< Back 12th – 13th June, 2024 Boston, MA The Festival Of Genomics & Biodata Discover, meet, learn and celebrate with the genomics and biodata community. Featuring ‘inspirational speakers, the latest research and clinical breakthroughs, cutting-edge technology and incredible networking opportunities, the Festival is designed to help attendees return to work armed with dozens of new ideas and contacts’ Previous Register now Next

Merck has entered into an exclusive global license agreement with Hansoh Pharma to develop and commercialize HS-10270, an investigational oral GLP-1 receptor agonist for the treatment of type 2 diabetes and obesity. < Back Merck Partners with Hansoh Pharma on Oral GLP-1 Receptor Agonist for Type 2 Diabetes Merck has entered into an exclusive global license agreement with Hansoh Pharma to develop and commercialize HS-10270, an investigational oral GLP-1 receptor agonist for the treatment of type 2 diabetes and obesity. Merck & Co., Inc. (NYSE: MRK) has entered into an exclusive global license agreement with Hansoh Pharmaceutical Group Company Limited (HKEX: 3692) for the development and commercialization of HS-10270 , an investigational oral GLP-1 receptor agonist aimed at treating type 2 diabetes and obesity. This strategic partnership marks a significant milestone in both companies' efforts to expand access to effective and convenient treatments for metabolic diseases. Under the terms of the agreement, Merck will gain exclusive rights to develop and market HS-10270 outside of China, while Hansoh Pharma will retain exclusive rights for its development and commercialization within China. The collaboration aims to advance the clinical development of this oral therapy, with the goal of offering a more accessible and patient-friendly alternative to the currently available injectable GLP-1 receptor agonists. A New Oral Option for Diabetes and Obesity HS-10270 is a novel oral formulation of a GLP-1 receptor agonist designed to help manage blood sugar levels and promote weight loss—two key therapeutic goals for patients with type 2 diabetes and obesity. This class of medications works by mimicking the natural GLP-1 hormone to regulate insulin secretion, reduce glucagon production, and suppress appetite. GLP-1 receptor agonists, such as semaglutide, have already proven highly effective in controlling blood glucose levels and aiding weight loss. However, the availability of these drugs in an oral form could expand patient access, as oral medications are generally preferred over injectable therapies for their ease of use and convenience. Early clinical trials of HS-10270 have shown positive results, including improvements in both glycemic control and body weight management. The oral formulation could provide a significant advantage over injectable alternatives, especially for patients who may have difficulty with injections or prefer non-injection-based treatments. Merck's Metabolic Disease Portfolio Merck’s collaboration with Hansoh Pharma will enhance its portfolio in the growing areas of diabetes and obesity management. "We are excited to collaborate with Hansoh Pharma on HS-10270 , an investigational oral GLP-1 receptor agonist that has the potential to offer patients a convenient and effective treatment option for managing type 2 diabetes and obesity," said Dr. Roger M. Perlmutter, President of Merck Research Laboratories. "This agreement further underscores our commitment to advancing breakthrough therapies for patients suffering from chronic conditions with significant unmet medical needs." In addition to its strong presence in oncology and vaccines, Merck has been expanding its diabetes and obesity pipeline, recognizing the increasing global burden of these diseases. The partnership with Hansoh Pharma represents a significant step toward providing more comprehensive solutions for metabolic disorders, which affect millions of people worldwide. Terms of the Agreement The agreement includes an upfront payment to Hansoh Pharma, as well as potential milestone payments tied to the successful development, regulatory approvals, and commercialization of HS-10270 . Hansoh Pharma will also receive royalties on the product's sales outside China. As part of the deal, Hansoh will continue to manage ongoing clinical trials in China and lead efforts toward regulatory approvals in that region. Merck’s global rights to HS-10270 outside of China reflect the company’s strategy to expand its leadership in metabolic disease treatments, with an emphasis on oral therapies, which are becoming increasingly preferred by patients. About Merck Merck is a global healthcare leader focused on creating innovative medicines, vaccines, biologic therapies, and animal health products. With a robust pipeline targeting critical areas such as oncology, cardiovascular diseases, and metabolic disorders, Merck is dedicated to improving patient outcomes and advancing healthcare worldwide. The company is committed to addressing unmet medical needs through science and innovation. About Hansoh Pharmaceutical Hansoh Pharmaceutical Group is one of China’s leading biopharmaceutical companies, focused on the discovery, development, and commercialization of novel therapies in oncology, central nervous system diseases, and metabolic diseases. The company has built a broad and diverse portfolio of innovative medicines and is expanding its presence in both domestic and international markets. Hansoh is particularly active in the development of treatments for type 2 diabetes and obesity, with a growing pipeline in these areas. Author BioFocus Newsroom Previous Next

