IL18R1

MONROVIA, Calif.--(BUSINESS WIRE)-- Xencor, Inc. (NASDAQ:XNCR), a clinical-stage biopharmaceutical company developing engineered antibodies and cytokines for the treatment of cancer and autoimmune diseases, today announced the presentation of data from the first patients in the Phase 2 combination study of vudalimab, a selective PD-1 x CTLA-4 XmAb® bispecific antibody, in patients with metastatic castration-resistant prostate cancer (mCRPC) and data from multiple preclinical-stage XmAb programs at the 37th Annual Meeting of the Society for Immunotherapy of Cancer (SITC) in Boston. “Evaluating chemotherapy combinations with vudalimab is an important part of our Phase 2 development plan due to the breadth of tumor types we could address with dual PD-1/CTLA-4 blockade and chemotherapy,” said Allen Yang, M.D., Ph.D., senior vice president and chief medical officer at Xencor. “Our initial combination data examines vudalimab with the aggressive chemotherapy regimen of a carboplatin and a taxane. Though we observed clinical activity, including multiple PSA50 responses and a partial response even in this small number of patients with advanced mCRPC, tolerability was a concern, so we are de-intensifying the chemotherapy regimen and maintaining the vudalimab dose. Consistent with our strategy of pursuing indications that checkpoint inhibitors have not yet addressed, we will continue to study a combination of platinum and taxane in patients with aggressive variant prostate cancer and a more broadly applicable chemotherapy combination with vudalimab and a taxane for other patients with mCRPC.” Posters will be available in the poster hall and virtually to registrants of the SITC Annual Meeting. In the poster hall, odd numbered posters will be displayed on Thursday, November 10, and even numbered posters will be displayed on Friday, November 11. The posters will be archived under "Events & Presentations" in the Investors section of the Company's website located at . Abstract 668, “A Phase 2 study of vudalimab, a PD-1 x CTLA-4 bispecific antibody, plus chemotherapy or targeted therapy in patients with molecularly defined subtypes of metastatic castration-resistant prostate cancer” Xencor is advancing vudalimab, a selective dual checkpoint inhibitor, in multiple Phase 2 clinical studies. The Company is conducting a Phase 2 study of vudalimab in patients with mCRPC, as a monotherapy or in combination with standard-of-care chemotherapy or a PARP inhibitor. A Phase 2 monotherapy study in patients with advanced gynecologic and clinically defined high-risk mCRPC is also ongoing. The trials in progress poster included clinical data from the safety run-in portion of the first Phase 2 study, which enrolled nine patients with mCRPC. Eight of the nine patients received vudalimab plus carboplatin and a taxane (either cabazitaxel or docetaxel). Patients were categorized into five cohorts, depending on their molecularly defined mCRPC subtype: aggressive variant prostate cancer (Cohort A; n=2), prior PARPi progressor (Cohort B; n=1), PARPi naïve (Cohort C; n=1), MSI-high or MMRD (Cohort D; n=0) and no targetable mutations (Cohort E; n=5). Efficacy Analysis As of the data cut on September 7, 2022, prostate-specific antigen (PSA) reductions of more than 50% from baseline (PSA50) had been observed in three of nine patients, inclusive of all cohorts and time on study. A patient in Cohort E with an 89% reduction in PSA from baseline experienced a partial response (PR) at week 18 and was continuing treatment at 35 weeks. Treatment was continuing for one additional patient in Cohort C, at 4 weeks. In addition to the patient experiencing a PR in Cohort E, six other patients were efficacy evaluable and experienced a best response of stable disease (n=5) or non-complete response/non-progressive disease (non-CR/non-PD; n=1). Safety Analysis The review of data from the safety run-in portion of the study guided the Company to revise the chemotherapy dosing regimens in combination cohorts in the study (Cohorts A, B and E). Vudalimab dosing in all cohorts remains at 10 mg/kg, administered every two weeks. The chemotherapy regimen was changed to taxane alone in Cohorts B and E or reduced dose intensity for the first cycle of treatment in Cohort A, the aggressive variant. Eight patients in Cohorts A, B and E received the combination of vudalimab, carboplatin and either cabazitaxel or docetaxel, depending on prior docetaxel exposure. Treatment-related