In addition to suffering seizures, many people with epilepsy also experience bursts of abnormal brain activity called interictal epileptiform discharges (IEDs). These can happen thousands of times a day and interfere with attention, memory, language, and sleep. New data from a study led by scientists at University of California, San Francisco (UCSF) shows that these brain blips are not random events as once thought. The data shows that they unfold in a predictable pattern that can be detected before they occur, suggesting it may be possible to prevent them.
Details of their work are published in Nature Neuroscience in a paper titled “Laminar organization of cellular microcircuits modulating human interictal epileptiform discharges.” In it, the scientists explain that they used a high-resolution technology recently adapted for humans that records individual neuron activity to track more than 1000 neurons in four patients undergoing surgery for epilepsy. The so-called Neuropixel probes provide “a view into new ways we might address a debilitating aspect of epilepsy that we haven’t been able to tackle,” said Jon Kleen, MD, PhD, an associate professor of neurology at UCSF and co-senior author of the study.
Preventing brain blips would be a boon for patients’ quality of life because over time, the effects of these mental disruptions can be significant and may account for some of the cognitive impairment experienced by about half of people with epilepsy.
Neuropixels probes, which are thin devices lined with hundreds of sensors, are designed to record activity throughout the human cortex. This means that unlike current sensors which are limited to brain signals on the surface of the brain, Neuropixels can provide a three-dimensional view of brain activity. For the study, the scientists implanted the probes seven millimeters deep into the part of the brain where patients’ seizures originate—this is the tissue that surgeons typically remove to reduce epilepsy symptoms.
Inserting the probes here made it possible to observe what happened in the neurons before, during, and after each IED. While seizures appear as a burst of neurons firing in synchrony, when IEDs occur, they unfold sequentially. Specifically, one set of neurons was active about a second before the IED started followed by another set that generated the sharp electrical spike at its peak, and then a third set became active as the IED faded. “We could see individual neurons that were just microns apart from each other playing different roles in the process,” said Alex Silva, the study’s first author and a medical student and doctoral candidate in the UCSF-UC Berkeley Joint PhD program in bioengineering. “It was really striking.”
Previous studies have demonstrated that most neurons involved in IEDs are used in normal cognitive processing. According to this study, nearly 80% of the neurons involved in IEDs were also involved in language and perception. Current implantable devices for epilepsy may be able to help. They include closed loop neurostimulators that can detect abnormal brain activity and deliver electrical pulses that interrupt it. So in the case of IEDs, devices that monitor single neurons could use the activity of the first set of neurons announcing the arrival of the abnormal pattern as a warning signal. “That would be a major step forward, changing treatment from reactively responding to abnormal brain bursts to proactively preventing them in the first place,” Kleen said.
Chair, Advanced Therapeutics University of Edinburgh, U.K.
Carrie Haverty
Vice President of Medical Affairs & Clinical Strategy Mirvie
Broadcast Date:
Time:
Welcome to the 2026 State of Precision Medicine virtual summit, hosted by Inside Precision Medicine. This year’s summit focuses on the existing gaps in precision medicine as we ask: How do we make treatment equitable and accessible for all patients across the disease continuum?
On June 3rd, the editors of Inside Precision Medicine will feature an outstanding line-up of guests highlighting the challenges and urgency of expanding access to disease therapies and empowering patients and consumers.
Agenda Highlights:
Becky Quick, co-anchor of CNBC’s Squawk Box and the founder of CNBC Cures, discusses her own family’s rare disease journey and her prescription to expand access to rare disease therapeutics
Anne Wojcicki, CEO of the 23andMe Research Institute, speaks on the consumer genetics pioneer’s recent renaissance leading the newly re-imagined organization
Brian Bigger, PhD, and Rob Wynn, MD, scientists and clinicians at Manchester University, share insights from their work on stem cell gene therapy and its potential to offer hope for patients with rare diseases such as Hunter syndrome. They are joined by Ricky Chu, father of two children with Hunter syndrome, a rare neurodevelopmental disorder
Carrie Haverty, president of the National Society of Genetic Counselors, hosts a panel on the current trends and challenges in genetic counseling
Saralyn Mark, MD, first senior medical advisor to both the Office on Women’s Health within the HHS and NASA, boldly explores lessons in women’s health with her guests Dorit Donoviel, PhD, and Kim Templeton, MD
Breakout sessions from the summit sponsors, including 10x Genomics and Illumina
Registration is entirely free. We look forward to seeing you on June 3.