StarDrop 8 integrates real-time collaboration into compound design and optimisation, streamlining decision-making and improving team productivity. < Back Optibrium Launches StarDrop 8, Bringing Real-Time Collaboration to Molecular Design StarDrop 8 integrates real-time collaboration into compound design and optimisation, streamlining decision-making and improving team productivity. Optibrium, a leading developer of software and AI solutions for molecular design, has announced the release of StarDrop 8, the most significant update to its comprehensive discovery platform in its 20-year history. StarDrop 8 introduces real-time collaboration across every stage of the compound design and optimisation workflow, enabling teams to make better decisions together and progress faster from hit to candidate. Unlike existing discovery collaboration software, StarDrop 8 delivers an all-in-one solution for medicinal chemists, embedding collaboration directly into a platform that combines interactive data visualisation, structure-activity relationship analyses, compound design, and a wide range of in silico modelling and generative chemistry capabilities. According to Optibrium, the integration of real-time collaboration means discovery teams can now “leverage their collective knowledge at every step to prioritise the compounds most likely to succeed and focus synthesis efforts where they matter.” A Connected Platform for Discovery Teams StarDrop 8 aims to improve how discovery teams work together by: Centralising all project information and analyses in a secure shared environment accessible to users working from any location or time zone. Ensuring everyone works with the latest compounds and data, preventing time lost from duplicated efforts. Allowing flexible, individual analysis while instantly sharing insights and results with colleagues. Capturing designs and decisions throughout the discovery process to identify successful strategies for future work. The latest release also strengthens StarDrop’s predictive capabilities, adding new and updated models for key ADME properties and additional molecular property calculators. “Drug Discovery Is Not a Solo Venture” “Drug discovery is not a solo venture,” said Edmund Champness, Chief Scientific Officer at Optibrium. “Our customers consistently tell us that to work effectively, chemists need to be sure they’re looking at exactly the same compounds and data as their colleagues. We’ve developed StarDrop 8 around this feedback, without compromising on StarDrop’s flexibility, which enables each user to analyse and visualise data in their own way.” “Its real-time collaborative environment ensures that teams stay aligned on the latest project information, regardless of distances or time zones,” Champness added. “The result is increased productivity and improved decision-making that help address the critical challenges of time and cost in discovery.” Author BioFocus Newsroom Previous Next

< Back Genetic Study Offers New Hope for Millions With ME and Long COVID Largest genetic investigation of ME to date points to clear biological drivers and future clinical trial paths. A major new genetic study has identified more than 250 core genes associated with myalgic encephalomyelitis (ME), offering what researchers describe as the most detailed genetic analysis of the disease ever completed. The findings, released by precision medicine company PrecisionLife, illuminate the underlying biology of ME, reveal substantial overlap with long COVID, and point to dozens of opportunities for drug repurposing that could accelerate the development of targeted treatments. ME and long COVID affect an estimated 400 million people worldwide, yet patients still face a landscape with no definitive diagnostic test and no approved cure. The newly published work could help shift that trajectory. PrecisionLife scientists used their AI-led combinatorial analytics platform to examine genomic data from two DecodeME cohorts alongside the UK Biobank. The approach confirmed consistent genetic signals across all three datasets. In total, the analysis identified 7,555 variants linked to increased disease risk, including the eight variants recently highlighted by the DecodeME GWAS. The findings reinforce that ME is driven by many different genes and involves at least four major biological pathways: neurological dysregulation, inflammation, cellular stress response, and calcium signaling. Researchers say this underscores the need for a more tailored approach to treatment, with therapies developed for specific biological subgroups rather than the disease as a whole. Dr Steve Gardner, CEO of PrecisionLife, said: “These results reinforce that ME has a clear biological and genetic basis and is a complex multisystemic disease. ME is highly