serious adverse events (SAEs) occurring within the first cycle of therapy were reported for five of eight patients. All events resolved with medical management, including steroids when appropriate, treatment interruption or treatment cessation. Overall, four patients discontinued treatment due to AEs. The types of irAEs observed were largely consistent with the Phase 1 vudalimab monotherapy study of 110 patients. No immune related adverse events (irAEs) or treatment-related AEs were reported for the patient in Cohort C, who received vudalimab and olaparib, a PARP inhibitor. Preclinical Program Posters Abstract 1067, “Synergistic combination of Natural Killer cell engagers (NKEs) with proinflammatory cytokines” Xencor’s XmAb natural killer cell engagers (NKEs) are multifunctional antibodies that target multiple activating receptors on the surface of NK cells and bind to tumor associated antigens. Xencor engineered a B7-H3 x NKG2D NKE bispecific antibody with a modified Fc domain to enhance FcγR binding. The molecule’s design is intended to engage NK cells through the simultaneous binding to B7-H3 on tumor cells and the activating receptors NKG2D and CD16. In addition to stimulating NK cells, NKG2D-targeting NKEs also provide costimulation to CD8 T cells, though this may induce the potential killing by the NK cells. Therefore, NKG2D affinity was tuned to balance desired anti-tumor activity with off-target effector cell effects. In parallel, Xencor also engineered NKEs targeting B7-H3 and NKG2D’s ligands, MICA and MICB (MICA/B). The molecule’s design is intended to engage the activating receptors NKG2D and CD16; however, indirect targeting of NKG2D via its ligands MICA/B may avoid off-target effector cell effects. In vitro, B7-H3 x NKG2D and MICA/B x B7H3 NKEs activated NK cells and enhanced NK cell mediated lysis of tumor cells. Additionally, in vitro anti-tumor activity was enhanced when combined with an analog of the proinflammatory IL15-Fc cytokine, XmAb306. Abstract 1073, “Costimulatory CD28 trispecific antibodies targeting PDL1 and PDL2 enhance T cell activation in solid tumors” T cells in the tumor microenvironment require both T cell receptor (TCR) and co-stimulatory receptor engagement to achieve full activation. CD28 is a key immune co-stimulatory receptor on T cells; however, the ligands that activate T cells through CD28 are usually not expressed on tumor cells. Xencor designed a PDL1 x PDL2 x CD28 XmAb trispecific antibody to provide CD28 costimulation in the presence of TCR engagement and either PDL1 or PDL2 antigens. Since PDL1 and PDL2 can engage PD-1 to suppress the immune system’s anti-tumor responses, the trispecific is designed to simultaneously block CD28's suppression by PD-1. In vitro, the trispecific enhanced the activity of a CD3 bispecific antibody, a modality known to indirectly promote PDL1 and PDL2 expression. Abstract 1079, “LAG3-targeted IL15/IL15Rα-Fc (LAG3 x IL15) fusion proteins for preferential TIL expansion via cis delivery of IL15 to LAG3+ cells” IL-2 and IL-15 are cytokines that cause the activation and proliferation of T cells and NK cells. Their therapeutic potential has been well established in preclinical models and clinical studies; however, when given systemically, these potent cytokines have historically provided a poor therapeutic window, as they are not well tolerated and are quickly cleared from circulation. LAG-3 is an immune checkpoint expressed on tumor-infiltrating lymphocytes (TILs), is frequently co-expressed with PD-1 and has limited expression in non-activated T cells. Xencor engineered LAG3-targeted, reduced potency IL15/IL15Rα-Fc cytokine/antibody fusion proteins (LAG-3 x IL-15) for selective activation of LAG3-positive immune cells, which may potentially avoid systemic toxicities arising from off-target activation and expansion of peripheral immune cells. An XmAb heterodimeric Fc domain serves as a molecular scaffold, and Xtend™ technology promotes longer circulating half-life. Recently, anti-LAG3 agents have generated promising results in clinical studies, and LAG-3 x IL-15 agents could be combined with anti-PD1 agents. Xencor’s LAG-3 x IL-15 candidate molecules demonstrated high selectivity for LAG3-positive cell populations in multiple in vitro and in vivo models. In a preclinical tumor model, a combination of LAG-3 x IL-15 and an anti-PD1 antibody inhibited tumor growth better than anti-PD1 antibody alone. Abstract 1372, “XmAb143, an engineered IL18 