clinical trials has shown that Fas signaling is fundamental to CAR T success, particularly in tumors that are genetically heterogeneous. Genetically heterogeneous tumors have a mix of different cell types, which can respond differently to treatment. A Fas agonist could generate a CAR-T bystander effect, in which the treatment destroys cancer cells that lack the molecule the tumor-targeting antibody is designed to hit. In other words, activating Fas may destroy cancer cells and improve CAR T efficacy, a potential one-two punch against tumors. In fact, the study showed tumors with a mutated version of the epitope of Fas receptors will not respond to CAR T at all. This finding could lead to new tests to identify which patients will benefit most from CAR T-cell immunotherapy. "We should know a patient's Fas status -- particularly the mutations around the discovered epitope -- before even considering giving them CAR T," Tushir-Singh said. "This is a definitive marker for bystander treatment efficacy of CAR T therapy. But most importantly, this sets the stage to develop antibodies that activate Fas, selectively kill tumor cells, and potentially support CAR T-cell therapy in solid tumors." Additional authors include Tanmoy Mondal, Himanshu Gaur, Brice E. N. Wamba, Abby Grace Michalak, Camryn Stout, Matthew R. Watson, Sophia L. Aleixo, Arjun Singh, Roland Faller, Gary Scott Leiserowitz and Sanchita Bhatnagar from UC Davis. and Salvatore Condello from Indiana University School of Medicine.

Using proprietary exosome tethering modification technology, Treg derived exosomes were engineered with a surface protein, cytotoxic T lymphocyte associated protein 4 (CTLA-4) to increase selective targeting to immune cells; This patented technology requires no genetic modifications, overcomes known limitations of exosome manipulation, and enables tethering of multiple potential proteins to an exosome surface and loading of therapeutic cargo in the exosome interior; CTLA-4-engineered Treg exosomes (CTLA-4-Treg exosomes) dramatically increased targeting of, binding to, internalization of, and uptake into immune cells including macrophages and T cells; This technology can serve as a platform to engineer the exosome surface with proteins of interest to target specific cell and tissue types to potentially treat epitope driven autoimmune diseases and cancer HOUSTON--(BUSINESS WIRE)-- Coya Therapeutics, Inc. (NASDAQ: COYA) (“Coya” or the “Company”), a clinical-stage biotechnology company developing multiple therapeutic platforms intended to enhance Treg function, including biologics and cell therapies, announced that Dr. Phil Campbell, Professor of Biomedical Engineering at CMU, presented his talk, “Rapid Functionalization of Treg Exosomes for Targeted Immunotherapy” at the 5th Exosome Based Therapeutic Development Summit in Boston, MA this morning (September 7, 2023). The presentation can be accessed here. Coya and CMU entered into a Research Collaboration Agreement and Option Agreement in 2022 to develop a unique patented technology intended to advance the potential use of exosomes for the treatment of diseases of unmet need. In this study, it was demonstrated that by using a proprietary cholesterol DNA tether technology, Treg exosome membranes could be engineered to controllably immobilize CTLA-4, a membrane surface active protein, onto the Treg exosome surface resulting in stable CTLA-4-Treg exosomes. It was also demonstrated that CTLA-4-Treg exosomes exhibited far better cell uptake then non-modified Treg EVs in representative immune cells, macrophages (J7774 murine cell line) and T-cells (human Jurket cell line). Previously, using the same technology, CMU demonstrated applications in Oncology by engineering mesenchymal derived exosomes with an immunomodulatory apoptotic inducing protein, Fas Ligand (FAS-L). The results demonstrate that targeted delivery of FASL-exosomes substantially increases its therapeutic effect with enhanced apoptosis in tumor cells and suppression of alloreactive T cells in mice, while minimizing potential off target effects. This publication is available here. Tregs are important immunomodulatory cells, with a key role controlling inflammation, enabling self-tolerance, and promoting regenerative processes. Treg-derived exosomes share many of the properties of the parent Treg cells making them able to modulate physiological and pathophysiological processes. The proprietary technology generates Exosome Polymer Hybrids (EPHs) which allow for efficient and versatile method of engineering and customizing cargos of Treg-derived exosomes using oligonucleotide tethers. Delivering EPHs to sites of inflammation or epitopes that drive specific diseases, while delivering customized loads, enables the next generation of selectively targeted and potent Treg-derived exosomes. Engineered exosomes may have multiple advantages, including low immunogenicity, improved stability, increased plasma retention after systemic delivery and increased residence time following local delivery, enhanced biodistribution, improved cell binding and uptake, and enhanced targeted therapeutic response. Dr. Fred Grossman, President and Chief Medical Officer of Coya stated, “This proprietary technology expands Coya’s pipeline to include autoimmune disorders and cancer. These engineered exosomes are a cell - free drug delivery system without genetic modification that can travel throughout the body unimpeded, including through the blood brain barrier, to provide specific targeted therapies.” 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 a 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 lead therapeutic programs includes Treg-enhancing biologics (COYA 300 Series product candidates) COYA 301 and COYA 302, which are intended to enhance Treg function and expand Treg numbers. COYA 301 is a proprietary investigational recombinant human low dose IL-2 biologic for subcutaneous administration intended to enhance Treg function and expand Treg numbers in vivo, and COYA 302 is a dual-mechanism investigational biologic combination comprised of proprietary low dose IL-2 and proprietary CTLA-4 Ig. The low dose IL-2 is intended to enhance anti-inflammatory regulatory T cell function and numbers while the fusion protein CTLA-4 Ig is intended to suppress pro-inflammatory cell function. These two mechanisms may be additive or synergistic in suppressing inflammation. 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.