polygenic and heterogeneous, so no single drug will help everyone. Stratifying patients by the mechanisms that are driving their disease will be essential for predicting who will benefit from which therapies and for developing accurate diagnostic tests.” The study also revealed a strong genetic relationship between ME and long COVID. Of 180 genes previously associated with long COVID, 76 were also linked to ME in DecodeME data. The overlap suggests that although the two conditions are not identical, they share biological pathways that may open the door to treatments that work for both. To speed progress across the field, PrecisionLife has made the full list of identified SNPs and genes publicly available. The company hopes this will support academic researchers, clinicians, and drug developers as they pursue repurposing opportunities, investigate new targets, and design mechanism-based therapies. Patient advocates welcomed the findings as a meaningful step forward after decades of limited progress. Sonya Chowdhury, CEO of Action for ME, said: “These findings offer further hope to people with ME around the world. For decades, people affected by ME have lacked recognition, access to proper diagnosis and effective treatments. PrecisionLife’s results represent a major step forward in understanding the biology of the disease and provide real opportunities for targeted therapies to move into clinical testing.” Prof Chris Ponting of the University of Edinburgh, an investigator on the DecodeME study, described the results as an example of what becomes possible when large-scale datasets are shared with research partners. He said: “DecodeME was designed to reveal the complex genetics of ME by providing a dataset of the scale and quality required for robust discovery. PrecisionLife has shown how making such datasets available can quickly generate new insights into ME disease biology.” For patients, the findings represent a source of validation and a signal that treatment avenues may finally be opening. Helen Baxter, patient advocate and PPI representative, said: “These results greatly enhance our understanding of the biology of ME and present opportunities for drug repurposing which affords hope to the millions of people living with ME and long COVID around the world.” The work forms part of the LOCOME program, funded in part by Innovate UK and delivered through a collaboration between PrecisionLife, Action for ME, and the University of Edinburgh. The partners expressed deep gratitude to the tens of thousands of participants who contributed data to DecodeME, many while managing severe symptoms such as pain, fatigue, and cognitive impairment. Author BioFocus Newsroom Previous Next

Long-term APEX results reinforce TREMFYA® as the only IL-23 inhibitor proven to slow structural joint damage in psoriatic arthritis. < Back Study Shows TREMFYA® Slows Psoriatic Arthritis Progression at 48 Weeks Long-term APEX results reinforce TREMFYA® as the only IL-23 inhibitor proven to slow structural joint damage in psoriatic arthritis. Johnson & Johnson has unveiled new long-term results from its Phase 3b APEX study, reinforcing TREMFYA® (guselkumab) as the only IL-23 inhibitor shown to substantially inhibit structural joint damage in active psoriatic arthritis (PsA). The findings, presented at the Inflammatory Skin Disease Summit (ISDS) 2025, demonstrate that TREMFYA® maintains robust protection against radiographic progression through 48 weeks while continuing to improve signs and symptoms of disease. At Week 24, TREMFYA® showed “two and a half times greater ability to inhibit joint structural damage versus placebo”, with similar results for patients receiving treatment every four weeks (Q4W)* or every eight weeks (Q8W), according to the PsA-modified van der Heijde-Sharp (vdH-S) score. Johnson & Johnson reported that “The inhibition of structural joint damage was sustained through Week 48.” For patients who initially received placebo and switched to TREMFYA® at Week 24, radiographic progression slowed substantially, from a mean vdH-S change of 0.96 at Week 24 to 0.41, marking a 57% reduction from Week 24 to Week 48. “Psoriatic arthritis is a chronic condition where joint damage can begin early and progress quickly if left untreated,” said Christopher Ritchlin, MD, MPH, University of Rochester Medical Center and APEX study investigator. “The APEX study results show that guselkumab can inhibit this process, even once it has begun, making it a valuable treatment option for both initiating treatment early and for patients who already show signs of joint damage.” Strong Symptom Improvement With No New Safety Signals Across both dosing groups, more than half of TREMFYA®-treated patients achieved a 50% improvement in signs and symptoms (ACR50) by Week 48. ACR50 response rates improved between Week 24 and Week 48, and nearly half of patients who switched from placebo at Week 24 achieved ACR50 by Week 48. The company confirmed that “no new safety signals” were observed and that the data remained consistent with TREMFYA®’s established safety profile. “These long-term data show that TREMFYA has set a new benchmark as the only IL-23 inhibitor proven to inhibit