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A BioFocus educational piece discussing important considerations when implementig perfusion and traditional bioprocessing workflows. < Back Comparing Perfusion Bioprocessing and Traditional Bioprocessing Methods A BioFocus educational piece discussing important considerations when implementig perfusion and traditional bioprocessing workflows. Bioprocessing is fundamental to the production of biologics, such as vaccines, monoclonal antibodies, and other therapeutic proteins. Traditional bioprocessing methods, including batch and fed-batch processes, have been the industry standard for decades. However, perfusion bioprocessing is gaining attention as a more efficient and productive alternative. This article compares perfusion bioprocessing with traditional methods, highlighting the key differences and advantages of each. Traditional bioprocessing methods Batch bioprocessing In batch bioprocessing, cells are grown in a fixed volume of nutrient medium, and the process runs until the nutrients are depleted or inhibitory waste products accumulate. The product is then harvested at the end of the cycle. Advantages: Simplicity: Easy to set up and manage. Lower initial investment: Requires simpler infrastructure and equipment. Disadvantages: Lower productivity: Limited by the volume of the initial nutrient medium. Variability: Greater batch-to-batch variability in product quality. Downtime: Requires time for setup, sterilization, and cleaning between batches. Fed-Batch bioprocessing Fed-batch bioprocessing improves upon batch processing by periodically adding fresh nutrients to the culture, which extends the growth phase and increases product yield. Advantages: Improved productivity: Extending the growth phase leads to higher product yields. Better control: Allows for more precise control over nutrient levels and growth conditions. Disadvantages: Intermediate complexity: More complex than batch processing. Still limited: While better than batch, it still experiences downtime and variability. Perfusion bioprocessing Perfusion bioprocessing is a continuous culture system where cells are constantly supplied with fresh nutrient medium while waste products and spent medium are simultaneously removed. This creates a steady-state environment conducive to optimal cell growth and consistent product production. Advantages: High Productivity: Continuous operation supports high cell densities, resulting in significantly higher yields. Consistent Product Quality: The steady-state environment minimizes batch-to-batch variability, ensuring consistent product quality. Efficiency: Smaller bioreactors can achieve the same production levels as larger batch systems, reducing costs. Real-Time Control: Advanced monitoring systems enable real-time adjustments to maintain optimal conditions. Scalability: Easily scalable from laboratory to commercial production. Sustainability: More efficient use of resources and reduced waste generation. Disadvantages: Complexity: Requires sophisticated equipment and control systems. Initial Investment: Higher initial capital investment for setup and equipment. Comparison Productivity and Yield Traditional Methods: Limited by the nutrient medium's initial volume and the growth phase's duration. Productivity is inherently lower. Perfusion: Continuous nutrient supply and waste removal support higher cell densities and extended production periods, significantly increasing overall yield. Product Quality Traditional Methods: Batch and fed-batch processes can lead to variability in product quality due to fluctuating growth conditions and nutrient levels. Perfusion: The steady-state environment ensures consistent conditions, leading to more uniform product quality. Operational Efficiency Traditional Methods: Require downtime for cleaning, sterilization, and setup between batches, reducing overall efficiency. Perfusion: Continuous operation eliminates downtime, maximizing bioreactor usage and operational efficiency. Resource Utilization Traditional Methods: Generally involve higher consumption of raw materials and generation of waste due to less efficient use of nutrients. Perfusion: More efficient nutrient use and continuous waste removal reduce raw material consumption and waste production. Scalability Traditional Methods: Scaling up involves larger bioreactors and more complex nutrient management, which can be challenging and costly. Perfusion: Easier to scale, as the process is continuous and can be maintained in smaller, more efficient bioreactors. Cost Implications Traditional Methods: Lower initial setup costs but higher operational costs due to inefficiencies and downtime. Perfusion: Higher initial capital investment but lower operational costs and higher long-term savings due to increased efficiency and productivity. Both traditional and perfusion bioprocessing methods have their respective advantages and disadvantages. Traditional methods offer simplicity and lower initial costs, making them suitable for smaller-scale operations or processes where high yield and consistency are less critical. However, for large-scale production and applications requiring high productivity and consistent product quality, perfusion bioprocessing presents a compelling alternative. As the biotechnology industry continues to evolve, the adoption of perfusion bioprocessing is likely to increase, driven by its superior efficiency, scalability, and sustainability. Author BioFocus Newsroom Previous Next

