People who are colorblind may be missing a life-saving warning sign of bladder cancer. Analysis of the electronic health records of hundreds of people found that those with color vision deficiency (CVD), or color blindness and bladder cancer had significantly worse outcomes than patients with normal vision, according to a study published in Nature Health.

Warning signs may go unnoticed

Bladder cancer is a major health concern and one of the most common cancers worldwide, according to the World Health Organization (WHO). For many individuals, the first warning sign is blood in their urine. However, people with color blindness may miss this early clue that something is wrong because they struggle to distinguish red from shades of brown or green. The study authors suspected that this blind spot in cancer detection leads to dangerous delays in seeking care.

To determine whether this was the case, the team analyzed data from the TriNetX electronic health records network. This is a massive global database of anonymous medical files.

The researchers compared 135 colorblind patients with bladder cancer to a group of 135 patients with the same condition but normal vision. Each pair had the same age, race, sex and even the same health histories, such as diabetes or high blood pressure. They also compared 187 matched pairs with colorectal cancer.

Increased risk

The researchers found that over a 20-year period, the CVD group experienced a 52% higher risk of death compared to the non-CVD group. According to the study, the possible explanation for this is not any difference in cancer biology, but the nature of the disease itself.

Bladder cancer is usually painless at first, meaning the red color of blood is often the only early warning a person receives. If someone doesn’t feel any pain and cannot see the color, they may not know anything is wrong until later, when the cancer has invaded deeper tissues and becomes harder to treat.

For colorectal cancer, there was no significant difference in survival between the two groups. The researchers believe this is because colorectal cancer is often caught through screening or because some symptoms are felt, such as stomach pain.

The study authors point out that their conclusions are not definitive proof but rather a starting point for more research. Even so, these findings could change the ways doctors treat colorblind patients, as they comment in their paper: “These hypothesis-generating findings should increase clinicians’ suspicion of bladder cancer among patients with CVD and nonspecific signs of malignancy.”

A News & Views article on the research is also published in Nature Health.

Stanford University-led researchers report that tumor cells hijack mitochondria from immune cells, reducing anti-tumor immune function and activating cGAS-STING and type I interferon signaling that promotes lymph node metastasis.

Lymph nodes hold dense networks of immune cells and can become a site of tumor colonization. Mechanisms that let tumor cells subvert tumor-immune microenvironments to favor spread to lymph nodes remain incompletely understood.

Mitochondrial transfer, the movement of mitochondria between cells, is a mode of intercellular communication that reshapes metabolism, stress responses, and cellular function across diverse physiological and pathological settings. Recruiting outside mitochondria into cancer cells can enhance oxidative phosphorylation, promote survival under metabolic stress, and influence therapy resistance.

Uncertainty remains around whether mitochondrial transfer from distinct cell types elicits unique features and clinical behaviors in cancer cells. The consequences of mitochondrial transfer and any impact on tumor dissemination have been poorly characterized.

Lymph node metastasis is a critical early step in cancer progression that can create a systemic impairment of tumor control. Mechanisms by which tumor cells subvert early immune surveillance in lymph nodes are also incompletely understood.

Previous reports have found that T cells and macrophages can transfer mitochondria to cancer cells. The extent of mitochondrial transfer by other immune cells remains unclear, along with any connections to lymph node colonization.

In the study, “Mitochondrial transfer from immune to tumor cells enables lymph node metastasis,” published in Cell Metabolism, researchers tracked mitochondrial movement from immune cells into tumor cells and tested whether that transfer links immune impairment with lymph node metastasis through cGAS-STING and type I interferon signaling.

Experiments set out to address uncertainty around how tumor cells subvert tumor-immune microenvironments to favor spread to lymph nodes, while also probing whether mitochondria arriving from immune cells carry consequences beyond metabolic support.

Flow cytometry and confocal microscopy tracked mitochondria movement into tumor cells after implantation of tagged colon, breast, and melanoma cancer cells into mitochondria reporter MtD2 mice.