structural damage in active psoriatic arthritis, which can develop in up to 30% of people living with psoriasis,” said Leonard Dragone, MD, PhD, Vice President, Rheumatology and Autoantibody Disease Area Leader, Johnson & Johnson Innovative Medicine. “It’s durable efficacy and established safety make TREMFYA an attractive first-line treatment option for patients with psoriatic disease.” Advancing Treatment Through Dual-Acting Mechanism The company highlighted that TREMFYA® is “the first and only fully-human, dual-acting monoclonal antibody approved to treat PsA that blocks IL-23 while also binding to CD64,” a receptor found on IL-23-producing cells. Findings related to CD64 binding are based on in vitro studies. The new results support Johnson & Johnson’s recent submission of a supplemental Biologics License Application (sBLA) to the U.S. FDA seeking approval to include evidence of structural damage inhibition in TREMFYA®’s label. About the APEX Study APEX (NCT04882098) is a multicenter, randomized, double-blind, placebo-controlled trial enrolling biologic-naïve adults with active PsA who had not adequately responded to standard therapies. The study includes: 24-week placebo-controlled period 24-week active treatment period 12-week safety follow-up Optional two-year extension Psoriatic Arthritis: A Complex, Chronic Condition Psoriatic arthritis is described in the release as a “chronic, immune-mediated, inflammatory disease” that can cause significant pain, stiffness, swelling, fatigue, and disability. The condition affects joints, skin, and multiple anatomical sites and is often accompanied by comorbidities such as obesity, cardiovascular disease, anxiety, and depression. Studies show that “up to 30% of people with plaque PsO also develop PsA.” Author BioFocus Newsroom Previous Next

< Back 12th – 14th January, 2026 San Francisco, CA ABD Capital Connect @ JPM Week 2026 High-efficiency life sciences partnering during JPM Week. ABD Capital Connect @ JPM Week 2026 is a curated partnering event designed to help life sciences startups, investors, and industry leaders make meaningful connections and advance strategic deals during the annual JP Morgan Healthcare Conference in San Francisco. Hosted January 12–13, 2026 at the Marines’ Memorial Club & Hotel, the conference streamlines the connection process with professionally compiled startup and investor books, over 50 structured partnering tables, expert plenaries, and premium networking opportunities. Attendees—from venture and private equity investors to biopharma companies, service providers, and economic development leaders—arrive informed, aligned and ready for purposeful conversations that maximize ROI and accelerate innovation across biotech, medtech and healthcare sectors. Previous Register now Next

< Back Artificial Intelligence: a Helper or Hindrance to Healthcare Provision AI is a promising tool for improving medical decision-making, but it requires careful regulation and ethical consideration to complement, not replace, human professionals. When we think of medical professionals, a few key players come to mind; surgeons, nurses and general practitioners to name a few. Patients rely on these individuals to carry them through routine to essential treatments - but what if there was another player emerging in this industry? Not a registered professional, but a technology that aims to contribute to healthcare using intricate algorithms and data-driven decisions . Artificial intelligence (AI) can be referred to as a computer system that is capable of performing tasks that typically require human intelligence. The recent advances in AI’s capability has gained traction, with businesses across varied industries vying to harness this technology. In the past few years, to call out just a few examples, we have witnessed Al-assisted predictive protein folding, bioprocessing and biomanufacturing optimization, psychotherapy, supply chain logistical problem-solving. This discussion piece aims to explore the benefits and drawbacks of implementing AI into medical decision making and healthcare provision. It’ll also explore changes that need to be made to the implementation of this technology that will allow it to serve as a complement to the existing healthcare systems around the world. Benefits of implementing AI into medical decision making AI holds excellent potential when integrated into healthcare, with there being multiple scenarios that it could work in - from clinical testing in the laboratory to decision making such as diagnosing and selecting treatments. The significance of incorporating AI into these departments is highlighted by the current healthcare workforce crisis. In a data analysis published by the British Medical Association in 2024, it was revealed that England had a substantially low proportion of doctors relative to the population. It went on to reveal that this lead to increased poor wellbeing and burnout among staff, impacting workforce retention and continuing the harmful unemployment cycle. This is why more and more researchers are seeing the potential for AI to help mitigate the effects of this - u tilising AI support tools could unlock additional time for doctors