< Back Digital Health Gains Still Out of Reach, BMJ Commission Finds Despite heavy investment, a BMJ Future Health Commission survey finds digital health has yet to ease workloads or cut costs, with EHR usability, interoperability, and training gaps undermining clinician trust. The BMJ Future Health Commission has published new findings suggesting that Europe’s rapid investment in digital health infrastructure is yet to yield the anticipated productivity benefits. Drawing on survey data from over 300 healthcare professionals (HCPs) and qualitative interviews across diverse care settings, the report documents a striking gap between optimism for digital transformation and its lived impact on clinical workflows. Fewer than half of respondents reported that digital systems had eased administrative burden (47%), reduced delivery costs (44%), or decreased clinical workload (38%). In contrast, a majority (80%) acknowledged improvements in care delivery, and 76% expressed optimism about healthcare’s digital future. Usability challenges with EHRs Electronic health records (EHRs), the most entrenched digital platform in European health systems, emerged as a paradoxical case. HCPs with the highest exposure to EHRs were significantly less likely to perceive efficiency benefits than their peers. This suggests that while EHRs have succeeded in digitising information, shortcomings in design, interoperability, and integration with clinical practice have limited their capacity to reduce workload. “These findings indicate that poor experiences with EHRs may erode clinician confidence in digital health more broadly, slowing adoption of emerging tools such as predictive analytics, patient-flow optimisation, and remote monitoring systems,” the Commission notes. Trust as a critical determinant The report positions trust as the decisive factor in digital health adoption. It distinguishes between: Foundational trust , established through transparent regulatory standards and certification processes. Operational trust , earned when frontline clinicians are actively involved in the design, selection, and training for new systems. Stephen McAdam, Segment Director for Digital Health at DNV, commented: “Trust is the critical currency of digital health. Rigorous standards ensure baseline safety, but confidence is ultimately secured on the ward, where usability and workflow fit determine whether technologies accelerate or obstruct care.” Five priorities for digital transformation The Commission sets out five evidence-based recommendations for closing the expectation–reality gap: Evaluate organisational confidence in EHRs , addressing usability deficits before scaling. Implement interoperability standards to facilitate secure, seamless data exchange. Commit to longitudinal training programmes that extend beyond deployment and target both clinical and non-clinical staff. Institutionalise clinician and patient involvement in procurement and design decisions to align systems with real-world practice. Strengthen risk management frameworks for data quality, security, and emergent threats. Implications for research and policy The findings arrive as European governments, including the UK, advance long-term digital strategies aimed at alleviating workforce shortages and rising demand. Yet, the Commission cautions that investment in infrastructure alone is insufficient. “Digital health’s promise will only be realised through rigorous implementation science, participatory design, and systematic evaluation of outcomes,” said Dr Helen Surana, Editor in Chief of BMJ Innovations. “Without these, digital transformation risks remaining a policy ambition rather than a clinical reality.” For researchers and policymakers, the report highlights a pressing need for translational studies that evaluate not only the technical capabilities of digital systems but also their impact on workflow, safety, and sustainability in practice. Author BioFocus Newsroom Previous Next