Researchers tagged colon, breast, and melanoma cancer cells so donor mitochondria could be detected inside tumor cells. Mouse experiments paired those tagged cancer cells with mice carrying a mitochondria reporter signal, allowing host mitochondria to be seen inside cancer cells at tumor sites and in draining lymph nodes.

Bone marrow transplantation created chimeric mice where the mitochondria reporter signal stayed within immune cells, tightening donor identity to hematopoietic compartments. Genetic differences in mitochondrial DNA between mouse strains provided a second way to detect donor mitochondrial material inside tumors.

Co-culture experiments placed tumor cells and immune cells together to watch transfer during direct contact and to test conditions that altered transfer rates, including low oxygen and inflammatory stimulation. Disruption of physical contact and of cell-to-cell transfer structures tested dependence on direct interaction.

Immune donor cells were separated into groups that retained mitochondria or lost mitochondria during contact with tumor cells, followed by readouts tied to antigen presentation and cytotoxic function.

Tumor cells that received mitochondria were compared with tumor cells that did not for immune-evasion markers and for gene expression patterns linked to type I interferon signaling and cytosolic DNA sensing.

Mitochondria caught crossing into tumor cells

Tumor cells acquired mitochondria from host cells across colon, breast, and melanoma models. Immune cells were identified as a donor source in bone marrow chimera experiments that restricted the reporter signal to hematopoietic cells. Draining lymph nodes carried a higher fraction of tumor cells with immune-derived mitochondria than primary tumors.

Direct physical contact supported transfer, with higher transfer under hypoxic stress and inflammatory cues. Disruption of transfer structures and knockdown of a transfer-related factor reduced transfer, paired with reduced lymph node metastasis incidence in reported mouse experiments. mtDNA polymorphism tracing added a second line of evidence that donor mitochondrial DNA could be detected in tumor material.

Immune weakening meets tumor escape programs

Immune cells that lost mitochondria showed reduced antigen-presentation and co-stimulatory machinery, with reduced activation and cytotoxic capacity reported for natural killer and CD8 T cells. Changes aligned with impaired immune surveillance in the co-culture systems described.

Tumor cells that received immune-derived mitochondria showed features linked to lymph node metastasis, including increased immune-evasion marker expression and activation of type I interferon pathways tied to cGAS-STING signaling.

Mitochondrial fusion and mtDNA leakage into the cytosol linked mitochondrial transfer to cGAS-STING activation. Inhibition of mitochondrial transfer machinery or inhibition of cGAS, STING, or type I interferon reduced lymph node metastasis in experiments.

Analyses of human datasets associated higher mitochondrial transfer signatures with lymph node metastasis and cGAS-STING pathway activation. Receiver prediction was limited when mitochondrial coverage was low and cell numbers were small.

Targets along the transfer chain

Authors identify immune-to-tumor cell mitochondrial transfer as a central mechanism that facilitates lymph node colonization through two coordinated effects. Loss of mitochondria disables anti-tumor immunity by diminishing antigen presentation and impairing cytotoxic function across multiple immune lineages, while immune-derived mitochondria activate the cGAS-STING pathway in tumor cells and induce a type I interferon program that promotes immune evasion and lymph node colonization.

Targeting mitochondrial transfer or the resulting cGAS-STING signaling represents a promising strategy to restrict lymph node metastasis, a critical early step in systemic cancer progression.

Engineers at the University of California have developed a new data structure and compression technique that enables the field of pangenomics to handle unprecedented scales of genetic information. The team, led by UC San Diego electrical and computer engineering professor Yatish Turakhia, describe their compressive pangenomics approach in Nature Genetics.

Pangenomics, a subset of bioinformatics, is the study of many different genomes from one specific species. This can provide a more holistic picture of the natural variation and mutations that occur within a species than using one singular reference genome. This has many practical applications, such as studying how genomic mutations lead to increased transmissibility or drug resistance in pathogens.