and nurses to focus on the nurturing side of care (and therefore benefitting patients), while also reducing stress and work overload for themselves. Success stories As discussed in the last section, AI has the potential to work alongside healthcare professionals to improve the industry, allowing the formation of what can be referred to as the human-AI hybrid team. Proof of the increased accuracy that AI can provide when supporting healthcare professionals was evidenced in a 2022 study, which involved an AI assisted colonoscopy. Here, endoscopists were asked to diagnose the same set of lesions in two separate sessions; one independently, and one assisted by AI. The results of this showed that when the endoscopists' confidence level was low, they were able to use the AI to direct their diagnosis to the AI opinion whose confidence perception was high, and vice versa. This highlighted how, while fully automated decision making is unfavoured, the hybridisation of human and AI opinion can work to produce more optimised outcomes. Ethical and legal drawbacks There are some issues to consider when it comes to incorporating AI into medical decision making, and these can be split into the categories of ethical and legal. In an issue published in the I nternational Journal of Medical Informatics , the following issues were highlighted: Accountability and responsibility How not discussing AI usage can harm the patient-physician relationship, undermining autonomy and trust Compromisation of informed consent Lack of appropriate regulation and liability, and accountability for patient harm. ...and potential ways around them When thinking about ways of combating the ethical and legal issues surrounding AI implementation in healthcare, we can look to the European Union’s AI act . This legal framework provides AI developers and deployers with regulations regarding AI usage, using a risk based approach. ‘Risk’ here is divided into 4 levels: minimal, limited, high and unacceptable. Healthcare falls into the category of high risk, given that it is an essential public service. This means that they are subject to strict obligations before implementation, including adequate risk assessment and mitigation systems, logging of activity to ensure traceability of results, and a high level of robustness, security and accuracy. Furthermore, numerous research papers have explored ideas around the ethical issues of AI implementation, including the idea that professionals must disclose when they are using AI tools (combating the issue of patient-physician distrust), and increased education for professionals who’ll be operating the tools. Conclusion In light of the presented arguments, my opinion stands that AI has an important role to play in medical decision making, but is to be used as a complement to human doctors rather than a replacement. Furthermore, I believe there are important ethical and legal implications to consider, which means that the use of AI in medical decision making is not universally applicable at present. Implementing AI in healthcare could have enormous benefits to both patient and physician well-being, so it is fundamental that the correct testing, continued education, and tight regulations are implemented to allow AI to work as a helper - not a hindrance - to the healthcare system. Author Monica Bhatia , freelance contributor Previous Next

The acquisition of Chimerix for $935 million will enhance Jazz’s oncology portfolio, particularly through the addition of dordaviprone, a lead drug candidate for treating a rare and aggressive brain tumor. < Back Jazz Pharmaceuticals to Acquire Chimerix, Enhancing Oncology Portfolio The acquisition of Chimerix for $935 million will enhance Jazz’s oncology portfolio, particularly through the addition of dordaviprone, a lead drug candidate for treating a rare and aggressive brain tumor. Jazz Pharmaceuticals is a global biopharmaceutical company headquartered in Dublin, Ireland, dedicated to developing life-changing medicines for people with serious diseases—often with limited or no therapeutic options. The company's diverse portfolio spans neuroscience and oncology, with a focus on addressing unmet medical needs through innovative therapies. The company has announced a definitive agreement to acquire Chimerix, a Durham-based biotech company, for approximately $935 million in cash. This acquisition aims to bolster Jazz's oncology research and development pipeline by adding Chimerix's lead drug candidate, dordaviprone, a novel therapy for treating H3 K27M-mutant diffuse glioma—a rare and aggressive brain tumor affecting children and young adults. The addition of dordaviprone aligns with Jazz's commitment to addressing significant unmet medical needs within oncology. Currently, there are no FDA-approved treatments for H3 K27M-mutant diffuse glioma, underscoring the urgency for effective therapeutic options. Bruce Cozadd, Chairman and CEO of Jazz Pharmaceuticals, stated, "Adding dordaviprone to our oncology R&D pipeline will further diversify our portfolio with a medicine that addresses a significant unmet need with no other FDA-approved therapies and limited treatment options for this patient population." Under