Camena Bioscience and Constructive Bio are partnering with global researchers to create the first fully synthetic chloroplast genomes. < Back International Team to Build First Fully Synthetic Chloroplast Genomes Camena Bioscience and Constructive Bio are partnering with global researchers to create the first fully synthetic chloroplast genomes. In a bold step for synthetic biology, Camena Bioscience and Constructive Bio have joined forces with the Max-Planck Institute of Molecular Plant Physiology (MPI-MP) to attempt what has never been achieved before: designing and assembling fully synthetic chloroplast genomes. The £9.1 million project, funded by the UK’s Advanced Research + Invention Agency (ARIA), unites global leaders in plant science and genome engineering, including researchers from the University of Essex and UC Berkeley. Their mission is to overcome the formidable complexity of chloroplast genomes; DNA molecules 120–170 kilobases long, highly AT-rich, and riddled with repetitive regions that make them notoriously difficult to sequence, synthesise, and assemble. Chloroplasts, the photosynthetic “powerhouses” of plant cells, play a central role in capturing energy and enabling plants to adapt to environmental change. Understanding and rewriting their genomes could transform plant biology, enabling crops to better withstand climate stress while creating sustainable platforms for producing biofuels, pharmaceuticals, and biomaterials. To tackle this challenge, Camena will deploy its enzymatic DNA synthesis platform, capable of building long, accurate DNA sequences at scale, while Constructive Bio brings its large-scale genome assembly toolkit, designed to precisely stitch together vast and complex genetic constructs. Together, these innovations will establish a robust pipeline for writing and assembling entire organelle genomes, an achievement that would mark a new era for synthetic biology. “Chloroplast genomes are among the most intricate DNA molecules in nature,” said Dr. Steve Harvey , CEO of Camena Bioscience. “By combining our strengths, we’re pushing the boundaries of what’s possible in DNA synthesis and plant genomics.” Dr. Ola Wlodek , CEO of Constructive Bio, added: “Synthetic chloroplasts could revolutionise both fundamental biology and sustainable innovation. This collaboration will lay the foundations for a new class of tools to study plant evolution, photosynthesis, and bioengineering at an unprecedented scale.” The project is led by Dr. Daniel Dunkelmann at MPI-MP, with contributions from Dr. Pallavi Singh (University of Essex) and Dr. Patrick Shih (UC Berkeley). Together, the team aims to deliver a proof-of-concept that could change how scientists design and study complex genomes, moving synthetic biology beyond microbes and into the intricate genomic landscapes of plants. By tackling one of the biggest technical hurdles in plant genomics, this ARIA-backed effort positions the UK and its partners as global leaders in synthetic biology innovation, advancing science toward a future where entire organelles, and eventually whole plants, can be written, redesigned, and optimized from the ground up. Author BioFocus Newsroom Previous Next

< Back Killing Mosquitoes With the Smell of Flowers Researchers manipulate killer fungi to lure in and eliminate malaria-carrying mosquitoes. As the fight against malaria and other mosquito-borne diseases continues, it is imperative that we introduce novel solutions to control mosquito populations. Inspired by mosquitoes’ attraction to flowers for finding nectar, scientists have engineered fungi to release a floral scent, leading the unsuspecting mosquitoes to their eventual demise. Despite the introduction of the malaria vaccines RTS,S in 2021 and R21 in 2023, malaria cases continue to rise, reaching approximately 282 million cases in 2024 – an increase of 9 million cases from the previous year. The WHO World Malaria Report highlights antimalarial drug and insecticide resistance as major barriers to eliminating malaria, emphasising the need for novel interventions. With current mosquito control methods facing growing limitations, what are the alternatives? In a study published in Nature , an international research team spanning China, Burkina Faso, and the US engineered the mosquito-killing fungi as a promising answer to this question. Co-author and Professor of Entomology at the University of Maryland, Raymond St. Leger, explained that “after observing that some types of fungi could trick mosquitoes into thinking they were flowers, we realized we could turbo-charge the attraction by engineering fungi to produce more longifolene, a sweet-smelling compound that’s already very common in nature. Before this study, longifolene wasn’t known to attract mosquitoes. We’re letting nature give us a hint to tell us what works against mosquitoes.” Metarhizium fungi were used thanks to their mosquitocidal spores and limited off-target effects. Longifolene-laced fungi present a more environmentally friendly alternative, with the chemical having a long safety record for its use in perfume. St. Leger said, “We've also designed the fungus and its containers to target mosquitoes specifically rather than any other insects and longifolene breaks down naturally in the environment”. The specificity of the fungus is a major advantage, as conventional insecticides used to control mosquito populations are toxic towards the environment, wildlife, and human health. Unlike insecticides, resistance to the killer fungi is less likely to arise as it builds upon an evolutionary necessary mechanism. “It'll be very difficult for them to overcome that hurdle, and we have the option of engineering the fungus to produce additional floral odors if they evolve to specifically avoid longifolene” St. Leger explained. These killer fungi are