Challenges in current pangenomic methods

Although advances in genome sequencing technologies have reduced the cost and increased the speed of sequencing, the data structures and analysis tools needed to study and graphically represent the relationships between millions of sequenced genomes remain a challenge.

While graph-based data formats for pangenomes have become popular and widely adopted, they only represent the genetic variation in a collection of genomes, not their shared evolutionary and mutational histories. They also have large storage requirements that do not scale well.

“The data structures used for pangenomics research are critical because they determine not only how efficiently genetic data is represented, but also what the data can represent,” said Sumit Walia, an electrical engineering Ph.D. candidate at the Jacobs School of Engineering and co-first author of the study.

The research team, which includes engineers from the Genomics Institute at UC Santa Cruz, pioneered a new data structure and file format, called Pangenome Mutation-Annotated Network (PanMAN).

How PanMAN works and its advantages

PanMAN not only provides unmatched compression for pangenomes but also significantly advances the representative power by encoding additional biologically relevant information, including phylogenies, mutations, and whole-genome alignments.Their compressive pangenomics approach can perform analysis on compressed pangenomic data, allowing researchers to handle vastly larger scales of genetic data than currently possible.

“Our compressive technique with PanMANs allows doing more with less, greatly improving the scale and scope of current pangenomic analysis,” said Turakhia, the study’s corresponding author.

PanMANs are composed of mutation-annotated trees, called PanMATs, which store a single ancestral genome sequence at the root and annotate mutations, such as substitutions, insertions, and deletions, on the different branches.

Multiple PanMATs are connected in the form of a network using edges to generate a PanMAN. These edges store complex mutations, such as recombination and horizontal gene transfer data, which result in sequences involving multiple parent sequences and violate the vertical inheritance assumption of single trees.

This representation is compact as it exploits the shared ancestry among genomes, representing each mutation only once on the branch where it arose instead of duplicating them across individual sequences.

In addition, PanMAN was crafted to represent a rich set of biologically meaningful information that current pangenome formats lack. Some information in PanMAN is explicitly stored, such as mutations, phylogeny, annotations, and root sequence, whereas other information can be derived, such as ancestral sequences, multiple whole-genome alignment, and genetic variation.

So far, the researchers have used PanMAN to study microbial genomes. They have found that this method is the most compressible format among variation-preserving pangenomic formats, providing up to hundreds or even thousands of times more compression. For example, the team built the largest pangenome for SARS-CoV-2, using more than 8 million separate genomes of the virus.

Using their PanMAN method, this vast amount of genetic data only required 366MB of file storage space, which is roughly 3,000 times less storage than its corresponding whole-genome alignment that PanMAN encodes.

Constructing an alignment for SARS-CoV-2 genomes at this scale was itself a formidable challenge, which was addressed by another computational tool developed at Turakhia’s lab, called TWILIGHT.

Future directions

Now, the researchers are expanding their use of TWILIGHT and PanMANs from microbes to human genomes. Turakhia and Melissa Gymrek, a professor of computer science and engineering at UC San Diego, received a Jacobs School Early Career Faculty Development Award to advance this effort.

“Extending compressive pangenomics to human genomes can fundamentally transform how we store, analyze, and share large-scale human genetic data,” said Turakhia.

“Besides enabling studies of human genetic diversity, disease, and evolution at unprecedented scale and speed, it can depict detailed evolutionary and mutational histories which shape diverse human populations, something that current representations do not capture.”

Much like humans, microbial organisms can be fickle in their productivity. One moment they’re cranking out useful chemicals in vast fermentation tanks, metabolizing feed to make products from pharmaceuticals and supplements to biodegradable plastics or fuels, and the next, they inexplicably go on strike.

Engineers at Washington University in St. Louis have found the source of the fluctuating metabolic activity in microorganisms and developed tools to keep every microbial cell at peak productivity during biomanufacturing.

