Revvity reports that its Signals Software business is launching Signals for Startups, a new program designed to help emerging biotech companies adopt scalable informatics capabilities earlier in their growth journey.
Built for early-stage biotechs, the program combines access to Signals software with guided onboarding and best-practice configurations for smaller biotechs to help accelerate innovation, improve scientific productivity and shorten time-to-value, according to a company spokesperson.
Startup biotechs are often under pressure to move quickly with limited IT, informatics, and operational resources while managing increasingly complex discovery data. Signals for Startups addresses this challenge with a purpose-built, scalable Signals environment that helps teams focus on science while establishing a strong digital foundation from day one, explains Kevin Willoe, president of Revvity Signals Software, adding that out-of-the-box configurations for large and small molecules enable companies to accelerate adoption, standardize data, and enhance collaboration on a proven, scalable informatics infrastructure.
“Signals for Startups addresses a critical need for emerging biotech companies that want to move fast without creating data and workflow challenges that limit their ability to scale,” he continues. “By combining startup-friendly access with guided onboarding and scalable Signals workflows, we are helping early-stage teams build the digital foundation they need to advance discovery, support investor readiness and grow with confidence.”
Signals for Startups is expected to be available in the U.S., Europe, the Middle East, and Africa later this month.
WASHINGTON — Biotech companies are lobbying the Trump administration to exclude treatments for rare diseases from programs that lower brand drug prices in Medicare.
The Rare Disease Company Coalition met last week with the White House Office of Management and Budget to discuss two pilot programs that are part of President Trump’s plan to get drugmakers to lower prices in the United States to levels charged in other rich countries, a policy generally referred to as most-favored nation.
Alzheimer’s disease (AD) and many other forms of neurodegeneration share a common culprit. In these diseases, tau proteins that normally stabilize neuronal microtubule filaments within nervous system networks instead form noxious knots and gradually disrupt the circuits they would otherwise preserve.
Scientists at Sanford Burnham Prebys have now shown that a different protein known as SORLA offers protection against the effects of these lethal loops. The results of the researcher’s’ study in mice suggests that future research may yield new treatments capable of boosting this protein’s ability to defend the brain.
Timothy Huang, PhD, assistant professor in the Center for Neurologic Diseases at Sanford Burnham Prebys, is senior and corresponding author of the team’s published paper in Science Advances, titled “SORLA up-regulation suppresses pathological effects in aged tauopathy mouse brain,” in which they concluded “These findings reveal a protective role for SORLA in multiple aspects of tauopathy pathogenesis and highlight its potential as a therapeutic target.”
Normally, tau proteins are found throughout the brain and nervous system, helping to maintain the shape and structure of our neuronal wiring. But in certain diseases, including Alzheimer’s disease, tau proteins clump together inside nerve cells, forming what are known as tau tangles. These toxic tangles are linked to cognitive impairment and nerve cell death in diseases known as tauopathies. “In AD, amyloid-β (Aβ) plaques and neurofibrillary tangles (NFTs) comprising hyperphosphorylated tau accumulate in brain,” the authors explained.
The new study focused on the safeguarding capabilities of protein known as SORLA. “A role for the trafficking receptor SORLA (Sortilin-related receptor containing LDLR class A repeats) in reducing Aβ levels has been well established,” the investigators continued. “… however, relatively little is known with respect to whether and how SORLA can potentially affect tau pathology in vivo.”
Timothy Huang added, “In the last 15 or 20 years, considerable data has come out from our lab and other groups showing that SORLA can suppress one of the hallmarks of Alzheimer’s disease—amyloid-beta generation and accumulation. Very little was known, however, about whether SORLA affected the tau tangles reflected on the other side of the coin in Alzheimer’s disease.”
SORLA is expressed in both neurons and glia in mouse and human brain, the authors noted. For their newly reported study the team began by crossbreeding mice that produce extra human SORLA protein, with PS19 (P301S) mice that develop tau tangles, brain atrophy and cognitive deficits. This new mouse model enabled experiments to determine SORLA’s effects on tau protein buildup and its resulting harms.