particularly exciting as they are easily cultivated using common scraps from harvesting, like rice husks. This presents a more sustainable solution for less economically developed countries in the global south, where malaria is most prominent. However, rising global temperatures threaten to spread mosquito growth to countries outside of tropical regions, carrying malaria and other mosquito-borne diseases with them. “Mosquitoes love many of the ways we are changing our world,” St. Leger said. “Right now, we’re hoping to use these approaches in Africa, Asia and South America. But one day, we may need them for ourselves.” Although laboratory and computer-based findings show promise, more research must be done to establish success in real mosquito environments. The international team, including St. Leger, are currently facilitating larger outdoor trials with the hope of approval from regulatory bodies. Author Will Smears , freelance contributor Previous Next

The FDA has approved a new plasma-based biomarker assay, the first blood-based diagnostic for Alzheimer's disease, offering a less invasive and more accessible alternative to traditional methods like PET scans and spinal taps. < Back FDA Clears Blood Test for Diagnosing Alzheimer’s Disease The FDA has approved a new plasma-based biomarker assay, the first blood-based diagnostic for Alzheimer's disease, offering a less invasive and more accessible alternative to traditional methods like PET scans and spinal taps. The U.S. Food and Drug Administration (FDA) has granted 510(k) clearance for the Lumipulse® G β-Amyloid 1-42/pTau217 Plasma Ratio test, marking a significant advancement in the diagnostic landscape for Alzheimer’s disease (AD). Developed by Fujirebio Diagnostics, this in vitro diagnostic is the first FDA-cleared blood test specifically designed to assist in the clinical evaluation of Alzheimer's by detecting key biomarkers linked to the presence of cerebral amyloid plaques. This regulatory milestone reflects a broader shift in the approach to diagnosing neurodegenerative conditions, moving away from highly invasive and resource-intensive methods such as cerebrospinal fluid (CSF) sampling and positron emission tomography (PET) imaging toward more scalable, minimally invasive assays. The Lumipulse G test quantifies the ratio of two critical proteins in blood plasma: β-amyloid 1-42 (Aβ1-42) and phosphorylated tau at threonine 217 (pTau217). These biomarkers are central to Alzheimer’s pathophysiology. Aβ1-42 is involved in the extracellular deposition of amyloid plaques, while hyperphosphorylated tau proteins contribute to the formation of intracellular neurofibrillary tangles, both recognized as defining features of AD. Rather than measuring amyloid deposition directly, the test leverages the pTau217/Aβ1-42 plasma ratio to infer the likelihood of amyloid plaque presence. This method provides clinicians with a biochemical signal that correlates closely with neuropathological status, supporting early-stage clinical decision-making. The FDA's clearance is supported by data from a pivotal clinical study involving 499 individuals with signs of cognitive impairment. Plasma test results were benchmarked against PET imaging and CSF-based assays. The Lumipulse G test demonstrated 91.7% positive predictive agreement and 97.3% negative predictive agreement, indicating a high degree of concordance with established reference standards. Furthermore, fewer than 20% of participants received indeterminate results, suggesting a high rate of diagnostic clarity for the majority of tested individuals. The assay is indicated for adults aged 55 years and older who are already exhibiting symptoms suggestive of cognitive decline, where differential diagnosis between Alzheimer’s and other dementias is clinically relevant. Until now, blood-based assays for Alzheimer’s have been confined to laboratory-developed tests offered by commercial providers such as Quest Diagnostics and Labcorp. These tests, while clinically useful, lacked FDA review and clearance. The Fujirebio assay represents the first step toward standardized, regulated blood biomarker diagnostics that could be implemented across a broader range of healthcare settings. By reducing dependence on CSF analysis and PET imaging, both of which are limited in availability and costly, this blood-based test can improve diagnostic equity and accelerate access to care. It is especially relevant as new disease-modifying therapies, such as monoclonal antibodies targeting amyloid, become available. These treatments are most effective when initiated early, underscoring the need for reliable tools to identify at-risk individuals before substantial neurodegeneration has occurred. Fujirebio’s progress aligns with a larger trend toward innovation in neurodegenerative disease diagnostics. In parallel, the company has expanded its partnership with Japanese pharmaceutical firm Eisai to jointly develop and promote blood-based biomarkers for Alzheimer’s and related disorders. This builds upon earlier collaborations focused on CSF diagnostics and supports the development of