Hacettepe University

BOSTON, May 23, 2024 (GLOBE NEWSWIRE) -- Aura Biosciences, Inc. (NASDAQ: AURA), a clinical-stage biotechnology company developing precision immunotherapies to treat solid tumors designed to preserve the function of the organ with cancer, today announced that it will host a virtual KOL event on Wednesday, May 29, 2024 at 2:00 PM ET. To register, click here. The event will feature Carol Shields, MD (Wills Eye Hospital), Hakan Demirci, MD (University of Michigan), and Mandeep Sagoo, MB, PhD, FRCS (Ed), FRCOPTH (Moorfields Eye Hospital), who will discuss the unmet medical need and current treatment landscape for patients suffering from ocular cancers, such as primary uveal melanoma, metastases to the choroid, and cancers of the ocular surface. It will also highlight Aura’s ocular oncology pipeline, focusing on its lead candidate bel-sar, which is currently in development as a potential vision-sparing therapy in the global Phase 3 CoMpass trial for the first-line treatment of adult patients with early-stage uveal melanoma. Aura's Therapeutic Area Head Ocular Oncology Anthony Daniels, MD will join the KOLs for a panel discussion moderated by Chris Howerton, PhD from LifeSci Advisors. A live question and answer session will follow the formal presentations. The live webcast of the event will be available on the “Investors & Media” page under the “Events & Presentations” section of Aura’s website at https://ir.aurabiosciences.com/events-and-presentations, where a replay of the webcast will be archived for 90 days following the presentation date. About Carol Shields, MD Carol Shields, MD completed her ophthalmology training at Wills Eye Hospital in Philadelphia and completed fellowship training in ocular oncology, oculoplastic surgery, and ophthalmic pathology. She is currently Director of the Oncology Service, Wills Eye Hospital, and Professor of Ophthalmology at Thomas Jefferson University in Philadelphia. She has authored or coauthored 12 textbooks, 341 chapters in edited textbooks, over 2000 articles in major peer-reviewed journals, and given over 1000 lectureships. Dr. Carol Shields is a member of numerous ocular oncology, pathology, and retina societies. She serves on the editorial or advisory board of 31 journals, including JAMA Ophthalmology and RETINA. She practices Ocular Oncology on a full-time basis with her husband, Dr. Jerry Shields and associates on the Oncology Service at Wills Eye Hospital. Each year the Oncology Service manages approximately 500 patients with uveal melanoma, 120 patients with retinoblastoma, and hundreds of other intraocular, orbital, and conjunctival tumors from the United States and abroad. About Hakan Demirci, MD Hakan Demirci, MD is the Richard N. and Marilyn K. Witham Professor of Ophthalmology and Visual Sciences at the Kellogg Eye Center, University of Michigan, where he also serves as Director of the Ocular Oncology Service. He specializes in the diagnosis and treatment of eye cancers, including intraocular, conjunctival, and orbital tumors. Dr. Demirci's research focuses on the early detection of eye cancers, targeted therapies, and metastasis prevention. He completed his medical degree at Hacettepe University in Turkey, followed by residencies at Istanbul University, Istanbul, Turkey in 1997 and in Ophthalmology at Henry Ford Hospital in 2010. He also completed fellowships in Ocular Oncology at Wills Eye Hospital, Thomas Jefferson University in 2001 and 2023 and in Eye Plastic, Orbital and Facial Cosmetic Surgery at Kellogg Eye Center, University of Michigan in 2006. About Mandeep Sagoo, MB, PhD, FRCS (Ed), FRCOPTH Mandeep Sagoo, MB, PhD, FRCS (Ed), FRCOPTH is Professor of Ophthalmology and Ocular Oncology at UCL Institute of Ophthalmology and a consultant ophthalmic surgeon with subspecialist interest in adult and pediatric eye tumors at the London Ocular Oncology Service at Moorfields Eye Hospital and St. Bartholomew’s Hospital and the London Retinoblastoma Service at Royal London Hospital. Mandeep graduated from Cambridge University and did his residency in ophthalmology at Oxford and then Moorfields Eye Hospital. His fellowship training was in ocular oncology, as a Fulbright Scholar, under Dr Jerry Shields and Dr Carol Shields at Wills Eye Hospital and his medical retina fellowship was at Moorfields. He holds over 20 academic awards and prizes, including the Gedge Prize of Cambridge University, John Glyn Young Fellows Prize of Royal Society of Medicine, PJ Hay Medal of the North of England Ophthalmology Society, the Syme Medal, and the King James IV Professorship of Royal College of Surgeons of Edinburgh. He has written multiple book chapters and over 200 academic papers. He is a member of Macula Society, council member of Oxford Ophthalmological Congress, and has served as honorary secretary of the International Society of Ocular Oncology. He led the clinical team that fitted the world’s first fully digitally made 3D printed ocular prosthetic. About Aura