Their studies showed that an overabundance of SORLA protein protected against a number of biological processes linked to the formation of tau tangles and progression of neurodegeneration. These include reducing the addition of too many phosphate groups to tau—known as hyperphosphorylation—and the ability of misshapen tau to serve as “seeds” that attract more tau and form clumps. This protection also extended to preservation of the synapses at the junction between neurons and the brain’s ability to adjust these connection points—which is called synaptic plasticity. “Using complementary approaches, we show that SORLA overexpression attenuates ventricular enlargement, tau phosphorylation and seeding, synaptic loss, impaired synaptic plasticity, and glial hyperactivation in the PS19 mouse brains,” the team wrote in summary.
An overabundance of SORLA protein protects against a number of biological processes linked to the formation of tau tangles and progression of neurodegeneration. These include reducing the addition of too many phosphate groups to tau, known as hyperphosphorylation. In these biopsy images, less phosphorylated tau—stained to appear green—has accumulated in the bottom sample overexpressing SORLA. [Tim Huang, Huijie Huang, Sanford Burnham Prebys]
“When you upregulate SORLA, you can suppress the negative effects found in tauopathies,” said first author Huijie Huang, PhD, a staff scientist in the Huang lab at Sanford Burnham Prebys. “We found there was less brain atrophy and less tau accumulation, which was very exciting to see.”
Because some people have mutations that disable the gene carrying the code for SORLA, Sorl1, the scientists wanted to compare the outcome of having extra SORLA to having none of it at all. Tests of mice genetically modified to lack Sorl1 told a very different story. “The opposite turned out to be true when we deleted the ability to produce SORLA proteins,” said Timothy Huang. “A lack of SORLA exacerbated the harmful effects observed in tauopathies.”
To address how extra SORLA or a lack of SORLA were either ameliorating or aggravating diseases featuring tau tangles, the research team used a combination of sequencing techniques capturing the levels of all proteins and gene expression in each cell, as well as mapping the spatial relationship of RNA and proteins within brain tissue. The scientists found that upregulated SORLA prevented problematic protein production changes in the synapses between neurons while also suppressing other drivers of tauopathy disease progression. They also observed that extra SORLA tamped down on disease-related gene expression patterns in brain cells known as glial cells that support and protect neurons in many ways. “One particularly notable finding that we can build on is the upregulation of a member of the plexin-B family of receptors in the absence of SORLA,” said Huijie Huang.
“There are unique drugs that can target this class of receptors that we may be able to apply to tau-related dementia disorders,” suggested Tim Huang. “One potential future direction is to repurpose these drugs to target overactivation of glial cells and perhaps reverse some of the phenotypes in tauopathies.”
The scientists also want to better understand what happens in each individual cell type when they upregulate or downregulate SORLA. “While it is not possible to specifically determine how cell-specific modulation of SORLA can affect tau using the global transgenic overexpression/deletion models used here, we are interested in further characterizing specific effects of SORLA on tau in neurons, and the extent of SORLA modulation on glia in influencing overall tau pathology,” they stated. The team plans to graft human neurons or glial cells into the mouse brain to study the effects of different SORLA mutations.
“Mouse cells and human cells are different,” said Tim Huang. “Because we’re looking at human disease, it’s more informative if we can observe the modulation and dysfunction of SORLA in the context of a human cell inside of a diseased brain environment.”
This continued research will reveal more knowledge about the ability of SORLA to safeguard against the toxic effects of tau tangles, and how to develop new treatments or repurpose existing therapies to benefit patients suffering from Alzheimer’s disease and other tau-related dementia disorders.
The human brain continues developing beyond the teenage years, with crucial changes involving decision-making and emotional regulation extending into the mid-to-late 20s. Researchers at Albert Einstein College of Medicine have identified a biological process in mice that offers new insight into how memory circuits mature during this period of brain development.
The study published in PLOS Biology titled, “Retrosplenial cortical reorganization during late adolescence introduces instability of contextual memory circuits,” found that a key memory region of the mouse brain undergoes a period of remodeling during late adolescence, causing memories formed earlier in life to become temporarily more difficult to retrieve before resurfacing with less precise detail. The findings identify a biological mechanism that may explain how access to memories changes during development.
The study focused on the retrosplenial cortex (RSP) and discovered that protective mesh-like structures, called perineuronal nets, stabilize memory circuits and unexpectedly diminish during late adolescence before rebuilding in adulthood. The changes were confined to the RSP and were not observed in the nearby hippocampus, another brain region essential for memory.