Officials at Ecolab Life Sciences report that the company is expanding its bioprocessing business with the launch of a new bioprocessing applications lab (BPAL) in Dongtan, Korea. They say the goal is to provide biopharmaceutical manufacturers across Asia with better local access to downstream process development support.
The site is Ecolab’s first bioprocessing facility in Asia and joins an established applications network in the U.S. and U.K.
BPAL Korea supports process development from early-stage resin screening through studies designed to replicate commercial manufacturing conditions, according to Jenny Tan, vice president and general manager, Ecolab Life Sciences APAC and India. On-site scientists work alongside customers across Asia to help optimize chromatography steps, improve yield and productivity, and accelerate regulatory pathways, with the aim of reducing the need to ship resins and reference materials overseas for development work, she continues.
Asia has become one of the world’s most active biopharmaceutical manufacturing regions, with Korea, China, Japan, India, and Singapore all home to growing pipelines in biosimilars and monoclonal antibody processes that scalable downstream purification. With local technical support now in place, manufacturers across the region can shorten development cycles and maintain consistency with global operations while working to tight regulatory and cost targets, continues Tan.
“Biopharmaceutical manufacturers across Asia are under increasing pressure to scale with speed while meeting demanding regulatory and performance expectations,” she explains. “BPAL Korea strengthens our ability to work side by side with customers, bringing local expertise together with Ecolab’s global, integrated bioprocessing network.”
By combining local scientific support with Ecolab’s innovative Purolite resin portfolio, Ecolab’s new BPAL was created to help enable manufacturers to address process challenges earlier, reduce development risk, and advance programs with greater confidence as they prepare for scaleup, says Tan.
This is the online version of Adam’s Biotech Scorecard, a subscriber-only newsletter. STAT+ subscribers can sign up here to get it delivered to their inbox.
I’m suffering from spring allergies + a nasty head cold this week. Not fun.
Mystery cloaks an ASCO plenary lung cancer survival result
The runup to next month’s annual meeting of the American Society of Clinical Oncology has started, and a good bit of the Wall Street chatter and speculation is centered on the Akeso-Summit Therapeutics drug ivonescimab.
SAN DIEGO, CA – At the 2026 American Association for Cancer Research (AACR) Annual Meeting, Verismo Therapeutics unveiled early data that could reshape CAR T-cell design. Built on a novel “KIR-CAR” platform, the experimental therapy SynKIR-310 uses a multi-chain, split-signaling architecture that mimics natural immune receptors, enabling T cells to stay active through repeated tumor attacks while potentially reducing exhaustion and safety risks that have long limited conventional approaches.
In preclinical studies, SynKIR-310 delivered potent anti-tumor responses in B-cell cancer models, including 100% survival in treated mice. The therapy targets CD19 using a canine-derived binding domain and is now being tested in patients with relapsed or refractory B-cell non-Hodgkin lymphoma in the Phase I CELESTIAL-301 trial.
Early clinical findings included a 70-year-old patient with follicular lymphoma who achieved a complete response just 28 days after receiving the lowest dose, an outcome still holding at six months. While preliminary, the results suggest that reengineering CAR T-cell biology itself may unlock more durable responses with fewer toxic side effects, tackling two of the field’s toughest challenges.
Two decades of rethinking CAR T
Laura A. Johnson, PhD, Chief Scientific Officer and Chief Operating Officer at Verismo Therapeutics
Verismo’s presentation of the data at AACR itself was understated, unfolding among rows of posters and quiet conversations. In the eyes of Laura A. Johnson, PhD, it was the culmination of a nearly two-decade-long scientific journey. It all began as a postdoc in the lab of immunotherapy trailblazer Steve Rosenberg, MD, PhD, who is currently chief of surgery at the National Cancer Institute, among several other appointments.