heterodimeric Fc-fusion, features improved stability, reduced potency, and insensitivity to IL18BP” IL-18 is a proinflammatory cytokine that modulates both the innate and adaptive immune responses. IL-18 receptor 1, the primary co-receptor for IL-18, is expressed on activated T cells and NK cells, which are critical for anti-tumor responses. Additional preclinical studies of IL-18 have demonstrated its anti-tumor activity, including synergy with immune checkpoint inhibitors and CAR-T therapies. In contrast with other potent cytokines, IL-18 has been well tolerated in clinical trials but demonstrated a lack of efficacy despite heavy dosing. IL-18 participates in a negative feedback loop with a high affinity natural inhibitor, IL18BP, which was observed to be upregulated in early phase clinical studies and may have directly resulted in IL-18’s limited clinical performance. Xencor engineered stabilized, potency-reduced, monovalent IL-18 cytokines fused to an XmAb heterodimeric Fc domain with Xtend Fc technology for longer half-life (IL18-Fc). Importantly, these IL18-Fc candidates were engineered to avoid binding its inhibitor IL18BP. In a preclinical mouse model of graft-versus-host disease, IL18-Fc led to the expansion and proliferation of target immune cells and induced high levels of interferon gamma. In a preclinical tumor model, IL18-Fc and an anti-PD1 antibody inhibited tumor growth and expanded NK cells and CD8 T cells more than the anti-PD1 antibody alone. Further, it was well tolerated in non-human primates and exhibited superior pharmacokinetics. Additional Posters (Clinical Trials in Progress) Abstract 667, “A Phase 1, multiple-dose study to evaluate the safety and tolerability of XmAb819 (ENPP3 x CD3) in subjects with relapsed or refractory clear cell renal cell carcinoma (RCC)” Abstract 733, “A Phase 2 study of vudalimab (XmAb717), an anti-PD-1/CTLA-4 bispecific antibody, in patients with selected gynecological malignancies and high-risk metastatic castration-resistant prostate-cancer” About Vudalimab Vudalimab is an XmAb bispecific antibody that simultaneously targets immune checkpoint receptors PD-1 and CTLA-4 and is designed to promote tumor-selective T-cell activation. Xencor’s approach to dual checkpoint inhibition reduces the need for multiple antibodies and allows for more selective targeting of T cells with high checkpoint expression of both targets, which may potentially improve the therapeutic index of combination immunotherapies. In preclinical studies, dual blockade of PD-1 and CTLA-4 with vudalimab significantly enhanced T cell proliferation and activation, and anti-tumor activity in vivo. Xencor is conducting a Phase 2 clinical study of vudalimab in patients with metastatic castration resistant prostate cancer (mCRPC), plus chemotherapy for certain patient populations, and a Phase 2 clinical study in patients with advanced gynecologic and genitourinary malignancies, as well as high-risk mCRPC. About XmAb®819 XmAb®819 is a tumor-targeted, T-cell engaging XmAb 2+1 bispecific antibody in development for patients with renal cell carcinoma (RCC). XmAb819 engages the immune system by activating T cells for highly potent and targeted killing of tumor cells expressing ENPP3, an antigen highly expressed on kidney cancers. ENPP3 is differentially expressed between RCC (high expression) and normal tissues (low expression). To attack RCC cells selectively, XmAb819 was engineered as an XmAb 2+1 bispecific antibody with two binding domains against ENPP3 and one cytotoxic T-cell binding domain against CD3, a component of the T-cell receptor (TCR) complex. Xencor’s XmAb Bispecific Fc Domain serves as the scaffold for these binding domains and provides long circulating half-life, stability and ease of manufacture. Xencor is conducting a Phase 1 study of XmAb819 in patients with advanced renal cell carcinoma. About Xencor Xencor is a clinical-stage biopharmaceutical company developing engineered antibodies and cytokines for the treatment of patients with cancer and autoimmune diseases. More than 20 candidates engineered with Xencor's XmAb® technology are in clinical development, and three XmAb medicines are marketed by partners. Xencor's XmAb engineering technology enables small changes to a protein's structure that result in new mechanisms of therapeutic action. For more information, please visit . Forward-Looking Statements Certain statements contained in this press release may constitute forward-looking