The work, published in Nature Communications, tracks hundreds of E. coli cells as they produce a yellow food pigment—betaxanthin—while growing, dividing and carrying out normal metabolic activities.

Understanding metabolic noise in microbes

“Like the behavior of a person, sometimes microbes are motivated to work hard, but they ‘get tired’ much more quickly and easily,” said Fuzhong Zhang, the Francis F. Ahmann Professor in energy, environmental and chemical engineering (EECE) and co-director of the McKelvey School of Engineering’s Synthetic Biology Manufacturing of Advanced Materials Research Center. Zhang is the corresponding author of the research, along with Ph.D. students Xinyue Mu and Alexander Schmitz.

Bioengineers and biologists have long observed large cell-to-cell variations in microbial metabolism, often called metabolic noise, or more generally, cellular noise. However, it has remained unclear what caused these differences and how frequently highly productive cells switch to low-productivity states. This lack of understanding has limited engineers’ ability to develop effective strategies to enrich hardworking, high-producing cells for biomanufacturing.

Answers lie in single cells’ fluctuating behavior, which is extremely challenging to study. Researchers must be able to measure a low-abundant metabolite along with the enzyme that produces it inside a tiny single cell while that cell grows and divides. To address this challenge, the team built microfluidic devices and engineered E. coli to produce a unique, bright-yellow metabolite—betaxanthin—that can be easily distinguished from thousands of other cellular metabolites.

New tools and strategies for productivity

These new advances allowed them to discover that betaxanthin production fluctuates rapidly, with cells switching from high-production to low-production states within a few hours. Approximately 50% of this betaxanthin noise comes from fluctuations in the enzyme responsible for producing betaxanthin, which arise from natural randomness (stochasticity) in gene expression. Fluctuations in cell growth rate account for less than 10% of the betaxanthin variability.

Using experimental data, the team developed computational models to test four different control strategies to ramp up bioproduction. The models showed that enriching cells that stochastically overproduce the enzyme leads to substantial increases in betaxanthin production. The team later confirmed this prediction in fermentation experiments.

“We create a gene circuit that allows cells with higher stochastic enzyme expression to grow faster,” Zhang said. “These cells also become high betaxanthin producers, giving us more product overall.”

The work is part of ongoing efforts at the McKelvey EECE department to develop new biomanufacturing capabilities in support of a zero-waste circular economy. This includes the challenging task of keeping microbial “workers” focused on making renewable products.

An international team of scientists, headed by a team at Nanyang Technological University, Singapore (NTU Singapore), has discovered a new way that could speed up the healing of chronic wounds infected by antibiotic-resistant bacteria.

Collaborating with researchers at the University of Geneva, the team’s preclinical study showed how a common bacterium, Enterococcus faecalis, actively prevents wound healing. The results of their collective studies in mice and in human cells showed that, unlike other bacteria, which produce toxins when they infect wounds, E. faecalis produces reactive oxygen species (ROS), which impairs the healing process of human skin cells.

The team identified extracellular electron transport (EET) as a previously unrecognized mechanism by which E. faecalis generates ROS, which, in turn, activates the unfolded protein response (UPR) in epithelial cells and impedes their migration following wounding. The study also demonstrated how neutralizing this biological process can allow skin cells to recover and close wounds.

Establishing a direct link between bacterial metabolism and host cell dysfunction, the study points to a potential new therapeutic strategy for chronic wounds. Co-senior and co-corresponding author, NTU associate professor Guillaume Thibault, PhD, at the School of Biological Sciences, and colleagues reported on their findings in Science Advances, in a paper titled “Enterococcus faecalis redox metabolism activates the unfolded protein response to impair wound healing,” in which they concluded, “Our findings establish EET as a virulence mechanism that links bacterial redox metabolism to host cell stress and impaired repair, offering new avenues for therapeutic intervention in chronic infections.”