Biosciences Aura Biosciences is a clinical-stage biotechnology company developing precision immunotherapies to treat solid tumors designed to preserve the function of the organ with cancer. Our lead candidate bel-sar is in late-stage clinical development for the treatment of patients with primary uveal melanoma, and other ocular oncology indications as well as in early-stage clinical development in bladder cancer. We are evaluating the safety and efficacy of bel-sar as a potential vision-sparing therapy in an ongoing global Phase 3 CoMpass trial for the first-line treatment of adult patients with early-stage uveal melanoma. Bel-sar is also being evaluated in additional solid cancers, including bladder cancer. Our mission is to develop vision and organ-sparing therapies to improve patient outcomes in cancer. Aura is headquartered in Boston, MA. For more information, visit aurabiosciences.com. Visit us @AuraBiosciences and on LinkedIn. Forward-Looking Statements This press release contains forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995, as amended, and other federal securities laws. Any statements that are not statements of historical fact may be deemed to be forward looking statements. Words such as “may,” “will,” “could,” “should,” “expects,” “intends,” “plans,” “anticipates,” “believes,” “estimates,” “predicts,” “projects,” “seeks,” “endeavor,” “potential,” “continue” or the negative of such words or other similar expressions that can be used to identify forward-looking statements. These forward looking statements include express or implied statements regarding Aura’s future expectations, plans and prospects, including, without limitation, statements regarding the therapeutic potential of bel-sar for the treatment of cancers including early-stage uveal melanoma. The forward-looking statements in this press release are neither promises nor guarantees, and investors should not place undue reliance on these forward-looking statements because they involve known and unknown risks, uncertainties and other factors, many of which are beyond Aura’s control and which could cause actual results to differ materially from those expressed or implied by these forward-looking statements, including, without limitation, uncertainties inherent in clinical trials and in the availability and timing of data from ongoing clinical trials; the expected timing for submissions for regulatory approval or review by governmental authorities; the risk that the results of Aura’s preclinical and clinical trials may not be predictive of future results in connection with future clinical trials; the risk that interim data from ongoing clinical trials may not be predictive of final data from completed clinical trials; the risk that governmental authorities may disagree with Aura’s clinical trial designs, even where Aura has obtained agreement with governmental authorities on the design of such trials, such as the Phase 3 special protocol assessment agreement with the U.S. Food and Drug Administration; whether Aura will receive regulatory approvals to conduct trials or to market products; whether Aura’s cash resources will be sufficient to fund its foreseeable and unforeseeable operating expenses and capital expenditure requirements; Aura’s ongoing and planned preclinical activities; and Aura’s ability to initiate, enroll, conduct or complete ongoing and planned clinical trials. These risks, uncertainties and other factors include those risks and uncertainties described under the heading “Risk Factors” in Aura’s most recent Annual Report on Form 10-K and Quarterly Report on Form 10-Q filed with the United States Securities and Exchange Commission (SEC) and in subsequent filings made by Aura with the SEC, which are available on the SEC’s website at www.sec.gov. Except as required by law, Aura disclaims any intention or responsibility for updating or revising any forward-looking statements contained in this press release in the event of new information, future developments or otherwise. These forward-looking statements are based on Aura’s current expectations and speak only as of the date hereof and no representations or warranties (express or implied) are made about the accuracy of any such forward-looking statements. Investor and Media Contact: Alex DasallaHead of Investor Relations and Corporate CommunicationsIR@aurabiosciences.com