companion diagnostics for therapeutics like lecanemab (Leqembi), Eisai’s anti-amyloid agent co-developed with Biogen. Importantly, commercialization of therapies like Leqembi has been hindered by delays in diagnosis and limited access to confirmatory testing. Scalable biomarker tests such as Lumipulse G may help bridge this diagnostic gap, enabling earlier and more confident identification of eligible patients. While this development represents a leap forward, its optimal use still requires careful integration into clinical workflows. Blood biomarker results must be interpreted in the context of comprehensive assessments, including neurological exams, cognitive testing, imaging, and family history. Clinicians must also consider individual variability in biomarker expression, comorbidities, and genetic factors such as APOE genotype when interpreting results. To support this evolving paradigm, the Alzheimer’s Association is preparing to release clinical practice guidelines focused on the use of blood biomarkers in specialty care. These will provide evidence-based recommendations for appropriate patient selection and test interpretation and are expected to debut at the 2025 Alzheimer’s Association International Conference (AAIC). With more than 6.9 million Americans currently living with Alzheimer’s, a number projected to nearly double by 2050, the need for scalable, cost-effective diagnostic strategies is pressing. Blood-based biomarker testing represents a crucial step in addressing this gap. Not only does it enable earlier intervention, but it also supports a more efficient clinical workflow that could ultimately reduce the economic and human burden of dementia. The FDA’s clearance of the Lumipulse G blood test signals the beginning of a new chapter in Alzheimer’s diagnostics, one that is rooted in molecular science, guided by robust clinical data, and oriented toward accessibility and earlier disease detection. As the field continues to mature, further innovations in blood-based biomarker platforms may pave the way for even broader regulatory approvals and integration into routine cognitive health assessments. 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

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< Back Defrosting Pandora’s Box: Eukaryotic Viruses Revived as Permafrost Melts The Claverie group reveal thirteen newly discovered 'zombie viruses' from ancient samples of Siberian permafrost. Last year, Jean-Michel Claverie and his research group in Information Genomique and Structurale at Aix Marseille University released ‘An update on Eukaryotic Viruses Revived from Ancient Permafrost’. Published in Viruses, the paper revealed thirteen newly discovered viral isolates from ancient samples of Siberian permafrost. Crucially, the study confirms the ability of these viruses to remain infectious after being frozen for over 48,500 years. This research followed on from the Claverie group’s previous findings in 2014 and 2015 from the Claverie group of two fully infectious eukaryotic viruses from a 30,000 year old permafrost sample in 2014 and 2015 . As noted in the most recent paper, the lack of new isolates uncovered since 2015 is not necessarily indicative of a lack of infectious viruses. The group reports findings of numerous infectious eukaryotic viruses, however they remain to be genomically categorised. The thirteen viral isolates reveal another concern as a result of global warming. Bacterial and eukaryotic viruses up to 48,500 years old have been reactivated by the group, and as the permafrost which contains them melts, there is a risk that these viruses will be revived outside of the lab. As permafrost melts Global rising temperatures act on permafrost much like a microwave on defrost setting. As the Earth warms, permafrost thaws and ice becomes liquid water. This change of state triggers the metabolic reactivation of microorganisms in the soil, such as bacteria, archaea and fungi. There can be two outcomes from this reactivation. One is that defrosted, active microorganisms are able to decompose organic material into CO2 and methane gas, which then further adds to greenhouse gases and so rising global temperatures. Another, one which poses a more immediate public health threat, is the physical release and reactivation of so-called “zombie” bacteria and archaea which have been trapped in cryptobiosis (the state of metabolic inactivation organisms enter upon extreme climate conditions) in the permafrost. Activating ancient viruses For the defrosted bacteria, this health threat is not a major concern. Antibiotics are effective at targeting a range of bacterial infections as they generally work similarly between bacteria types meaning ancient bacteria are likely to be able to be treated with our modern antibiotics. Defrosted ancient viruses, on the other hand, may pose a much greater risk. Within modern viral infections, each different type of virus requires different vaccines or antiviral agents. This is because viruses often work in different ways, targeting different pathways in the body; viruses don’t have universally