The study was headed by Thibault and co-senior author Kimberly Kline, PhD, a professor from the University of Geneva, who is a visiting professor at the NTU Singapore Centre for Environmental Life Sciences and Engineering. The paper’s first author is NTU Research Fellow Aaron Tan, PhD.

Worldwide, chronic wounds represent a major health challenge, with an estimated 18.6 million people developing diabetic foot ulcers each year, according to figures cited by the NTU. Such wounds are a leading cause of lower-limb amputations and are frequently complicated by persistent infections that prevent healing. In Singapore, chronic wounds, including diabetic foot ulcers, pressure injuries, and venous leg ulcers, are increasingly common, with over 16,000 cases annually, particularly among older adults and people with diabetes.

E. faecalis is an opportunistic pathogen frequently found in chronic infections such as diabetic foot ulcers. These wounds are difficult to treat and often fail to heal, increasing the risk of complications and amputation. “Enterococcus faecalis is a gut commensal and opportunistic pathogen that causes difficult-to-treat biofilm-associated infections, including catheter-associated urinary tract infection, infective endocarditis, and chronic wound infections,” the authors wrote. “We previously showed that E. faecalis infection impairs wound healing.”

Antibiotic resistance is also an increasing concern in E. faecalis, with some strains resistant to several commonly used antibiotics, making certain infections difficult to treat. While such infections are known to delay healing, the biological mechanism behind this disruption has remained unclear to doctors and scientists. “… the extent to which E. faecalis metabolism actively interferes with host repair mechanisms is poorly understood,” the team further noted.

Through their newly reported research, Thibault and colleagues found that in E. faecalis, a metabolic process known as extracellular electron transport continuously produces hydrogen peroxide, a highly reactive oxygen species that can damage living tissue. Laboratory experiments showed that oxidative stress triggers a cellular defense mechanism known as the unfolded protein response (UPR) in keratinocyte skin cells, which are responsible for skin repair.

The unfolded protein response is normally used by cells to cope with damage by slowing down protein production and other vital activities, so that they can recover. Once activated, the stress response effectively paralyses the cells, preventing them from migrating to close the wound. “E. faecalis is the first example, to our knowledge, where a defined EET system is shown to drive ROS production that directly alters host stress signaling and function,” the scientists commented.

The researchers showed that a strain of E. faecalis genetically modified to lack the EET pathway produced significantly less hydrogen peroxide and was unable to block wound healing. This confirmed that the metabolic pathway was central to the bacterium’s ability to disrupt skin repair.

The team then tested whether neutralizing the hydrogen peroxide could reverse the damage. By treating affected skin cells with catalase, a naturally occurring antioxidant enzyme that breaks down hydrogen peroxide, the researchers reduced cellular stress and restored the cells’ ability to migrate and heal.

This, they suggest, offers a potential approach to tackle antibiotic-resistant E. faecalis strains other than trying to kill or inhibit them with antibiotics. In their paper, they concluded, “These findings not only establish a role for EET in ROS generation but also, through its interaction with the host UPR, establish it as a metabolic virulence mechanism by which E. faecalis disrupts epithelial repair, thereby presenting new opportunities for targeting chronic E. faecalis-driven pathologies.”

Added Thibault, who is also the assistant dean, international engagement, at the College of Science, “Our findings show that the bacteria’s metabolism itself is the weapon, which was a surprise finding previously unknown to scientists. Instead of focusing on killing the bacteria with antibiotics, which is becoming increasingly difficult and leads to future antibiotic resistance, we can now neutralize it by blocking the harmful products it generates and restoring wound healing. Instead of targeting the source, we neutralize the actual cause of the chronic wounds—the reactive oxygen species.”

As the study used human skin cells to demonstrate the mechanism, the findings are relevant to human physiology and may pave the way for new treatments for patients with non-healing wounds. The researchers suggest that wound dressings infused with antioxidants such as catalase could be an effective treatment in the future.