statements within the meaning of applicable securities laws. Forward-looking statements include statements that are not purely statements of historical fact, and can generally be identified by the use of words such as “potential,” “can,” “will,” “plan,” “may,” “could,” “would,” “expect,” “anticipate,” “seek,” “look forward,” “believe,” “committed,” “investigational,” and similar terms, or by express or implied discussions relating to Xencor’s business, including, but not limited to, statements regarding presentations of clinical trial data for vudalimab generally, planned clinical trials, the quotations from Xencor's senior vice president and chief medical officer and other statements that are not purely statements of historical fact. Such statements are made on the basis of the current beliefs, expectations, and assumptions of the management of Xencor and are subject to significant known and unknown risks, uncertainties and other factors that may cause actual results, performance or achievements and the timing of events to be materially different from those implied by such statements, and therefore these statements should not be read as guarantees of future performance or results. Such risks include, without limitation, the risks associated with the process of discovering, developing, manufacturing and commercializing drugs that are safe and effective for use as human therapeutics and other risks, including the ability of publicly disclosed preliminary clinical trial data to support continued clinical development and regulatory approval for specific treatments, in each case as described in Xencor's public securities filings. For a discussion of these and other factors, please refer to Xencor's annual report on Form 10-K for the year ended December 31, 2021 as well as Xencor's subsequent filings with the Securities and Exchange Commission. You are cautioned not to place undue reliance on these forward-looking statements, which speak only as of the date hereof. This caution is made under the safe harbor provisions of the Private Securities Litigation Reform Act of 1995, as amended to date. All forward-looking statements are qualified in their entirety by this cautionary statement and Xencor undertakes no obligation to revise or update this press release to reflect events or circumstances after the date hereof, except as required by law.

Medikine’s first therapeutic candidate, MDK-703, an Interleukin-7 (IL-7) mimetic with an extended half-life, will be studied in healthy volunteers, with top-line results expected in the fourth quarter of 2022 Company plans to investigate MDK-703 in solid tumors following completion of the Phase 1 clinical trial MDK-703 is an immunoglobulin Fc fragment-peptide fusion protein incorporating an IL-7 PEPTIKINE™ discovered using Medikine’s innovative platform technology to improve drug properties MENLO PARK, Calif.--(BUSINESS WIRE)-- Medikine, Inc., a biopharmaceutical company developing transformative therapeutics for cancer, autoimmune disorders, and infectious diseases using its novel PEPTIKINE™ technology, today announced it has initiated dosing of MDK-703, an extended half-life IL-7 mimetic. The Phase 1 clinical trial, in healthy volunteers, will evaluate the safety, tolerability, pharmacokinetics, and pharmacodynamics of single, ascending intramuscular doses of MDK-703 compared to placebo. Top-line results from the clinical trial are expected in the fourth quarter of 2022. MDK-703 is the First IL-7 Mimetic to be Studied in Humans MDK-703 is an investigational biologic drug incorporating an IL-7 PEPTIKINE discovered using Medikine’s platform technology. Medikine’s PEPTIKINES are substantially smaller molecules than the cytokines they emulate, structurally unrelated to natural cytokines, engineered for low immunogenicity, and readily amenable to incorporating targeting and other pharmacological features. IL-7 is a cytokine critical for the development and maintenance of T cells, including enhancing generation, function, and survival of memory T cells. In oncology, treatments with these biological attributes, alone or in combination with other immune-based therapies, may enhance the rate, depth, and durability of clinical response. In addition to these anti-tumor properties, MDK-703 has the beneficial property that it will not generate anti-drug antibodies (ADAs) that neutralize native IL-7, an issue previously observed with IL-7 agents that have been studied in humans. The