“We’ve known for years that the brain continues developing through adolescence and young adulthood,” said senior author Jelena Radulovic, MD, PhD, professor of neuroscience, psychiatry, and behavioral sciences at Einstein. “Our findings begin to explain what that developmental process looks like in one of the brain’s memory circuits and how it can influence the way earlier experiences are recalled.
Previous studies suggested that the memory circuits reached maturity during early adolescence. Instead, results showed that an important stabilizing system temporarily weakened during late adolescence before recovering in adulthood.
The timing is notable because it corresponds to a period now recognized as one of continued brain maturation in humans. According to the National Institutes of Health, the brain continues developing and maturing into the mid-to-late 20s.
“The behavior matched the biology,” said lead author Hui Zhang, PhD, a research fellow at Einstein. “The retrosplenial cortex is responsible for older, more established memories. As its stabilizing structures declined, access to memories formed earlier in life became less reliable.”
To determine how these brain changes affected behavior, the researchers trained mice to associate a specific environment with a mild foot shock. The mice remembered the experience and froze when returned to the same chamber. Weeks later, many of the mice trained during early adolescence no longer showed that fear response, while mice trained during adulthood retained stable memories over the same period.
When the adolescent mice later experienced another test in a different environment, they once again responded to the original setting, demonstrating that the memories had become temporarily inaccessible rather than erased.
The researchers traced these changes to a decline in key structural proteins that help build and maintain perineuronal nets, along with reduced activity of growth factor, TGFβ2. When TGFβ2 activity was restored, the mice regained their ability to retrieve memories formed earlier in life.
By mid-adulthood, many of those memories resurfaced spontaneously, although they had become less precise. Rather than responding only to the original environment, the mice generalized their fear to unfamiliar settings. The researchers note that this pattern resembles the “reminiscence bump,” a well-known phenomenon in which adults disproportionately recall memories from adolescence and early adulthood while often remembering the emotional significance of an experience more readily than its specific details.
The findings may also have implications beyond memory. Schizophrenia and major depression often emerge in humans during late adolescence. The authors suggest that changes in this developmental process could contribute to vulnerability to psychiatric disorders in genetically susceptible individuals. Additional research is needed to evaluate whether similar mechanisms occur in humans.
One of Rhode Island’s most-wanted fugitives — a former doctor convicted of sexual assault but on the run for 20 years — appears to have been living a secret life as a biotech executive.
Ronald Fischer, 70, was arrested last week by federal and Rhode Island authorities after they tracked and boarded a 56-foot sailboat cruising off the coast of New Jersey. The former anesthesiologist disappeared in 2005 while on trial for first-degree sexual assault.
The boat was registered under the name Richard Graydon, an alias used by Fischer, U.S. Marshals said. That is the same name as a doctor and seasoned drug development executive hired last March by Immix Biopharma, a Los Angeles-based biotech company, as its new chief medical officer.
MilliporeSigma opened a new €25 million BioReliance® testing facility at the company’s global headquarters in Darmstadt, Germany. The facility expands access to commercial drug substance and drug product release testing as well as stability testing for biopharmaceutical companies developing and commercializing therapies in Europe, according to the company.
“As demand for biologics and novel therapies continues to grow, our customers need reliable, compliant testing capabilities closer to where their products are developed and commercialized,” said Paolo Carli, head of advanced solutions for the life science business of Merck KGaA. “Our new testing facility combines best-in-class analytical characterization services with more than 75 years of BioReliance expertise to help our European customers move critical therapies toward patients with greater speed and confidence.”
The 2,000-square-meter facility is designed to help customers meet European requirements for in-region drug substance and drug product release testing and to expand the company’s ability to support customers from drug development through commercialization. The site will also offer GMP-compliant stability studies for monoclonal antibodies and cell therapies, addressing the growing demand for biologics testing across Europe.
Located close to major clinical trial sites in Germany, France, Spain, the Netherlands, Belgium and Italy, the Darmstadt facility is strategically positioned to support biopharmaceutical companies seeking to release drug products into European markets, pointed out Carli. By adding these capabilities in the heart of Europe, the company is strengthening its support for customers managing increasingly complex development, quality and regulatory requirements, he added.