Because antioxidants such as catalase are already widely used and well understood, the scientists believe this strategy could shorten the path from laboratory research to clinical application, compared with developing a new drug. The team aims to move toward human clinical trials after determining the most effective way to deliver antioxidants through ongoing studies in animal models.

In their paper, the scientists suggested, “Future studies should examine the role of EET in vivo, its regulation and contribution within polymicrobial settings, and the potential for targeting redox metabolism to mitigate E. faecalis infections that are increasingly recalcitrant to antibiotic therapy.”

Liver failure claims thousands of lives each year as patients in the United States wait for a donor organ. Now, a research project at the University of California San Diego, funded by the Advanced Research Projects Agency for Health (ARPA-H), aims to change that by developing a fully functional, patient-specific, 3D bioprinted liver. The project, which falls under ARPA-H’s Personalized Regenerative Immunocompetent Nanotechnology Tissue (PRINT) program, provides up to $25,771,771 for a 60-month period.

The multidisciplinary team has the goal of creating “made-to-order” livers grown from a patient’s own cells. The approach could offer a safe, scalable alternative to transplantation that eliminates the need for donor organs and lifelong immunosuppressant drugs.

“When people think about 3D printing, they often imagine making gadgets like cellphone holders or toys, not human organs,” said Shaochen Chen, PhD, professor in the Aiiso Yufeng Li Family Department of Chemical and Nano Engineering at the UC San Diego Jacobs School of Engineering. “But the need for organ transplants is enormous, and 3D bioprinting is uniquely suited to address that challenge, as it allows us to personalize each organ to the patient. Our ultimate goal—the holy grail—is to help solve the organ shortage by printing real, living human organs that can restore health and quality of life.”

Chen and his lab have developed a technology capable of rapidly fabricating high-resolution biological tissues with complex, multi-cellular structures in just seconds rather than hours. Recently, they integrated artificial intelligence into the design and manufacturing process to help engineer sophisticated vascular networks. This, Chen explained, is one of the key challenges in scaling up from small tissue samples to full-sized, living organs.

The project could provide an on-demand source of functional liver tissue for transplantation, potentially saving the lives of more than 12,000 patients in the United States each year who are currently on the transplant waiting list. The approach could also significantly reduce healthcare costs and improve long-term outcomes for patients with chronic liver disease.

“For decades, the transplant community has dreamed of a future where the fate of thousands of patients each year is no longer determined by the scarcity of donor organs,” said Gabriel Schnickel, MD, professor of surgery at UC San Diego School of Medicine, chief of the Division of Transplantation and Hepatobiliary Surgery at UC Dan Diego Health. “This work has the potential to fundamentally change countless lives by moving that vision from aspiration to reality.”

The researchers are collaborating with Allele Biotechnology, an industry partner with expertise in personalized stem cell generation technologies and methods to efficiently produce different types of cells needed to bioprint livers for transplantation. The San Diego company also owns specialized facilities for cell manufacturing that meet regulatory standards. Together, the team plans to advance the process from laboratory-grade to clinical-grade production.

Unlike conventional 3D printing methods, this technology uses digitally controlled light patterns to solidify cell-laden materials layer by layer, allowing researchers to precisely recreate the fine microarchitecture found in living tissues, including intricate networks of blood vessels. Chen and his team launched a startup company, Allegro 3D (now Cellink), to translate the technology beyond the laboratory. As they worked to commercialize the bioprinting platform, they progressively advanced the system from an experimental prototype to an industrial-scale printer capable of producing much larger, more complex structures.

The investigational cancer vaccine, NOUS-209, was found to safely stimulate the immune system to target precancerous and cancerous cells in individuals with Lynch Syndrome (LS), according to a study from researchers at The University of Texas MD Anderson Cancer Center.

The results of a Phase Ib/II clinical trial, published today in Nature Medicine, provide early evidence that immune-based approaches, such as NOUS-209, may be able to intercept cancer before it develops, offering a potential new avenue for preventive care for high-risk individuals.