Johnson, who is chief scientific officer and chief operating officer at Verismo, told Inside Precision Medicine, “My postdoc project was literally taking, finding, and choosing an antigen; finding a shared antigen T cell receptor; subcloning it; and making it into a T cell. Not a CAR drug, but a TCR engineered drug that worked so well in the first year that they used to have money on tap there, turned it into a clinical trial, and then put me as an academic in charge of overseeing the clinical trial, the making of the drug, and getting to go and visit and shake the patient’s hands. In the four years since then, we saw literally pounds of tumor fall off these patients when we visited them in the clinic.”
That dramatic and deeply personal experience showed Johnson the promise and limitations of immune-based cancer therapies. Even as she saw tumors regress in ways that seemed almost implausible, she saw that those responses were not universal or durable and that toxicity could complicate even the most striking successes.
She continued to gain experience and try out different things, eventually leading her to the University of Pennsylvania (UPenn) with CAR T-cell therapy pioneer Carl June, MD. Working with June at UPenn, Johnson expanded CAR T-cell research rapidly, supported by industry investment and a mandate to investigate engineered immune cells’ effects on a variety of cancers. It was during those “great five years” that Johnson began to tackle solid tumors with CARs. Even as the field struggled with relapse, toxicity, and solid tumor efficacy, she led the way in clinically implementing experimental therapies.
Johnson’s subsequent move into industry, including a leadership role at GlaxoSmithKline (GSK), broadened her perspective further. “At the time, I did not see myself as an industry kind of person,” said Johnson. “I didn’t know what that was, but I did go to GSK for five years. It was amazing. I learned so much there. You know how to run clinical trials across the globe for registration. These huge teams of support. It was great.”
Johnson added, “I also had a sponsored research agreement with GSK, which was then exploring cell therapy, and after a year of that, they decided to open up a whole cell therapy unit and invited me to come and lead the group.”
By the time she returned to academic collaborations, she had seen the field from multiple angles—scientific, clinical, and operational—and had developed a growing sense that the limitations of CAR T therapy might be rooted in something more fundamental than incremental improvements could fix.
The origins of KIR-CAR
That realization sharpened when she reconnected with colleagues at UPenn, including Carl June and Michael Milone, PhD, MD, the co-inventors of Kymriah, the first-ever approved CAR T, who had already begun questioning the underlying design of conventional CAR T systems. “Back then, Mike and Carl already saw that it worked, but they felt something was not right about it. You know that patients can have recurrences of cancer, and it doesn’t work in solid tumors, no matter what they do. So they were already in the background trying to tinker and figure it out.”
The success of Kymriah had proven that engineered immune cells could be transformative, but it had also exposed persistent problems that could not be ignored. “At the time, Mike had a great idea that the artificiality of the single-chain CAR T was causing these problems because it was not evolutionarily selected for. It’s not natural. Maybe this has something to do with it.”
That insight led Milone to revisit the basic biology of immune receptors, examining how natural systems separate recognition from activation rather than fusing them into a single, continuously active structure. “They all have the same receptor format to bind to the target on the cell’s outside. The receptor is anchored in place by a neck in the cell membrane, while a completely separate internal signaling mechanism is also anchored by a neck in the membrane and is activated from the inside. And these two actually don’t interact. They have nothing to do with each other unless and until that target is found unbound, which brings the two together.”
From this observation emerged the concept of KIR-CAR, a multi-chain system inspired by natural killer (NK) cell biology that attempts to restore a more controlled and conditional activation process. “T cells, their main job, is actually not to kill you but rather to kill bad things, so they try and shut everything down,” Johnson explained. “So, we said, ‘Let’s use NK cells.’ They’re the other main lymphocyte that attacks tumors, and they’re innate. Maybe they won’t have the same problems with shutting down. Let’s throw it at the wall and see what sticks.’”
