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Preclinical data from the next generation eyedrop platform to be unveiled for the first time at ARVO 2024 DAEJEON, South Korea, April 22, 2024 /PRNewswire/ -- PharmAbcine, Inc. ("PharmAbcine" or the "Company") (KOSDAQ: 208340), a clinical-stage public company developing next generation therapeutics to treat medical unmet needs, announced today that the Company's U.S. subsidiary, Wincal Biopharm, Inc. ("WincalBio"), will present preclinical findings on its innovative ocular drug delivery platform at the upcoming conference, Association for Research in Vision and Ophthalmology (ARVO), the world's largest ophthalmology conference which will be held from May 5th to 9th, 2024 in Seattle, WA, United States. Based in South San Francisco, California, WincalBio is an emerging biotech dedicated to developing next-generation ocular drug delivery platforms and therapeutics for vascular diseases. Its proprietary Ocular Penetration Carrier (OPC) screening platform has shown high potential in treating various ocular diseases using eyedrop formulation of antibody therapeutics, thereby replacing the need for intravitreal injections. This novel OPC platform has a mechanism in facilitating the delivery of antibody therapeutics through the vitreous humor of the eye, reaching critical structures such as the aqueous chamber, vitreous, retina, and choroid. WincalBio stands as a pioneer in biotech industry with a leading program validated in mouse CNV models for anti-VEGF antibody therapies, a significant advancement in treating age-related macular degeneration (AMD) and diabetic macular edema (DME). These breakthroughs, along with preclinical data from various animal models, will be unveiled for the first time at ARVO 2024. While anti-VEGF antibody therapies are the standard of care for AMD treatment, they are currently limited to intravitreal injections. Dr. TaeWeon Lee, Chief Scientific Officer of WincalBio, underscored the importance of presenting these groundbreaking findings at ARVO, noting, "The OPC platform, developed internally over the past few years, has never been publicly disclosed. Presenting the preclinical data for the first time at ARVO holds tremendous significance." Additionally, Dr. Venice Chiueh, Director at WincalBio and the oral presenter, expressed gratitude for the keen interest of ARVO meeting organizers. "We appreciate the opportunity provided by ARVO reviewers to present advancements in eyedrop development. We are committed to ensuring the success of clinical studies aimed at transitioning existing patients from intravitreal injections to eyedrop applications." Eyedrop applications of therapeutics offer significant advantage of being non-invasive, as well as enhancing patient convenience with minimum side effects. While effectively delivering sufficient quantities of the therapeutics to the back of the eye remains the primary challenge for topical applications, WincalBio's OPC platform aims to overcome this challenge. ARVO, founded in 1928, is the world's largest ophthalmology conference with over 10,000 members from over 75 countries. The schedule of the presentation is as follows: Presentation Number: 2159 Presentation Title: Development of eyedrops for anti-VEGF therapeutic antibodies as a substitute for IVT injection for posterior ocular disease indications Session Number: 240 Session Title: Advancements in age-related macular degeneration: Novel drugs, delivery systems, and mechanistic insights Session Date/Start Time: May 6, 2024 from 3:00 PM to 3:15 PM Room: Yakima 1 (Seattle Convention Center - Arch Building) About Wincal Biopharm, Inc. Wincal Biopharm (WincalBio) is focused on developing vascular therapeutics. Our current focus is on developing eyedrop formulations for therapeutic antibodies using proprietary Ocular Penetration Carrier (OPC) screening platform to identify a matching antibody:carrier pair that allows therapeutic antibodies reach intraocular space including aqueous chamber, vitreous, retina and choroid, which is difficult without injection. This non-invasive eyedrop delivery of therapeutic antibodies without intravitreal injections opens up broader treatment opportunities for multiple intraocular diseases including wet AMD, DME, diabetic retinopathy, uveitis, geographic atrophy, thyroid eye disease and uveal melanoma to lower the treatment burden for both patients and clinicians. It can be used as a monotherapy with already FDA approved anti-VEGF antibodies as well as combination with other novel target antibodies including cytokine targets such as ILs (IL-1, IL-4, IL-6, IL-10, IL-17, IL-18, IL-23), TNFa, TGFb, FGF, PDGF, FasL, EGFR as well as ocular cancer targets (PD-1, PD-L1, CTLA4). Currently, anti-VEGF antibody is a lead program with preclinical efficacy demonstration in mouse CNV model, and planning to do clinical studies in 2026 followed by other novel target antibody programs and combination programs. At WincalBio, our commitment to in vivo science with a needle free drug delivery underpins to improve patient's quality of life and compliance. About OPC Platform Ocular Penetration Carrier (OPC) platform is an in vivo ocular penetration screening to quickly identify a matching cargo protein to carrier formulation from our proprietary carrier library. Delivered target protein localization from cornea, anterior chamber, vitreous, retina, choroid and optic nerve can be monitored with a labeled fluorescent signal. A wide variety of large molecule therapeutic candidates including Fab, scFv, IgGs, Fc fusion proteins, recombinant proteins and growth factors can be delivered to the back of eye. Our proprietary carriers were designed to facilitate large molecules to intraocular target area. About Aflibercept-ED (WBP-101) Aflibercept-ED (WBP-101) is an aflibercept/OPC eyedrop formulation to target retinal area without using needles. Aflibercept has been clinically well proven anti-VEGF therapeutics with the delivery route of intravitreal injections. WBP-101 eyedrop application can significantly improve ease of use and avoid injection related issues including pain, bleeding, infection or inflammation and may improve patient adherence rate by lowering treatment related burdens. Patients can easily apply eyedrops at home, which can replace IVT injection procedures for ocular disease treatment. WBP-101 can be a primary monotherapy or can be used as a maintenance therapy after an initial IVT injection. Combination therapy is also possible by delivering different pathway blocking antibodies in a single formulation. Preclinical PoC in mouse CNV model demonstrated a comparable efficacy profile to the IVT injected. For additional information about Wincal Biopharm, Inc., visit . SOURCE PharmAbcine

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.