A MilliporeSigma spokesperson noted that the BioReliance sites form a global testing network that allows customers to scale across geographies and work with the company across continents. Among the company’s leading technologies is the Blazar® platform, which moves the biosafety testing paradigm from traditional methods to rapid molecular approaches to significantly reducing testing timelines for virus detection.
The Aptegra® CHO genetic stability testing streamlines a previously complex and time-intensive process into a single assay, continued the spokesperson.
MilliporeSigma lists the opening of the Darmstadt facility as one of several significant investments the company has made to grow its global contract testing footprint. In 2024, the company opened a €290 million biosafety testing facility in Rockville, MD, and expanded biosafety testing capacity by 40% across its Glasgow and Stirling sites through a €22 million investment. The company also cites the new BioReliance facility as reflecting the firm’s continued commitment to its global headquarters in Darmstadt, where €2.5 billion has been invested since 2015.
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Data from a new study suggest that a form of hyperhidrosis, or excessive sweating, may be due to genetic mutations that result in the overstimulation of the nerves that control the sweat glands. These findings, which are reported in Science Advances, could open a door to targeted treatments for the condition using existing medicines. Full details of the findings are provided in the paper titled “A neurocutaneous NaV1.8 channelopathy underlies a genetic subtype of primary idiopathic hyperhidrosis.” The international study is led by scientists at Vrije Universiteit Brussel.
Excessive sweating, which affects roughly two to five percent of the population, causes more than just discomfort. The impact of the condition on the daily lives of people living with it can be very severe. Patients often sweat so profusely that they have to change clothes several times a day. Many avoid social contact, experience shame, and develop depression. Yet the condition is often seen as a superficial skin problem and patients often do not receive appropriate care.
That could change thanks to the findings from this study which is the culmination of 10 years of research done by scientists in the lab of Frank Bosmanbs, PhD, at Vrije Universiteit Brussel and their collaborators at Johns Hopkins University. To pinpoint a genetic basis for hyperhidrosis, the scientists analyzed the DNA of more than 180 patients. They discovered defects in the Nav1.8 ion channel, which normally functions as a biological gate that regulates electrical signals in the nervous system.
Specifically, in patients with hyperhidrosis, the gate is left too wide open due to a genetic predisposition. As a result of this, the nerves are constantly overstimulated and in a state of activity, which results in excessive sweating often triggered by emotional or stress-related stimuli. To dig deeper into their theory, the scientists developed an experimental mouse model. Because mice only sweat from their paws, the team developed a microscopic measurement method to count sweat droplets using an iodine-starch mixture.
They found that mice that had the same genetic defect as hyperhidrosis patients also sweated excessively. Furthermore, once the scientists administered a substance that blocked the overactive nerve signals, their symptoms decreased significantly and reversibly. However the genetic picture is more complex. Bosmanbs and his team found a patient who had inherited an inhibitory nerve mutation but still sweated excessively due to a separate mutation in a local water channel within the sweat gland. It suggests that there are different biological pathways that can lead to the same overstimulation that results in hyperhidrosis.
Though the genetic picture is a complex one, the scientists believe that their findings offer the prospect of better treatments for this condition. Currently, some severe forms of hyperhidrosis are treated by severing the sympathetic nerve pathways in the chest. While effective, this treatment is both invasive and can have unwanted side effects. With a deeper understanding of the genetic basis of the condition, scientists may be able to better predict which patients are likely to get the most benefit from localized treatment of the sweat glands, systemic medication or nerve-targeted therapies. Another potential treatment avenue is drug repurposing, which is supported by the evidence from the mouse studies. However, further testing via controlled clinical trials is required.
A vaccine to prevent pancreatic cancer, targeting common KRAS mutations, was found to be safe and stimulated KRAS-specific T-cell responses in 90% of study participants who were at high risk of developing pancreatic ductal adenocarcinoma (PDAC), according to Phase I clinical trial results. After a median follow-up of 16.5 months, none of the participants developed pancreatic cancer, and some of the precancerous lesions shrank or stopped growing. The study represents the first proof of concept for the use of vaccines for interception of pancreatic cancer in human patients.