The resulting design combined elements of NK cell receptors with T-cell machinery, creating what Johnson describes as a more natural on-off switch. The combination of the killer immunoglobulin receptor (KIR), which acts as the outside binder, with existing intracellular signaling machinery used for CARs resulted in the name KIR-CAR. “A chimera has the head of a lion, the body of a goat, and the tail of a snake,” said Johnson, using the hybrid from Greek mythology in describing a traditional CAR. “We’ve un-Frankensteined them and put them back. What we end up with is just a more natural on/off switch. Why would we think we can do better than a million years of evolution at figuring out a way to trigger and turn off these cells to get rid of bad things?”
Early signals of efficacy and safety
In early preclinical experiments, KIR-CAR cells were compared to single-chain CAR T cells, showing subtle differences in vitro but greater differences in complex systems. By the time Johnson presented SynKIR-310 at AACR, those differences had become a consistent pattern across preclinical studies and early clinical observations, suggesting that the KIR-CAR approach may improve tumor control without the toxicity of conventional CAR T therapies.
Johnson said, “It’s been surprising, but great news. Our preclinical team has reversed the process, gone back to mice, and successfully reproduced the same findings. Not only is the KIR-CAR superior at eliminating tumors, but it also has a shorter duration of interferon gamma. In contrast, the single-chain CAR T cells that everyone else on the planet is using appear to be frighteningly toxic because they go off script.”
Johnson vividly described that uncontrolled activation. “If you do any assay with them, presumably including in vivo, lasting more than a day, they start killing everything around them,” she said. “They start spitting out interferon gamma. They infect every cell they come into contact with; they proliferate; they produce cytokines; they cause lysis; and they have many other harmful off-target effects.”
That behavior aligns with her broader description of how conventional CAR T cells can become overactivated and exhausted. Johnson elaborated, “The CAR T cell is hyperactivated, and it’s going down. It knows it’s exhausted, but it also detects an activated state, so it sets off fireworks and hopes the grenade response will take out whatever is bad too.”
In contrast, biomarker data from SynKIR-310 suggest a more controlled and physiologic immune response. “When we look at the biomarkers, they’re not making a ton of interferon or TNF alpha,” said Johnson. “Even from the first dose we used, we showed clearly biological activity where the T cells go in; as of day seven, you start to see interferon pickup. It peaks out at about ten days.”
Johnson continued, “Then it’s textbook as for how a T cell activates when it sees its target; this process is crucial for the immune response. It showed that it’s very clearly encountering a target, activating and doing what it’s supposed to do. However, the blood levels we observed were significantly lower than expected due to hematologic malignancies, which involve widespread tumors throughout the body, including the bone marrow and blood.”
Clinical observations, though limited, reinforce that pattern. “The results were announced today for the first nine patients. It’s a basket study for both ovarian cancer and cholangiocarcinoma. So, there are three very high unmet and urgent needs for patients. Most of these have one line of approved therapy, or maybe two, and once they become advanced refractory or metastatic, there’s nothing for these patients. Overall survival is measured in weeks, not months.”
Within that context, even modest responses carry significance. “Four of the nine showed measurable tumor reductions and the last patient treated, the last one in cohort three, had a response that continued past our data cutoff and keeps going. So, it’s very good news.”
Perhaps most striking, however, is the KIR-CAR’s apparent safety profile. “The biggest thing they were worried about is toxicity. Everybody knows that CAR causes cytokine release syndrome (CRS), and interferon gamma causes neuropathic disease, leading to brain damage and other severe symptoms. It’s got a bad rap. I think they got a headache one night that was called ‘CRS.’ That was gone the next morning. That’s it.”
A broader vision for cancer treatment
For Johnson, the significance of these findings lies less in any single result than in their consistency across different models and targets, reinforcing her belief that the KIR-CAR platform reflects a fundamentally different—and potentially more effective—approach to engineering immune cells. “You can want something to work as much as you want, but if it doesn’t, it doesn’t, and you accept it,” said Johnson. “So it’s okay that the data was the same for both our platform assets, the CD19 and mesothelioma KIR-CARs; this result is real.”
That reproducibility has given her confidence to draw comparisons with existing therapies. “When we see the same things again, there are fewer CRS cytokines, less duration of toxicity, and way better treatment. It is better than both Kymriah and Yescarta. We did the in vivo models, but it’s a little better than Kymriah and a lot better than Yescarta.”