company plans to investigate MDK-703 in solid tumors following the completion of the Phase 1 clinical trial in healthy volunteers. Medikine has shown that MDK-703 behaves similarly to IL-7 in human immune cell in vitro studies and in humanized mice and non-human primates in vivo studies. In addition to increasing the total number of CD8 T cells and CD4 T cells, MDK-703 increased the number of memory T cells, particularly T memory stem (TSCM) cells. TSCM cells are a subset of memory T cells that have the potential to self-renew and differentiate, thereby reconstituting the entire spectrum of memory and effector cell types.1 In addition, MDK-703 had negligible-to-no impact on the expansion of CD4 T regulatory and natural killer (NK) cell populations. “Based on preclinical data, we believe that MDK-703 has best-in-class potential, with biology consistent with facilitating the differentiation, maintenance, and survival of the T cell subsets that are critical for durable anti-tumor activity in humans. The initial study of MDK-703 in healthy subjects is designed to provide important proof-of-pharmacology that is relevant to cancer treatment, including the impact on specific T-cell populations and the lack of neutralizing IL-7 ADAs,” commented Dr. Joseph Leveque, president and chief medical officer of Medikine. Medikine Applies Expertise in PEPTIKINE Technology to Next-Generation Cytokine Drug Development Medikine’s founding team of Ronald W. Barrett, Ph.D. (chief executive officer and chairman of the Board), William J. Dower, Ph.D. (scientific advisor), and Michael C. Needels, Ph.D. (chief technology officer), have worked together since the 1990s. They are experts in peptide library technology and its application to the discovery of cytokine receptor agonists and antagonists. Their groundbreaking work at the Affymax Research Institute resulted in the discovery of peptide mimetics of erythropoietin and thrombopoietin. At Medikine, they have been taking this concept to a new level of sophistication and utility by engineering novel PEPTIKINES for multi-subunit cytokine receptors. As Medikine moves from PEPTIKINE discovery research into clinical development, the company’s leadership team is well prepared with the recent addition of Joseph Leveque, M.D., as president and chief medical officer, and Marcos Milla, Ph.D., as interim chief scientific officer. Dr. Leveque previously has held senior executive and therapeutic area leadership roles at Mirati Therapeutics, Synthorx, ARMO BioSciences, Bristol Meyers Squibb, and Amgen. Dr. Milla is currently a venture partner at Samsara BioCapital and was previously chief scientific officer at Synthorx, head of Therapeutics Discovery at Adaptive Biotechnologies, and head of Emerging Science and Innovation of Janssen Discovery Sciences. Research by Drs. Leveque and Milla at Synthorx to discover and develop a “non-alpha” IL-2 derivative led to Synthorx’s acquisition by Sanofi for $2.5 billion in late 2019. Dr. Milla commented, “With its versatile drug discovery platform, Medikine is well-positioned to develop transformative therapies for cancer and other serious diseases. I am particularly intrigued by the pharmacology of MDK-703, with its unique action on key T cell memory populations of great importance to find and destroy cancer cells―one that I believe could offer advantages over other cytokine-based therapies in development. I am thrilled to help realize the possibilities of this lead program and the rest of Medikine’s pipeline.” Medikine’s Pipeline of PEPTIKINE Therapeutics In addition to its lead product candidate, MDK-703, Medikine also has identified novel PEPTIKINES that activate the IL-2/15βγ receptor complex. The company is exploring their use for engineering bispecific cytokine mimetics with differentiated pro including an IL-7 and IL-2/15βγ dual receptor agonist, and a cell-targeted IL-2/15βγ attenuated receptor agonist. Medikine also has identified multiple high-affinity peptide ligands for both subunits of the IL-18 receptor that do not bind to the IL-18 decoy soluble receptor. Medikine is exploring the use of these peptide ligands as part of IL-18 PEPTIKINES. ABOUT MEDIKINE Medikine is a biopharmaceutical company with a mission to transform the discovery of oncology, autoimmune disorder, and infectious disease therapeutics by employing a versatile drug discovery platform that generates modular “PEPTIKINES”- peptide mimetics of cytokines that are smaller in molecular size than, and structurally unrelated to, the natural cytokines they emulate. These PEPTIKINES are engineered for low immunogenicity and are readily amenable to the incorporation of targeting and other pharmacological features. Medikine’s lead candidate, MDK-703, currently in a Phase 1 clinical trial in healthy volunteers, is an IL-7 PEPTIKINE fused to an immunoglobulin Fc-domain. MDK-703 emulates the beneficial properties of IL-7, a cytokine critical for maintenance of T cell responses. For more information, please visit . REFERENCES Gattinoni L, Speiser D, Lichterfeld M, et al. T memory stem cells in health and disease. Nat Med. 2017;23:18–27. doi:10.1038/nm.4241