PDAC is an aggressive cancer that is often diagnosed at advanced stages and carries a low (five-year) survival rate. Approximately 10% of cases are associated with hereditary predisposition caused by pathogenic mutations in specific cancer susceptibility genes that are passed down from parent to child. The disease evolves over time from precursor lesions such as pancreatic intraepithelial neoplasia and intrapapillary mucinous neoplasms.
“Individuals at high risk due to hereditary predisposition or to the presence of a concerning pancreatic lesion detected on imaging usually undergo surveillance to monitor for changes over time,” said Neeha Zaidi, MD, associate professor of oncology at the Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins University. “If there is a high enough concern for transformation to cancer or if early cancer is detected, the current standard of care is surgical resection. However, the chances of recurrence are up to 80%, and many precursor lesions to pancreatic cancer are microscopic and thus undetectable by imaging.”
The researchers wanted to test if intercepting cancer development through noninvasive approaches could provide an effective strategy to prevent PDAC and improve survival in high-risk individuals. “Prevention and interception save lives and reduce the morbidity associated with cancer development and progression. This is especially important for cancers whose early-onset frequency is increasing and for which we do not have effective methods for early detection,” said Elizabeth Jaffee, MD, FAACR, deputy director of the Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins.
Mutations in the KRAS gene are the main oncogenic drivers in more than 90% of PDACs. The researchers previously developed mKRAS-VAX, an off-the-shelf synthetic long peptide vaccine targeting the six most common KRAS mutations found in PDAC and in most pancreatic precancer lesions.
In the new study, the team conducted a Phase I clinical trial to assess vaccination with mKRAS-VAX in 20 individuals at high risk of PDAC due to hereditary predisposition and radiographic evidence of a pancreatic lesion, typically in the form of a small cyst.
“The goal of this study was to test the safety of the vaccine and induction of durable immune responses,” said Jaffee. She added that the trial was based on preclinical data demonstrating the ability of a KRAS-targeted vaccine to prevent progression of early precancers in a genetically engineered mouse model of KRAS-driven pancreatic cancer.
Study participants received mKRAS-VAX via subcutaneous injections according to a prime-boost vaccination strategy, with priming doses on weeks one, three, and five and a boost dose on week 13. Blood was collected at different time points, and optional annual follow-up visits were offered for long-term immune monitoring.
Results showed that the vaccine stimulated mutant-KRAS-specific effector and central memory T-cell responses in 90% of participants. These responses remained detectable in the blood for up to two years after vaccination. “This long-lasting response is particularly noteworthy when assessing for possible interception of cancer, which requires long-lasting immunity,” said Zaidi. “In addition, the vaccine was safe and well tolerated, supporting its use in larger cancer interception studies.”
After a median follow-up of 16.5 months, none of the vaccinated individuals developed cancer. The researchers evaluated changes in cyst size as an exploratory clinical endpoint and found a higher rate of cyst reduction or resolution among the vaccinated individuals (37.5%) relative to an unvaccinated cohort with similar characteristics (6.8%).
“This research underscores the need for further funding to support the development of strategies that can intercept and prevent cancer development in high-risk individuals. More studies are needed to find the best vaccine approaches, the best targets, and the ideal timing for vaccination,” concluded Jaffee.
According to the authors, the study’s limitations include the small size and the fact that the trial was not designed to assess the clinical efficacy of the vaccine. “We observed evidence of stability or regression of the pancreatic cysts in association with the induction and durability of KRAS-specific T-cell responses,” said Michael G. Goggins, MD, professor of pathology, medicine, and oncology and the Sol Goldman Professor of Pancreatic Cancer Research at Johns Hopkins University School of Medicine. “However, larger studies are needed to demonstrate that this effect was in fact due to the vaccine.”
![An overabundance of SORLA protein protects against a number of biological processes linked to the formation of tau tangles and progression of neurodegeneration. These include reducing the addition of too many phosphate groups to tau, known as hyperphosphorylation. In these biopsy images, less phosphorylated tau—stained to appear green—has accumulated in the bottom sample overexpressing SORLA. [Tim Huang, Huijie Huang, Sanford Burnham Prebys]](https://www.genengnews.com/wp-content/uploads/2026/07/Low-Res_FIGURE1-panel-G-300x223.jpg)