conserved druggable processes. Ancient viruses, despite being dormant in permafrost for tens of thousands of years, when woken from cryptobiosis could be equally tricky to protect against. An example of the havoc wreaked by such defrosted infectious diseases can be seen in the devastated reindeer populations in 2015 and 2016, which have been linked to the release of Bacillus anthracis spores from permafrost after exceptionally hot summers. Such devastation, according to Claverie, is not a small threat but a large hazard which we are quite likely to see as a result of melting permafrost. Knowing more about the potential strains that may be released as a result of permafrost defrosting due to climate change could act as some protection against them. Acanthamoeba safety Awakening ancient infectious bacteria and eukaryotes raises obvious safety concerns. Certain labs can facilitate exploration of viruses more safely due to their safety procedures. Another way to activate viruses without creating a risk of infection to humans/plants/animals is to use a species which is genetically very far removed. Acanthamoeba spp . was used by the Claverie group as the safest way to infect a species without risk of infection, due to its evolutionary distinction from the human/plant/animal genus. Acanthamoeba is useful not only for its safety but also for its ability to live in a multitude of environments: water taps, flowerpots, dust particles, marine waters and more. Detecting their viruses may be an indicator for other live viruses in a given setting. With this safety blanket in place, the Claverie group was able to reactivate thirteen viral isolates from the different samples. Seven of the thirteen isolates were found to be new members of the Pandoraviridae family. Each of the isolates are thought to be distinct both from each other and also contemporary viral strains, and using radiocarbon dating techniques, the oldest sample was dated as being more than 48,500 years old. After tens of thousands of years spent dormant in permafrost, large DNA viruses are still infectious to Acanthamoeba . Limits of Detection These findings, and unpublished findings from the same group, indicate a large population of potential viruses which could be reawakened as permafrost defrosts. However, the detection of positive viral cultures in the study was conducted using light microscopy. This means that smaller, non-lytic viruses are likely to have passed through microscopy studies undetected; there is likely an even greater population of viruses that can survive in ancient permafrost and more still which may exist that do not infect Acanthamoeba . Author Frances Briggs , freelance contributor Previous Next

The National Institute for Health and Care Excellence (NICE) has granted approval for the life-changing cystic fibrosis modulator drugs—Kaftrio, Symkevi, and Orkambi—to be made available through the NHS in England. < Back NICE Approves Vertex’s Modulator Drugs for Cystic Fibrosis: A Landmark Decision for the NHS The National Institute for Health and Care Excellence (NICE) has granted approval for the life-changing cystic fibrosis modulator drugs—Kaftrio, Symkevi, and Orkambi—to be made available through the NHS in England. The National Institute for Health and Care Excellence (NICE) has granted approval for the life-changing cystic fibrosis (CF) modulator drugs—Kaftrio, Symkevi, and Orkambi—to be made available through the NHS in England. This milestone follows extensive advocacy by the Cystic Fibrosis Trust and the broader CF community, marking a pivotal moment for thousands affected by this debilitating condition. CF is a chronic, life-limiting genetic disorder with no current cure. The availability of these modulator therapies on the NHS offers new hope and a significantly improved quality of life for patients. However, despite being a hugely positive moment, David Ramsden, chief executive of Cystic Fibrosis Trust, advised that ‘We should not forget though, that these treatments are not a cure and simply don’t work for some people. With the support of our incredible community, clinicians and researchers, a lot has been achieved, but we know there is still lots more to do” In November 2023, NICE acknowledged the clinical efficacy of Vertex’s CF treatments in draft guidance but stopped short of recommending them as cost-effective, causing disappointment in patients and their families. The draft stated that "even when considering the condition’s severity ... the most likely cost-effectiveness estimates for [Kaftrio], [Symkevi], and [Orkambi] are above the range that NICE considers an acceptable use of NHS resources." This echoed a prolonged standoff over the pricing of Vertex’s CF drugs that had previously been resolved in 2019 with a four-year government reimbursement deal, which included Orkambi and other CF drugs. Kaftrio was added to this scheme in 2020. Vertex announced the updated long-term reimbursement deal with the NHS on Thursday, ensuring access to Kaftrio, Symkevi, and Orkambi for all existing and future eligible cystic fibrosis patients in England. This