the terms of the agreement, Jazz will acquire all outstanding shares of Chimerix for $8.55 per share in cash, representing a 72.4% premium over Chimerix's last closing share price. The transaction is expected to close in the second quarter of 2025, subject to customary closing conditions. Jazz plans to fund the acquisition through existing cash and investments. Dordaviprone is currently under review by the U.S. Food and Drug Administration (FDA) for the treatment of H3 K27M-mutant diffuse glioma. The FDA has set a target action date of August 18, 2025, for the accelerated approval decision. If approved, dordaviprone has the potential to become a standard of care for this patient population and contribute to Jazz's revenue streams in the near term. Author BioFocus Newsroom Previous Next

University of Iowa researchers have uncovered an unexpected double-ring structure in the DNA repair protein RAD52, revealing new insights that could guide the development of next-generation cancer drugs. < Back Unexpected Protein Structure May Lead to New Cancer Treatments University of Iowa researchers have uncovered an unexpected double-ring structure in the DNA repair protein RAD52, revealing new insights that could guide the development of next-generation cancer drugs. A University of Iowa -led study ( published in April 2025) has revealed the unexpected structure adopted by the DNA repair protein RAD52 as it binds and protects replicating DNA in diving cells. This new structural and mechanistic understanding of the RAD52-DNA complex may help researchers develop new anti-cancer drugs. “RAD52 is a coveted drug target for treating cancers that have DNA repair deficiencies, including breast and ovarian cancers, and some glioblastomas,” explains Maria Spies, PhD, UI professor of biochemistry and molecular biology in the UI Carver College of Medicine and senior author of the new study that was published April 2 in Nature. “This protein is an attractive target for new anti-cancer drugs because while it is dispensable in healthy human cells, RAD52 becomes essential for survival of cancer cells, which are deficient in DNA repair function, such as those with defects in BRCA1 and BRCA2 genes.” Cancers with DNA repair deficiencies depend on other proteins to provide backup pathways for DNA repair, which allows the cancer cells to proliferate fast and survive despite DNA damage. RAD52 is one of those proteins. This means that molecules that block RAD52 and prevent it from functioning could be useful for treating these types of cancer. It has already been shown that RAD52 inhibitors can selectively kill cancerous cells and minimize the toxicity associated with radiation and chemotherapy. This ability is similar to the action of the first drugs approved to target BRCA1/2 deficient cancers, the so-called PARP (poly-ADP-ribose polymerase) inhibitors, which are now in clinical use. While almost 15% of patients treated with the PARP inhibitor olaparib remain disease free for more than five years, many develop resistance within the first year. “Targeting RAD52 (independent of or together with PARP inhibition) will increase the repertoire of available therapies,” Spies says. “However, to develop drugs that will inhibit RAD52 in cancer cells, we first need to understand how RAD52 functions at the molecular, structural, and cellular level.” A new shape reveals possible targets for drug therapy The fact that RAD52 appears to be dispensable in normal human cells but essential for survival of cancer cells experiencing defective DNA repair creates both an advantage and a challenge. The advantage is that inhibiting RAD52 should kill cancer cells with minimal negative effect on the patient’s healthy cells. The challenge is figuring out what functions and features of RAD52 should be targeted. In the new study Spies and her UI team, collaborating with Pietro Pichierri at the Istituto Superiore di Sanità, in Rome, Italy, and M. Ashley Spies, PhD, in the UI College of Pharmacy, have discovered structural and functional information about RAD52 that may help them develop new, specific ways to inhibit this protein. Double ring structure protects DNA Spies and Pichierri had previously discovered that RAD52 is important in protecting stalled DNA replication forks. Their work suggested that this new function of RAD52 facilitates the survival of cancer cells. In the new study, Spies’ team used cryogenic electron microscopy (CryoEM) to show that RAD52 proteins form an unexpected spool-like structure composed of two rings of RAD52, each containing 11 copies of protein, that engages all three arms of the “DNA replication fork”, rearranges the fork structure and protects it from unscheduled activity of motor proteins. To obtain this image, the team created a DNA substrate, which resembles a stalled DNA replication fork. The substrate fixes the RAD52 complex in place by bringing the two rings together with all three DNA arms. Both single and double stranded DNA features interact with RAD52 and hold the structure in place, allowing the team to obtain a detailed 3D structure of the whole protein-DNA complex. Using specialized microscopes built in Spies’ lab, the researchers