MONT-SAINT-GUIBERT, Belgium, Aug. 04, 2021 (GLOBE NEWSWIRE) -- Celyad Oncology SA (Euronext & Nasdaq: CYAD) (the “Company”), a clinical-stage biotechnology company focused on the discovery and development of chimeric antigen receptor T cell (CAR T) therapies for cancer, today announced an update on its financial results and recent business developments for the fiscal quarter ended June 30, 2021. "We continue to blaze a path forward by developing new technologies to advance allogeneic CAR T therapies, including our proprietary shRNA platform for allogeneic CAR T production and ‘armored’ CAR capabilities with co-expression of secreting cytokines, starting with IL-18. The innovations we are making through our clinical development pipeline and new technologies were the focus of our R&D day last month. This is an exciting time in our Company’s history as we plan for a steady stream of milestones in the second half of 2021,” commented Filippo Petti, Chief Executive Officer of Celyad Oncology. “We plan on announcing multiple clinical updates in the next six months that are expected to help further the progress of our lead programs and proprietary shRNA platform for the development of next-generation allogeneic CAR Ts.” Second Quarter 2021 and Recent Business Highlights Pipeline Update CYAD-101 – Allogeneic TIM-based NKG2D CAR T for mCRC CYAD-101 is the Company's first-in-class, allogeneic CAR T candidate engineered to co-express a chimeric antigen receptor (CAR) based on the NKG2D receptor and the novel inhibitory peptide TCR Inhibitory Molecule (TIM). CYAD-211 – Allogeneic shRNA-based, anti-BCMA CAR T for r/r MM CYAD-211 is an investigational, shRNA-based allogeneic CAR T candidate for the treatment r/r MM. CYAD-211 is engineered to co-express a B cell maturation antigen (BCMA) targeting CAR and a single shRNA, which interferes with the expression of the CD3ζ component of the T-cell receptor (TCR) complex. CYAD-203 – Allogeneic shRNA-based, IL-18-armored NKG2D CAR T for Solid Tumors CYAD-203 is the Company’s first armored CAR T candidate engineered to co-express the cytokine interleukin-18 (IL-18) with the NKG2D CAR receptor. To the Company’s knowledge, this therapy is on track to be the first IL-18 secreting allogeneic CAR T candidate. IL-18 is a proinflammatory cytokine that directly potentiates the anti-cancer activity of CAR T cells while also altering the balance of pro- and anti-inflammatory cells within tumor tissue. CYAD-02 – Autologous NKG2D CAR-T for r/r AML and MDS CYAD-02, the Company’s autologous CAR T candidate with shRNA technology that targets the NKG2D ligands MICA and MICB, is currently being evaluated for the treatment of r/r acute myeloid leukemia (AML) and myelodysplastic syndromes (MDS) in the Phase 1 CYCLE-1 dose-escalation trial. Upcoming Anticipated Milestones First Half 2021 Financial Results Key financial figures for the first half of 2021, compared with the first half of 2020 and full year 2020, are summarized below: Research and Development expenses were €10.0 million for the first half of 2021, compared to €11.1 million for the first half of 2020. The €1.1 million decrease was mainly driven by lower preclinical expenses, including process development, as well as decreased clinical costs associated with the autologous r/r AML and MDS franchise. General and Administrative expenses were €4.8 million for the first half of 2021, compared to €4.8 million for the first half of 2020. An increase in insurance costs for the period were compensated by savings on travel and living expenses due to COVID-19 pandemic travel restrictions and a decrease in expenses associated with the share-based payments related to the Company’s warrants plan. A fair value adjustment of €2.0 million (non-cash expense) related to the reassessment of the