Acclaimed academic researcher has led 40+ multicenter phase 2 and phase 3 clinical studies CHICAGO--(BUSINESS WIRE)-- MAIA Biotechnology Inc., (NYSE American: MAIA) (“MAIA”, the “Company”), a clinical-stage biopharmaceutical company developing targeted immunotherapies for cancer, today announced the appointment of Professor Saadettin Kilickap, M.D. to its Scientific Advisory Board (SAB). This press release features multimedia. View the full release here: Professor Saadettin Kilickap, M.D., Scientific Advisor to MAIA Biotechnology (Photo: Business Wire) Dr. Kilickap is a professor at the Istinye University Faculty of Medicine, Department of Medical Oncology, Liv Hospital in Turkey. His research focuses on medical oncology and cancer epidemiology, including solid tumors such as lung cancer, breast cancer, melanoma, and gastrointestinal system cancers, as well as targeted therapies and immunotherapy. “Saadettin has served as principal or sub-investigator in more than 40 national and international multi-center phase 2 and phase 3 studies, many of which were related to lung cancer,” said Chief Executive Officer Vlad Vitoc, M.D. “He is a prominent voice on medical oncology and cancer epidemiology, with a special interest in quality of life for cancer patients. We are delighted to welcome him as Scientific Advisor as we begin to clear major clinical inflection points this year and progress with our groundbreaking cancer research.” Prior to his current appointment, Dr. Kilickap was a professor at the Preventive Oncology Department of Hacettepe University Cancer Institute of Turkey. Earlier he worked in the Department of Hematology-Oncology at Regensburg University in Germany and was a faculty member at the Sivas Cumhuriyet University Faculty of Medicine, Department of Internal Medicine, in Turkey. Dr. Kilickap graduated with honors from Gazi University Faculty of Medicine and went on to complete his internal medicine residency training at Hacettepe University Faculty of Medicine, both located in Ankara, Turkey. He completed his fellowship training at Hacettepe and became a medical oncology specialist in 2009. In the same year, he graduated from the Cancer Epidemiology Master's Program at the Hacettepe University Oncology Institute, Department of Preventive Oncology. Dr. Kilickap has authored more than 240 scientific articles published in international peer-reviewed journals, and delivered more than 50 poster presentations at international congresses. About MAIA Biotechnology, Inc. MAIA is a targeted therapy, immuno-oncology company focused on the development and commercialization of potential first-in-class drugs with novel mechanisms of action that are intended to meaningfully improve and extend the lives of people with cancer. Our lead program is THIO, a potential first-in-class cancer telomere targeting agent in clinical development for the treatment of NSCLC patients with telomerase-positive cancer cells. For more information, please visit . Forward Looking Statements MAIA cautions that all statements, other than statements of historical facts contained in this press release, are forward-looking statements. Forward-looking statements are subject to known and unknown risks, uncertainties, and other factors that may cause our or our industry’s actual results, levels or activity, performance or achievements to be materially different from those anticipated by such statements. The use of words such as “may,” “might,” “will,” “should,” “could,” “expect,” “plan,” “anticipate,” “believe,” “estimate,” “project,” “intend,” “future,” “potential,” or “continue,” and other similar expressions are intended to identify forward looking statements. However, the absence of these words does not mean that statements are not forward-looking. For example, all statements we make regarding (i) the initiation, timing, cost, progress and results of our preclinical and clinical studies and our research and development programs, (ii) our ability to advance product candidates into, and successfully complete, clinical studies, (iii) the timing or likelihood of regulatory filings and approvals, (iv) our ability to develop, manufacture and commercialize our product candidates and to improve the manufacturing process, (v) the rate and degree of market acceptance of our product candidates, (vi) the size and growth potential of the markets for our product candidates and our ability to serve those markets, and (vii) our expectations regarding our ability to obtain and maintain intellectual property protection for our product candidates, are forward looking. All forward-looking statements are based on current estimates, assumptions and expectations by our management that, although we believe to be reasonable, are inherently uncertain. Any forward-looking statement expressing an expectation or belief as to future events is expressed in good faith and believed to be reasonable at the time such forward-looking statement is made. However, these statements are not guarantees of future events and are subject to risks and uncertainties and other factors beyond our control that may cause actual results to differ materially from those expressed in any forward-looking statement. Any forward-looking statement speaks only as of the date on which it was made. We undertake no obligation to publicly update or revise any forward-looking statement, whether as a result of new information, future events or otherwise, except as required by law. In this release, unless the context requires otherwise, “MAIA,” “Company,” “we,” “our,” and “us” refers to MAIA Biotechnology, Inc. and its subsidiaries.

