This past week delivered another gut punch for science in the US. This time, the target was the National Science Foundation—a federal agency that funds major research projects to the tune of around $9 billion. The foundation’s efforts were overseen by a board of 22 prominent scientists. On Friday last week, they were all fired.
The NSF has been without a director since April 2025, when former director Sethuraman Panchanathan stepped down in the wake of DOGE-led funding cuts and mass firings. Trump’s nominee for the role is Jim O’Neill, an investor and longevity enthusiast who does not have a science background.
It’s hard to predict exactly how things will shake out for science. But it’s not looking great.
The NSF was established in 1950 to “promote the progress of science,” among other goals. It has served as a major source of support for research and education since then. In 2024, the agency spent $9.39 billion—a substantial figure but only 0.1% of all federal spending.
Key decisions about how that money is spent have been made by the National Science Board. Each of the scientists who made up the board until last week was appointed by a US president to serve, at least initially, a six-year term. Those members were responsible for establishing NSF policies, authorizing major expenditures and providing oversight, says Keivan Stassun, a physicist and astronomer at Vanderbilt University who was appointed to the board in late 2022.
“It’s a relatively small group with a tremendous amount of responsibility and authority,” says Stassun. He viewed his appointment as “a tremendous honor.”
Then, last Friday, the email landed in his inbox. “It said: On behalf of President Trump, this letter is to notify you that your position as a member of the National Science Board is terminated effective immediately. Thank you for your service,” says Stassun. “It was deeply disappointing.”
Still, Stassun wasn’t surprised, given the administration’s actions across federal science agencies over the past year.
Since Donald Trump took office at the start of 2025, the NSF—along with many other federal agencies—has frozen, unfrozen, and terminated grants. “The board was not involved in any of those [terminations],” says Stassun. Members had no say in the firing of agency staff either, he says. Staff numbers are currently down 40%, he adds.
In a 2026 budget request, the Trump administration sought to cut the NSF’s budget by around 57%. Last summer, NSF staffers wrote a letter of dissent arguing that such substantial cuts would “cripple American science.” The proposed cuts would have hit biological sciences, engineering, and STEM education particularly hard.
Those cuts were rejected by Congress earlier this year. But grant terminations and firings are essentially allowing them to take effect regardless, says Stassun. “The funds that the White House has been dispersing to the agency … have been far less than what Congress intended,” he says.
Many ambitious research projects are grinding to a halt as a result. “The Extremely Large Telescope Program appears to be dead in the water for now,” says Stassun. And the NSF arm dedicated to science education “has effectively zeroed out,” he says.
But not all of them. While the administration’s 2027 budget request states that NSF will “close out” its directorate for social, behavioral, and economic sciences, it describes AI and quantum information science as key “frontier initiatives.” Biotechnology is described as a “focal point.”
When asked for comment, the NSF directed MIT Technology Review to the White House press office. The White House did not respond directly to questions about the firing of NSB members and said in a statement, “The National Science Foundation’s work continues uninterrupted.”
Jim O’Neill, Trump’s current candidate for the position of NSF director, is certainly interested in biotechnology. Specifically, when I spoke to O’Neill in February, he told me that he supposes he is a Vitalist—a hardcore supporter of efforts to extend human longevity who believes that death is wrong.
O’Neill was deputy secretary of the Department of Health and Human Services and acting director of the Centers for Disease Control and Prevention until a leadership shakeup a couple of months ago. But he isn’t a scientist. And that has some scientists worried. He has yet to be confirmed by the Senate for the role.
In the meantime, the administration’s efforts are having a real impact on research. “We [NSB members] tried to stand for a continued investment in science, engineering, and technology, and in science education broadly,” says Stassun. “The administration will now be able to operate the agency the way that [it wants to, with] no governance body in the way.”
The big takeaway from a new government survey of infant formula is that the U.S. supply is largely safe. But experts and health officials say there are still steps that can be taken to make a product consumed by two-thirds of infants in the U.S. even safer.
One noteworthy finding from the Food and Drug Administration’s testing of 312 formula samples concerned per- and polyfluoroalkyl substances, or PFAS, also known as “forever chemicals.” The FDA detected five PFAS in the samples it tested, with the most common one — PFOS — found in half of all samples. Of those samples, the vast majority (95%) contained less than 2.9 parts per trillion (ppt) of PFOS.
What, exactly, does that mean? The FDA analysis doesn’t explain the PFAS results in much detail. But parents are bound to wonder, given that higher levels of exposure to PFAS, man-made chemicals used in products like nonstick cookware and stain-resistant clothing and rugs, have been linked to conditions including higher cholesterol, kidney and testicular cancer, and reduced vaccine efficacy.
NEWARK, N.J. — OxyContin maker Purdue Pharma is set to be dissolved and replaced by a company focused on the public good by the week’s end, as a massive legal settlement resolving thousands of lawsuits takes effect.
A federal judge on Tuesday delivered a criminal sentence to the company to resolve a Department of Justice probe — a last necessary step to clear the way for the settlement.
U.S. District Judge Madeline Cox Arleo made her decision after listening to hours of impact statements from people who lost loved ones or struggled with addiction themselves and requested she reject the negotiated sentence. While she didn’t go that far, she said she sympathized with people who bore the brunt of an epidemic linked to more than 900,000 deaths in the U.S. since 1999.
WASHINGTON — The Food and Drug Administration has named Katherine Szarama as the acting director of the Center for Biologics Evaluation and Research, which regulates vaccines, gene therapies, and the blood supply.
A Health and Human Services official confirmed the move, which was first reported by Politico, to STAT.
She is replacing Vinay Prasad, who left the agency on Thursday after a tumultuous tenure during which he issued a series of controversial decisions on rare disease drugs and vaccines. FDA Commissioner Marty Makary said in March that Prasad would return to the University of California San Francisco.
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.
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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.
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.