“Current management strategies for Lynch Syndrome patients—frequent screenings or elective preventive surgery—are life-changing interventions that help prevent cancer development but can significantly affect quality of life,” said principal investigator Eduardo Vilar-Sanchez, M.D., Ph.D., chair ad interim of Clinical Cancer Prevention. “By teaching the immune system to recognize and attack abnormal cells, this therapy offers a promising new approach to this patient population, who face a significantly higher risk of colorectal, endometrial, urothelial and other cancers.”

What is Lynch Syndrome?

Lynch syndrome is caused by inherited mutations in mismatch repair (MMR) genes, which normally help fix DNA errors. Patients with LS have a genetic predisposition to develop cancers with microsatellite instability and often develop cancers at a younger age than the general population, meaning they may benefit from increased screening and preventive strategies.

What is NOUS-209 and what did the researchers learn about the therapy in this study?

NOUS-209 is an experimental cancer vaccine that helps the immune system recognize cancer cells. It works by showing your immune system clear “practice targets” from cancer cells so it can learn to spot and attack the real ones in your body.

NOUS-209 was generally well tolerated, with no serious side effects related to treatment. All participants developed strong immune responses from T cells that recognize and attack cancer-related targets, and these responses increased further with annual retreatment. In laboratory testing, the vaccine-induced T cells were able to kill tumor cells and showed signs of long-lasting immune memory.

One year after treatment, researchers observed fewer precancerous lesions and no new advanced polyps, providing early evidence that NOUS-209 may help stop cancer before it develops.

What are the limitations of this study?

The Phase Ib/II study was relatively small (45 patients) and designed to evaluate safety and immunogenicity, rather than definitive clinical outcomes.

Next, researchers will work to understand how NOUS-209 can induce immune responses in larger and higher-risk populations of LS carriers. Optimal dosing schedules and durability of immune protection over multiple years also is under investigation.

Robert Kramer, former CEO of Emergent BioSolutions, allegedly earned more than $10.1 million by executing trades with information related to the company’s manufacturing operations that had yet to be made public.

The New York Attorney General has sued Robert Kramer, former CEO of Emergent BioSolutions, for allegedly engaging in insider trading by selling off stocks before an anticipated dip in the company’s shares.

“Kramer entered into the illegal trades while in possession of material nonpublic information regarding serious and unresolved contamination issues Emergent faced,” the complaint reads. Kramer gained more than $10.1 million in proceeds from these stock trades, the suit alleges. The lawsuit was filed Thursday with the Supreme Court of the State of New York.

At the heart of the lawsuit is a series of partnerships in mid-2020 between Emergent and AstraZeneca, which had an aggregate value of more than $260 million. Under the agreement, Emergent promised to manufacture the pharma’s virus-based COVID-19 vaccine, while also providing other contract development services such as analytical testing and drug substance processing.

Soon after the deals were forged, Emergent ran into “serious manufacturing difficulties,” Thursday’s lawsuit claims, namely the contamination of AstraZeneca’s vaccine. The contract manufacturer encountered “excess bioburden (bacteria) and elevated endotoxin” concentrations in several vaccine batches, which ultimately resulted in “the rejection and destruction of multiple batches.”

Kramer was aware of these issues as early as Oct. 6, 2020, the suit alleges.

Later that same month, the complaint claims, Kramer instructed his investment adviser to put in place a trading plan, which the former CEO executed on Nov. 13, 2020—“still in the midst of an internal investigation of the unresolved contamination and manufacturing problems that had not been disclosed to the public.” Ultimately, Kramer earned more than $10.1 million in proceeds from this trading plan.

Kramer had not engaged in such a trade since 2016, the lawsuit states.

The ex-CEO continued to carry out a handful of similar trades through January and early February 2021, acquiring and then immediately selling Emergent shares. Shortly thereafter, Emergent’s contamination problems became public, sending the company’s share prices on a decline “from which it has not recovered,” according to the lawsuit. Kramer announced his retirement from Emergent in June 2023.