contingent consideration and other financial liabilities associated with the advancement in the Company’s NKG2D-based CAR T candidates as of June 30, 2021 required by International Financial Reporting Standards (IFRS) was mainly driven by time accretion as well as updated assumptions to discount rate and revaluation of the U.S. dollar foreign exchange rate. The Company also posted €1.8 million in net other income for the first half of 2021, compared to a net other income of €1.8 million for the first half of 2020. Other income for the first half of 2021 is primarily due to grant income from the Walloon Region and from the Federal Belgian Institute for Health Insurance (Inami) of €1.6 million. Net loss for the first half of 2021 was €14.9 million, or € (1.02) per share, compared to a net loss of €16.6 million, or €(1.19) per share, for the first half of 2020. Net cash used in operations, which excludes non-cash expenses, was €12.2 million for the first half of 2021, compared to €14.6 million for the first half of 2020. As of June 30, 2021, the Company had cash and cash equivalents of €12.0 million ($14.3 million). During the first half of 2021, the Company raised proceeds of €8.1 million ($9.7 million) from the sale of American Depositary Shares (ADSs), in aggregate, to Lincoln Park Capital Fund, LLC (LPC) and through its At-the-Market facility. The Company believes that its existing cash and cash equivalents combined with the remaining access to the equity purchase agreement established with LPC should be sufficient, based on the current scope of activities, to fund operating expenses and capital expenditure requirements to the end of the third quarter of 2022. As of June 30, 2021, the total number of basic shares outstanding were 15.494 million, as compared to 13.942 million as of June 30, 2020. Celyad Oncology First Half 2021 Conference Call Details Date: Thursday, August 5, 2021Time: 2 p.m. CEST / 8 a.m. EDTDial-in: +1 412 317 6060 (International), + 1 866 652 5200 (United States) or +32 (0) 800 389 13 (Belgium)Please ask to be joined into the Celyad Oncology SA call The conference call will be webcast live and archived within the “Events” section of the Celyad Oncology website. About Celyad Oncology Celyad Oncology is a clinical-stage biotechnology company focused on the discovery and development of chimeric antigen receptor T cell (CAR T) therapies for cancer. The Company is developing a pipeline of allogeneic (off-the-shelf) and autologous (personalized) CAR T cell therapy candidates for the treatment of both hematological malignancies and solid tumors. Celyad Oncology was founded in 2007 and is based in Mont-Saint-Guibert, Belgium and New York, NY. The Company has received funding from the Walloon Region (Belgium) to support the advancement of its CAR T cell therapy programs. For more information, please visit . 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. Forward-looking statements include statements regarding the clinical activity and safety and tolerability of CYAD-211, CYAD-203, CYAD-101 and CYAD-02; expectations regarding enrollment and the announcement of additional clinical data; outcomes and timelines for the IMMUNICY-1 and CYCLE-1 clinical trials and plans for initiating KEYNOTE-B79 Phase 1b trial; the timeline for submission an IND application for CYAD-203; and the Company’s cash runway. Forward-looking statements may involve known and unknown risks and uncertainties which might cause actual results, financial condition, performance or achievements of Celyad Oncology to differ materially from those expressed or implied by such forward-looking statements. Such risk and uncertainty include the duration and severity of the COVID-19 pandemic and government measures implemented in response thereto. A further list and description of these risks, uncertainties and other risks can be found in Celyad Oncology’s U.S. Securities and Exchange Commission (SEC) filings and reports, including in its Annual Report on Form 20-F filed with the SEC on March 24, 2021, 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. Investor and Media Contacts:Sara ZelkovicCommunications & Investor Relations DirectorCelyad Oncology investors@celyad.com Daniel FerryManaging DirectorLifeSci Advisors, LLCdaniel@lifesciadvisors.com Source: Celyad Oncology SA Celyad Oncology SAInterim Consolidated Statement of Comprehensive Income (Unaudited) Celyad Oncology SAInterim Consolidated Statement of Financial Position (Unaudited)