agreement follows NICE’s positive recommendation for Vertex’s CFTR modulators, reflecting successful negotiations that address both clinical efficacy and cost concerns. The new deal, a result of collaboration among Vertex, NICE, and the NHS, ensures not only immediate access to these critical drugs but also includes provisions for future license extensions and rapid access to new treatments. Vertex is working on a next-generation CF therapy combining vanzacaftor, tezecaftor, and deutivacaftor, which will also be covered under this agreement pending regulatory approval. Ludovic Fenaux, Senior Vice President of Vertex International, expressed his satisfaction with the agreement: “We are delighted to have agreed extended long-term access to Kaftrio, Symkevi, and Orkambi for eligible CF patients in England. I would like to acknowledge the collaboration of NHS England, NICE, and the Scottish Medicines Consortium (SMC), and thank the CF community for highlighting the value these innovative medicines bring to patients.” This decision represents a significant advancement in the treatment of cystic fibrosis, promising to transform the lives of those affected by this challenging condition. Similar access agreements are anticipated to be formalized soon in Scotland, Wales, and Northern Ireland, ensuring consistent availability of these therapies across the UK. Vertex’s portfolio of CF medicines is broadly available in over 60 countries, including Australia, France, Italy, Germany, the Republic of Ireland, the Netherlands, Spain, and the U.S. The company continues to work closely with regulatory and health authorities worldwide to ensure broad access to its innovative treatments. As the pharmaceutical community reflects on this landmark decision, it underscores the importance of collaboration and negotiation in bringing life-saving treatments to patients while balancing cost-effectiveness and accessibility. Author BioFocus Newsroom Previous Next

< Back World Health Summit 11th - 13th October, 2026 Berlin, Germany From Crisis to Resilience: Innovating for Health. ! Widget Didn’t Load Check your internet and refresh this page. If that doesn’t work, contact us. Previous Next

Ascletis advances oral GLP-1 drug ASC30 after Phase 1b shows strong weight loss and safety, shifting focus to obesity with a slower dose-escalation strategy. < Back Ascletis Enters the Obesity Drug Spotlight with Bold Play on Oral GLP-1 Candidate Ascletis advances oral GLP-1 drug ASC30 after Phase 1b shows strong weight loss and safety, shifting focus to obesity with a slower dose-escalation strategy. Ascletis Pharma has unveiled promising topline results from its U.S.-based Phase 1b trial of ASC30, its once-daily oral GLP-1 receptor agonist, positioning the molecule as a serious contender in the booming obesity market. The data support a pivot toward a slower, more tolerable dose-escalation strategy ahead of a Phase 2a study set to launch in Q3 2025. The randomized, double-blind, placebo-controlled Phase 1b multiple ascending dose (MAD) study enrolled adults with obesity (BMI 30–40 kg/m²) and evaluated three weekly titration schemes over four weeks. Schemes 1 and 2 (starting at 2 mg) demonstrated placebo-adjusted weight loss of 4.5% and 6.5%, respectively. Scheme 2 achieved a maximum individual weight loss of 9.1%, with no evidence of plateauing. Importantly, gastrointestinal (GI) side effects were mostly mild and transient—Scheme 1 reported no vomiting at all. Scheme 3, which began at a higher dose (5 mg) and escalated rapidly to 60 mg, showed similar efficacy—6.1% placebo-adjusted weight loss after excluding two low-response outliers—but with worsened GI tolerability. This reinforced the case for a “low and slow” dose titration, particularly given the absence of serious adverse events or liver enzyme elevations across all cohorts. ASC30 is a first-in-class small molecule GLP-1R biased agonist, designed in-house to be administered either as a once-daily oral tablet or once-monthly subcutaneous injection. The oral formulation is central to Ascletis’ metabolic disease strategy as the company aggressively reallocates R&D resources from virology and oncology toward obesity. Phase 2a plans are already in motion. Ascletis has submitted a 13-week protocol to the FDA, incorporating a gradual weekly titration based on learnings from Phase 1b. With robust safety and early efficacy signals, and patent protection secured through 2044, Ascletis is gearing up to challenge major players like Novo Nordisk and Eli Lilly in the next generation of anti-obesity therapeutics. Author BioFocus Newsroom Previous Next