At the same time, she remains grounded in the understanding that these are early results, requiring validation in larger trials and over longer follow-up periods, even as they point toward a broader shift in how the field might approach the design of next-generation immunotherapies. Rather than continuing to build increasingly complex artificial systems, the KIR-CAR approach suggests that aligning more closely with the immune system’s natural architecture—its built-in checks, balances, and conditional activation mechanisms—may offer a path to therapies that are both more effective and less toxic.
That idea, rooted in the biology she has spent her career studying, connects her earliest experiences watching tumors disappear in clinical trials to the work she now presents. It formed a narrative for Johnson that is less about a single product than about a way of thinking: that progress in cancer immunotherapy may ultimately depend not on pushing the immune system harder but on understanding it more deeply and working within the logic it has evolved over millions of years to follow.
Researchers at the Mass General Brigham Heart and Vascular Institute and collaborators have developed and validated a new integrated polygenic risk score (PRS) that estimates inherited risk across eight cardiovascular conditions using a single genetic test. The tool is a combination of a handful of genetic risk models collected into a comprehensive risk tool and is designed to improve identification of individuals at elevated risk for coronary artery disease (CAD), atrial fibrillation, type 2 diabetes, venous thromboembolism, thoracic aortic aneurysm, extreme hypertension, severe hypercholesterolemia, and elevated lipoprotein(a).
The validation study, published in the Journal of the American College of Cardiology, showed that individuals with high genetic risk scores had significantly higher odds of developing disease compared with those at average risk, including a 3.7-fold higher odds for CAD and a 4.1-fold higher odds for severe hypercholesterolemia.
“Interpreting DNA risk is new for the public as well as clinicians,” said co-senior author Pradeep Natarajan, MD, director of preventive cardiology at Mass General Brigham Heart and Vascular Institute. “It was very important to us to provide a clear genetic risk report that would be accessible and patient-friendly.”
The researchers developed the integrated PRS tool using PRSmix, an elastic-net approach that combines previously published polygenic risk scores from the Polygenic Score Catalog. The model was trained using genotype and clinical data from 245,394 participants in the NIH All of Us Research Program and validated using data from 53,306 people from the Mass General Brigham Biobank. In the validation cohort, the integrated scores demonstrated strong discrimination across all eight conditions, with individuals in the top 10% of genetic risk showing increased odds of disease, including CAD (odds ratio 3.7), type 2 diabetes (3.1), atrial fibrillation (3.0), venous thromboembolism (1.9), hypertension (2.1), and lipoprotein(a) (41.0).
Current cardiovascular risk assessments typically rely on age, sex, blood pressure, cholesterol, and other clinical factors. The Mass General team noted that these methods may miss individuals with substantial inherited risk who do not yet show clinical symptoms. By comparison, the new PRS tool gives a single genetic assessment that can be applied early in life and across multiple disease pathways simultaneously.
“Although PRS have typically been evaluated one condition at a time, a single genotyping assay enables calculation of PRS for any heritable trait without significant additional cost, creating an opportunity to assess inherited risk across multiple cardiovascular conditions simultaneously,” the researchers wrote noting the value of this new method.
In this study, the integrated PRS improved risk classification when incorporated into clinical prediction models, including better stratification of individuals near clinical decision thresholds for cardiovascular disease. The system also generated standardized risk categories—high, average, or low—for each condition and presented results in clinician-facing and patient-facing formats that can be integrated into electronic health records.
Clinically, the new PRS is could be use to identify people whose inherited risk could provide the opportunity for preventive interventions such as increased monitoring, lifestyle modification, or preventive therapies, even when conventional risk factors appear normal. For CAD specifically, the findings suggest that individuals with high polygenic risk may have risk levels comparable to other established high-risk groups, despite modest or normal cholesterol levels.
The researchers also evaluated how the tool could work across diverse populations and clinical settings. They found that while the PRS performed consistently across ancestry groups, predictive strength was reduced in individuals with greater genetic variation from people of European ancestry, exposing the inherent limitations in current genomic reference datasets. Despite this, the integrated framework was designed to allow updating as new data become available.