The New York Attorney General is asking the court to direct Kramer to “disgorge all amounts obtained” from the alleged insider trading scheme and to pay all direct and indirect damages related to the incident.

The office has also filed a case against Emergent, but on Thursday announced that it had reached a settlement, with the company agreeing to pay $900,000. Emergent has also promised to bake more protections into its anti-insider trading policies.

Buying vaccine biotech Dynavax was an easy choice for Sanofi despite antivaccine moves by the Trump administration.

“It’s a good time to do vaccine BD and M&A,” according to Sanofi CEO Paul Hudson.

While vaccine sentiment is suffering amid the Trump administration’s rhetoric, Hudson says he’s playing the long game with Sanofi’s acquisition of Dynavax.

“With the uncertainty, if you’re a short-term thinker, you don’t move. If you’re a long-term thinker—which is what we have to be—then there are less people to compete against to make acquisitions,” Hudson told reporters at a media breakfast in San Francisco on day three of the J.P. Morgan Healthcare Conference.

To end 2025, Sanofi offered $2.2 billion to buy Dynavax. The center of that deal is the hepatitis B vaccine Heplisav-B. That the vaccine is for adults could help Sanofi overcome some of the vaccine hesitancy that is rising, particularly in America, Hudson said. “We know that the sensitivities are less in the adult context.”

And it was those sensitivities that set the stage for the French drugmaker to pay what Hudson called an “appropriate price” for Dynavax. Elsewhere on the company’s business development (BD) bingo card, he also pointed to Sanofi’s July 2025 acquisition of Vicebio for $1.6 billion, scooping up a combination vaccine for respiratory syncytial virus (RSV) and human metapneumovirus (hMPV).

“Those things will launch 5, 6, 7, 8 years from now. And so we have to assume that there’ll be a new administration or two between now and then,” Hudson said. “We don’t know what their sensitivities will be, but it’s okay, as long as there’s some objectivity in the regulator.”

Hudson hinted that there could be more deals to come in the vaccine space.

Sanofi’s legacy vaccine sales fell 8% in the third quarter and Hudson is predicting similar “softness” in the quarters to come. Hudson reiterated that the sales decline can be pinned on the “misinformation that is going around.” He noted the rise in measles cases as people opt out of vaccines.

“We think it will settle down and we’ll move through it,” Hudson said. Sanofi has not provided guidance for 2026 yet.

Hudson also spoke to recent vaccine schedule updates and other antivaccine actions at the Department of Health and Human Services (HHS). The CEO suggested that people are capable of educating themselves when it comes to vaccines in partnership with their care providers.

“The vast majority of people understand the benefit of vaccines and their lives and generations of their family have been protected that way,” Hudson said. “Not everybody looks to the top of the HHS to get people with their guidance on how to live their lives.”

He continued: “So I think people should be respectful of all guidance given, but I think talking to their own healthcare professional is still probably the best thing to do.”

The Next Moment

Vicebio and Dynavax’s programs may be years out from FDA review, but Sanofi’s flu-COVID combo, licensed from Novavax, is not. Hudson expects regulatory review to happen in 2027 or 2028.

That shot is “going to be the next moment, I think, for an acceleration on vaccine utilization,” Hudson said. The product will offer convenience with a one-and-done approach for both infectious diseases. And it will be the only non-mRNA COVID shot available in the U.S. for those who do not want to receive a shot featuring that technology.

“We think people are still very vaccine literate. We think they understand the reactogenicity or the tolerability challenges of mRNA,” Hudson said. Those post-vaccine reactions may have been tolerated during the global pandemic, but that’s not the case anymore, the CEO explained. He expects Sanofi will garner the over-55 and over-65 markets, particularly as the combo can offer a high dose needed for older people, who are at higher risk of death from the flu.

“While there may be debates on Facebook and other places, the over-65s, I think, are highly motivated to get protected,” Hudson said, “because they know they are the ones that are most vulnerable.”