< Back Training the Immune System to Outlast Cancer Personalized RNA vaccines show long-term promise in pancreatic cancer, new study reports. Pancreatic cancer, particularly pancreatic ductal adenocarcinoma (PDAC), is one of the deadliest forms of cancer, with limited treatment options and a high rate of recurrence after surgery. However, a new study published in Nature reports that personalized RNA vaccines can train the immune system to fight back, potentially delaying or even preventing the return of the disease. One of the biggest hurdles in cancer treatment is getting the immune system to recognize and attack cancer cells. Cancer vaccines aim to do just that by targeting specific proteins, or "neoantigens," that are unique to the tumor. But in pancreatic cancer, which has relatively few mutations, this has been particularly challenging. The new study, led by researchers at Memorial Sloan Kettering Cancer Center, tackles this problem head-on with a novel approach: personalized RNA vaccines designed to prime the immune system to recognize and destroy cancer cells. A Personalized Approach The researchers conducted a phase I clinical trial involving 19 patients who had undergone surgery to remove their pancreatic tumors. After surgery, patients received a combination of treatments: a single dose of atezolizumab (an immune checkpoint inhibitor), followed by a personalized RNA vaccine called autogene cevumeran , and then a standard chemotherapy regimen known as mFOLFIRINOX. The vaccine was tailor-made for each patient, targeting up to 20 unique neoantigens—mutated proteins found only in their tumors. The goal was to train the immune system, specifically CD8+ T cells, to recognize and attack any remaining cancer cells, reducing the risk of recurrence. The results were striking. At a median follow-up of 3.2 years, patients who responded to the vaccine—meaning their immune systems produced a strong T cell response—had significantly longer recurrence-free survival compared to non-responders. In fact, the median recurrence-free survival for responders had not yet been reached, while non-responders had a median survival of just 13.4 months. Even more impressive was the longevity of the immune response. The vaccine-induced T cells were estimated to persist for an average of 7.7 years, with some clones potentially lasting for decades. These T cells not only stuck around but also remained functional, retaining their ability to recognise and attack cancer cells. This is a critical finding, as long-lasting immunity is essential for preventing cancer from coming back. How does it work? The vaccine works by introducing RNA sequences that encode the neoantigens into the body. These RNA sequences are packaged in lipid nanoparticles, which help deliver them to immune cells. Once inside, the immune cells use the RNA to produce the neoantigens, effectively training the immune system to recognize and attack cancer cells that display these same proteins. The study also revealed that the vaccine-induced T cells were mostly "de novo," meaning they were newly generated in response to the vaccine rather than pre-existing in the body. This is important because it suggests that the vaccine can kickstart an immune response even in patients whose immune systems haven’t naturally recognized the cancer. Using advanced single-cell RNA and TCR sequencing, the researchers tracked the behavior of these T cells over time. They found that the T cells went through several phases: first proliferating rapidly, then contracting, and finally settling into a long-lasting memory state. Importantly, these memory T cells retained their ability to kill cancer cells, even years after vaccination. In patients who experienced a recurrence, the tumors showed signs of "clonal pruning," meaning that the cancer cells targeted by the vaccine were largely eliminated. This suggests that the vaccine-induced T cells were actively working to keep the cancer in check. What does this mean for patients? For patients with pancreatic cancer, these findings are a beacon of hope. The study shows that it’s possible to generate a strong, long-lasting immune response against a cancer that has historically been very difficult to treat. While the results are still early and need to be confirmed in larger trials, the potential is enormous. The personalized nature of the vaccine is particularly exciting. By targeting the unique mutations in each patient’s tumor, the vaccine can potentially be adapted to treat a wide range of cancers, not just pancreatic cancer. This approach could be especially beneficial for cancers with low mutation rates, where traditional immunotherapy has struggled to make an impact. The researchers are already planning the next steps. A global randomized trial, called IMCODE 003, is underway to further test the efficacy of the vaccine in a larger group of patients. If successful, this could pave the way for a new era of personalized cancer vaccines, offering hope to patients with some of the most challenging forms of the disease. This study represents a significant leap forward in the fight against pancreatic cancer. By harnessing the power of personalized RNA vaccines, researchers have shown that it’s possible to train the immune system to recognize and attack cancer cells, potentially preventing recurrence and improving survival. While there’s still much work to be done, the results are a promising step toward a future where cancer vaccines could become a standard part of treatment, offering new hope to patients worldwide. Author BioFocus Newsroom Previous Next