The PRS is currently available through Mass General Brigham Laboratory for Molecular Medicine and Broad Clinical Labs. The researchers said that next steps to further refine the tool include broader prospective validation across diverse populations, evaluation its cost-effectiveness, and research to determine how genetic risk information should influence clinical decision-making.
As cancer survival rates improve, a new challenge is coming into sharper focus: what happens after the first cancer is treated. A large population-based study drawing on decades of U.S. registry data offers one of the most comprehensive looks yet at the risk of subsequent primary cancers (SPCs)—and reveals a complex, evolving landscape shaped by age, sex, and generational exposure. The work was published in PLOS Medicine.
Using data from more than 3.3 million individuals diagnosed with a first primary cancer between 1975 and 2019, investigators from the Virginia Commonwealth University (VCU) School of Medicine analyzed nearly 30 million person-years of follow-up, identifying more than 510,000 second cancers. Their findings, based on Surveillance, Epidemiology, and End Results (SEER) registries, show that SPC risk is not static but varies significantly depending on when patients were born, how old they were at diagnosis, and the type of cancer they initially had.
“We have follow-up guidelines after treatment for the primary cancer, but we don’t really know what risk profile these patients fall into for another cancer,” said Susan Hong, MD, who co-directs a cancer survivorship outcomes research program at VCU and co-directed the study. “They’re not average-risk individuals—but they’re not necessarily at extremely high risk across the board either. That’s where it becomes very nuanced and complex.”
Age and sex drive risk—but not uniformly
The analysis confirmed that SPC incidence increases with age at first cancer diagnosis, rising substantially in both men and women, though more steeply in males. Among women, rates climbed from 915 per 100,000 person-years at ages 35–39 to 1,980 at ages 75–79; in men, the increase was from 1,228 to 2,945.
But these patterns were not consistent across all cancer types. For breast cancer survivors, the risk of developing a second cancer remained relatively stable regardless of age at diagnosis—a finding that surprised the investigators.
“I was kind of surprised that the risk of subsequent cancer didn’t vary by age among breast cancer survivors,” said Hui Cheng, PhD, the study’s lead analyst. “I thought older patients would have higher risk, but that wasn’t necessarily the case.”
By contrast, survivors of lung and bladder cancers and melanoma showed a clear age-related increase in SPC risk, suggesting that surveillance strategies may need to differ significantly by index cancer type.
Cohort effects point to environmental and behavioral drivers
One of the study’s most striking findings emerged from its age–period–cohort modeling: SPC risk peaked among individuals born between 1935 and 1945, then declined in more recent birth cohorts—with notable exceptions.
Researchers observed rising risks among female lung cancer survivors and male bladder cancer survivors, even as overall SPC incidence declined in more recent decades. The cohort-specific patterns hint at underlying environmental or behavioral exposures that vary across generations.
“We observed higher risk in cohorts born in the ’40s and ’50s,” Cheng said. “If we think back, those individuals were young adults during peak tobacco use, which may be a contributing factor. But we don’t have individual-level smoking data, so we can’t confirm that directly.”
This limitation underscores a key challenge of large registry-based studies: while they offer statistical power and long-term follow-up, they often lack granular data on treatment exposures, genetics, and lifestyle factors.
Treatment advances and unintended consequences
The findings also reflect the dual-edged nature of cancer treatment progress. As therapies improve and patients live longer, the window for developing late effects—including second malignancies—widens.
“We’re doing so well treating primary cancers, and people are living longer,” Hong said. “But we also need to think about what risk profile these patients fall into over time.”
Radiation therapy and certain chemotherapies are known contributors to secondary malignancies, with risks often emerging 10 to 15 years after exposure. Yet without detailed treatment data, the current analysis cannot disentangle these effects.
Instead, the study serves as what investigators describe as a “hypothesis-generating” effort—mapping broad patterns that can guide more targeted research.
Toward risk-stratified survivorship care
“We’re trying to figure out how to risk-stratify patients and pay attention to their long-term health care needs without overreacting or underreacting,” Hong said.