Researchers have identified the genetic causes of three mitochondrial diseases by figuring out what dozens of poorly understood mitochondrial proteins do. The functions of hundreds more mitochondrial proteins remain unknown, indicating that this approach could be a promising path to finding better ways to diagnose and treat the bewildering array of conditions linked to malfunctioning mitochondria. When something goes wrong in mitochondria, the tiny organelles that power cells, it can cause a bewildering variety of symptoms such as poor growth, fatigue and weakness, seizures, developmental and cognitive disabilities, and vision problems. The culprit could be a defect in any of the 1,300 or so proteins that make up mitochondria, but scientists have very little idea what many of those proteins do, making it difficult to identify the faulty protein and treat the condition. Researchers at Washington University School of Medicine in St. Louis and the University of Wisconsin-Madison systematically analyzed dozens of mitochondrial proteins of unknown function and suggested functions for many of them. Using these data as a starting point, they identified the genetic causes of three mitochondrial diseases and proposed another 20 possibilities for further investigation. The findings, published May 25 in Nature, indicate that understanding how mitochondria's hundreds of proteins work together to generate power and perform the organelles' other functions could be a promising path to finding better ways to diagnose and treat such conditions. "We have a parts list for mitochondria, but we don't know what many of the parts do," said co-senior author David J. Pagliarini, PhD, the Hugo F. and Ina C. Urbauer Professor and a BJC Investigator at Washington University. "It's similar to if you had a problem with your car, and you brought it to a mechanic, and upon opening the hood they said, 'We've never seen half of these parts before.' They wouldn't know how to fix it. This study is an attempt to define the functions of as many of those mitochondrial parts as we can so we have a better understanding of what happens when they don't work and, ultimately, a better chance at devising therapeutics to rectify those problems." Mitochondrial diseases are a group of rare genetic conditions that collectively affect one in every 4,300 people. Since mitochondria provide energy for almost all cells, people with defects in their mitochondria can have symptoms in any part of the body, although the symptoms tend to be most pronounced in the tissues that require the most energy, such as the heart, brain and muscles. To better understand how mitochondria work, Pagliarini teamed up with colleagues, including co-senior author Joshua J. Coon, PhD, a UW-Madison professor of biomolecular chemistry & chemistry and an investigator with the Morgridge Institute for Research; and co-first authors Jarred W. Rensvold, PhD, a former staff scientist in Pagliarini's lab, and Evgenia Shishkova, PhD, a staff scientist in Coon's lab, to identify the functions of as many mitochondrial proteins as possible. The researchers used CRISPR-Cas9 technology to remove individual genes from a human cell line. The procedure created a set of related cell lines, each derived from the same original cell line but with a single gene deleted. The missing genes coded for 50 mitochondrial proteins of unknown function and 66 mitochondrial proteins with known functions. Then, they examined each cell line for clues to the role each missing gene normally plays in keeping the mitochondria running properly. The researchers monitored the cells' growth rates and quantified the levels of 8,433 proteins, 3,563 lipids and 218 metabolites for each cell line. They used the data to build the MITOMICS (mitochondrial orphan protein multi-omics CRISPR screen) app, equipping it with tools to analyze and identify the biological processes that faltered when a specific protein went missing. After validating the approach with mitochondrial proteins of known function, the researchers proposed possible biological roles for many mitochondrial proteins of unknown function. With further investigation, they were able to tie three proteins to three separate mitochondrial conditions. "It is very exciting to see how our mass spectrometry technology platform can generate data on this scale but more importantly, data that can directly help us to understand human disease," Coon said. One condition is a multisystemic disorder caused by defects in the main energy-producing pathway. Co-author Robert Taylor, PhD, DSc, a professor of mitochondrial pathology at Newcastle University in Newcastle-upon-Tyne, U.K., identified a patient with clear signs of the disorder but no mutations in the usual suspect genes. The researchers identified a new gene in the pathway and showed that the patient carried a mutation in it. Separately, Pagliarini and colleagues noticed that disrupting one gene, RAB5IF, eliminated a protein encoded by a different gene, TMCO1, that has been linked to cerebrofaciothoracic dysplasia. The condition is characterized by distinctive facial features and severe intellectual disability. In collaboration with co-author Nurten Akarsu, PhD, a professor of human genetics at Hacettepe University in Ankara, Turkey, the researchers showed that a mutation in RAB5IF was responsible for one case of cerebrofaciothoracic dysplasia and two cases of cleft lip in one Turkish family. A third gene, when disrupted, led to problems with sugar storage, contributing to a fatal autoinflammatory syndrome. Data regarding that syndrome were published last year in a paper led by Bruno Reversade, PhD, of A*STAR, Singapore's Agency for Science, Technology and Research. "We focused primarily on the three conditions, but we found data connecting about 20 other proteins to biological pathways or processes," said Pagliarini, a professor of cell biology & physiology, of biochemistry & molecular biophysics and of genetics. "We can't chase down 20 stories in one paper, but we made hypotheses and put them out there for us and others to test." To aid scientific discovery, Pagliarini, Coon and colleagues have made the MITOMICS app available to the public. They built in several user-friendly analysis tools so anyone can look for patterns and create plots just by clicking around. All of the data can be downloaded for more advanced analysis. "The hope is that this large dataset becomes one of a number in the field that collectively help us to devise better biomarkers and diagnostics for mitochondrial diseases," Pagliarini said. "Every time we discover a function of a new protein, it gives us a new opportunity to target a pathway therapeutically. Our long-term goal is to understand mitochondria at sufficient depth to be able to intervene therapeutically, which we can't do yet."