were also able to monitor the RAD52-DNA transactions at the single-molecule level, revealing that the fork protection occurs through dynamic protein-DNA interactions. “Although the single ring structure had been observed previously, this is the first structure showing the two rings together on the DNA, doing something unexpected,” Spies says. “This new structure provides clues about which important areas of the protein can be targeted for future drug discovery.” Targeting RAD52 to create new cancer drugs Spies’ team already has small molecules that bind and inhibit RAD52, but to develop these molecules into testable drugs, they need to be further refined and modified to make them more effective and more specific. The results of Spies lab’s structural and biophysical work were complemented by computational studies by Ashley Spies (UI College of Pharmacy), and cell-based and super resolution imaging by the Pichierri group in Rome. In combination, the labs’ efforts revealed the importance of the two-ring RAD52 architecture to its ability to act as a DNA replication gatekeeper and to the survival of cancer cells. “This work and our structure-activity knowledge gained in this study sets up future work on understanding the RAD52 activities and regulation, and offers new targets for its inhibition,” Spies says. “Hopefully, this information will help us develop new inhibitors of this protein and tap the potential of RAD52 as an anti-cancer drug target.” The project was led by Maria Spies, PhD, Professor of Biochemistry and Molecular Biology at the University of Iowa Carver College of Medicine. Under her direction, the Spies laboratory conducted and coordinated the study, with significant contributions from shared first authors Masayoshi Honda, PhD, and Mortezaali (Ali) Razzaghi, PhD. Dr. Honda performed the biochemical and single-molecule fluorescence analyses, while Dr. Razzaghi led the cryo-electron microscopy (cryo-EM) studies. Paras Gaur, PhD, served as a second author, contributing his expertise by carrying out the mass photometry experiments and assisting in the interpretation of single-molecule data. The study further benefited from collaborations with Pietro Pichierri, PhD (Istituto Superiore di Sanità, Rome), M. Ashley Spies, PhD (University of Iowa College of Pharmacy), and Nicholas J. Schnicker, PhD (University of Iowa Protein and Crystallography Core), who provided additional structural and computational insights. The study was funded in part by grants from the National Cancer Institute, part of the NIH (R01 CA232425 and P30 CA086862, which supports HCCC); Ali Razzaghi was supported by a postdoctoral fellowship from the NIH NCI T32 in Free Radicals and Radiation Biology training program CA078586. Overall, the work led by the Spies laboratory highlights a newly identified RAD52 structure and its implications for cancer therapy. If you're interested in learning more you can read the original research paper in Nature here . You can also find out more about the study lead, Maria Spies, via her profile on the University of Iowa website here . Author Jennifer Brown with corrections from Dr Maria Spies Previous Next

< Back LIVX 2026 8th – 10th December, 2026 Dubai, UAE Hosting the most powerful global ecosystem for longevity, biotech, and investment. ! Widget Didn’t Load Check your internet and refresh this page. If that doesn’t work, contact us. Previous Next

< Back LIVX 2026 8th – 10th December, 2026 Dubai, UAE Hosting the most powerful global ecosystem for longevity, biotech, and investment. ! Widget Didn’t Load Check your internet and refresh this page. If that doesn’t work, contact us. Previous Next

< Back 10th – 11th June, 2026 Abu Dhabi, UAE Global Biotech Summit 2026 The premier event to connect, convene, and collaborate. The Global Biotech Summit is the UAE's most important integrated platform for strategic innovation, investment, and breakthrough collaboration in biotechnology and life sciences. Taking place at Beach Rotana, Abu Dhabi on 10 – 11 June 2026, the Summit combines a world-class conference program with a comprehensive exhibition, uniting global and regional leaders, visionary scientists, investors, policymakers, and innovators under one roof. Aligned with Abu Dhabi’s vision of Future Health, the Global Biotech Summit is uniquely positioned to showcase cutting-edge solutions, connect decision-makers with transformative technologies, and unlock new market opportunities across the region. The Global Biotech Summit uniquely brings the entire value chain together from researchers presenting to investors, entrepreneurs meeting pharmaceutical executives, service providers connecting with biotech leaders, and policymakers engaging with innovators. This integrated approach accelerates deal-making, partnership formation, and the deployment of capital into breakthrough science. The event aims to position Abu Dhabi as the nexus where biotech innovation converges with unparalleled opportunity, fueling partnerships that advance next-generation therapies, enabling capital to reach the companies shaping the future of healthcare, and creating long-term impact across the regional biotech landscape. Previous Register now Next