In practice, that could mean more intensive surveillance for older survivors of certain cancers, while maintaining consistent monitoring across age groups for others, such as breast cancer.
The findings also highlight gaps in the current survivorship infrastructure—particularly for adult-onset cancers. While pediatric oncology has long benefited from coordinated long-term follow-up systems, similar frameworks are less developed for adult survivors.
“There’s been a long-standing effort to follow childhood cancer survivors, but we don’t have that kind of system in place for adults,” Hong noted. “Now that we’re seeing more cancers in younger adults, we need to think about how to address decades of survivorship.”
A starting point for deeper investigation
Ultimately, the study raises as many questions as it answers. Why do certain cohorts carry higher risks? How do treatment regimens, genetics, and lifestyle interact to drive SPC development? And which risk factors are modifiable?
The research team is already looking ahead to studies that can incorporate more detailed patient-level data, with a focus on identifying actionable prevention strategies.
“We’re very interested in understanding what factors are associated with better or worse outcomes—especially modifiable risk factors,” Cheng said.
Digital twins help optimize drug production processes by modeling the thousands of interactions that cells, raw materials, and reagents undergo in culture. And new analysis suggests they could do the same thing for supply chains.
Researchers at the U.S. National Institute of Standards and Technology (NIST) and EMD Millipore put forward the idea, arguing that twins could make drug distribution, which is also characterized by thousands of interactions, more resilient and efficient.
Lead author Perawit Charoenwut, a logistics researcher at NIST’s systems integration division, tells GEN, “A digital twin could be extremely helpful in all phases of the biopharmaceutical supply chain. Starting from demand planning triggered by global events such as pandemics, regional disease outbreaks, aging demographics, etc., through to being able to provide visibility on capacity requirements and limitations.”
In silico models could also provide solutions to disruption by identifying alternative supply options, such as distribution centers or regional inventories, in less time, Charoenwut says.
“Digital twins could also be helpful in evaluating different suppliers by running simulations on their potential performance, based on different demand scenarios versus their individual capacities and capabilities,” he continues.
Standards
In theory, digital twins are a good option for supply chain modeling and management. In practice, however, firms interested in the approach will need to overcome some technical challenges.
For example, one major hurdle is the lack of data standardization, according to study co-author Boonserm Kulvatunyou, PhD, a computer engineer at NIST. “Supply chain digital twins require data from across organizations and third-party sources,” he tells GEN. “The lack of industry standards creates challenges in obtaining all the necessary data.”
Kulvatunyou says, “The aim is to provide a semantic foundation for connecting data and knowledge across the manufacturing and supply chain operations.
“Further work is being conducted to cover broader materials, processes, and quality data,” he says. “We would like to invite industry and academia to join this effort and benefit from these new standards.”
Industry interest
Biopharma firms interested in digital supply chains will also need to establish a solid data infrastructure, according to Charoenwut, who says companies should start small and pace themselves.
“We think that biopharma companies do believe that digital twins could make a significant difference in their supply chain efficiency and resiliency. Many of them are probably building prototypes and proofs-of-concept to demonstrate the value and potential benefits, but then soon realize the digital data foundation gaps that need to be addressed in parallel in order to fully adopt this technology.
“As digital twins can vary in detail and complexity, companies should strategize digital twin adoption by starting with lower-complexity cases based on available digital data and progressively moving up the scale to gain greater precision and new capabilities. In other words, the implementation of digital twins should be viewed as an evolution rather than a breakthrough,” he says.
New contamination testing results from the Food and Drug Administration confirm the safety of infant formula in the U.S., the agency said Wednesday.
The FDA tested 312 samples from 16 infant formula brands for contaminants like heavy metals, pesticides, and the “forever chemicals” known as per- and polyfluoroalkyl substances, or PFAS. The vast majority had undetectable or very low levels of contaminants, the agency said, with levels of lead, mercury, cadmium, and arsenic coming in below federal requirements for drinking water across all samples.
resin portfolio, Ecolab’s new BPAL was created to help enable manufacturers to address process challenges earlier, reduce development risk, and advance programs with greater confidence as they prepare for scaleup, says Tan.