A once-nightly oral pill helped control obstructive sleep apnoea in a large, phase 3 clinical trial presented at the 2026 ATS International Conference. The drug, called AD109, is the first therapy to treat OSA by addressing its underlying mechanisms and targeting the neuromuscular causes of airway collapse. The trial results will be published in the American Journal of Respiratory and Critical Care Medicine.
The trial, called SynAIRgy, showed that patients who took AD109 had fewer breathing interruptions during sleep, less oxygen deprivation, and improved blood oxygen levels overall. More than 40 percent of patients saw their OSA disease severity category improve, and 18 percent achieved complete disease control.
“These results provide encouraging evidence that targeting neuromuscular dysfunction can translate into meaningful clinical outcomes, aligning with our evolving understanding of the disease biology,” said first author Patrick John Strollo, MD, a sleep medicine physician at the University of Pittsburgh Medical Center.
Continuous Positive Airway Pressure (CPAP) is the gold standard treatment for OSA, but many patients are unable to tolerate treatment. AD109 could help fill that gap with an easier treatment option, Dr Strollo said.
“In many other chronic diseases, such as cardiovascular disease, asthma, or type 2 diabetes, it would be unthinkable for the majority of diagnosed patients to remain untreated or undertreated. Yet that remains the reality in OSA,” he said. “An oral pill that targets the underlying neuromuscular drivers of airway collapse during sleep could help address this gap and broaden the range of effective options for patients who remain untreated today.”
AD109 combines two medications, aroxybutynin and atomoxetine, which work together to support muscles in the throat and prevent the airway from sagging or collapsing during sleep.
For the trial, which ran for six months at 69 sites across the U.S. and Canada, researchers enrolled 646 adults with mild to severe OSA who couldn’t tolerate or refused CPAP.
Patients taking AD109 saw their apnea-hypoxia index, which measures the number of breathing interruptions per hour, decrease by about 44 percent, compared with 18 percent in the placebo group. Oxygen desaturation index (the number of times during the night that blood oxygen drops) and hypoxic burden (oxygen deficiency) also improved in the AD109 group.
Importantly, improvements were observed consistently across a broad range of patients, including those with varying severity levels and body types.
Along with improved outcomes, the drug showed an acceptable safety profile with mild, expected side effects. The most common side effects were dry mouth, nausea, insomnia, and difficulty urinating. Around 21 percent of patients discontinued therapy due to side effects.
Dr Strollo noted that the results will be published alongside a companion mechanistic review by ATS in the American Journal of Respiratory Cell and Molecular Biology.
“Together, these peer-reviewed articles connect late-stage clinical outcomes with the biological mechanisms that drive the disease, targeted by the mechanism of action of AD109, providing a more complete and integrated view of OSA and strengthening confidence in the approach,” he said.
AD109 has received Fast Track designation from the FDA for the treatment of OSA, recognising the significant unmet need for effective, well-tolerated pharmacologic therapies for OSA. Apnimed has submitted its New Drug Application (NDA) for AD109 to the FDA. Based on FDA feedback, Apnimed expects a potential PDUFA target action date in 1Q 2027, subject to FDA acceptance of the NDA for review.
Icing a sprained ankle or sore muscle, long used to reduce pain and swelling, may in the longer run delay recovery and prolong pain, new research suggests.
In a preclinical study published in Anesthesiology, McGill University researchers found that even though cryotherapy (icing) eased pain in the short term, recovery time was more than doubled in some cases.
“These results highlight a paradox: treatments that reduce inflammation and relieve pain in the short term may, in some cases, interfere with the biological processes required for full recovery,” said lead author Lucas Lima, a research associate at the Alan Edwards Centre for Research on Pain.
The findings add to a growing body of research questioning the long-term benefits of common anti-inflammatory strategies, said Lima. Previous studies have shown that medications such as acetylsalicylic acid (Aspirin) can also extend the duration of pain, and animal research has suggested icing may delay tissue repair.
The new study provides, for the first time, direct evidence that icing can also affect the duration of pain itself, based on experiments with mice mimicking inflammatory and exercise-related injuries.
Icing is commonly used as part of the RICE protocol, a standard approach to managing injuries that includes rest, ice, compression and elevation. It is widely used by athletes, clinicians and in everyday injury care, but there is limited evidence for its long-term benefits, said the researchers.
“Our results suggest we need to better understand when anti-inflammatory strategies are helpful and when they are not,” said senior author Jeffrey Mogil, James McGill Distinguished Professor and E. P. Taylor Chair in Pain Studies.
He emphasized the results are not yet directly applicable to humans. A clinical trial is underway to test whether the same effect appears in patients recovering from procedures such as wisdom tooth removal.
About the study
“Cryotherapy and Duration of Inflammatory Pain in Mice” by Lucas Lima and Jeffrey Mogil et al. was published in Anesthesiology. The study was supported by the Canadian Institutes of Health Research Foundation and the Louise and Alan Edwards Foundation.
A large South Korean study published by The BMJfinds no increased risk of psychiatric or neurodevelopmental disorders, such as ADHD and autism, in children whose mothers used sedative drugs (benzodiazepines or Z-hypnotics) during pregnancy.
Benzodiazepines and Z-hypnotics are used to alleviate anxiety and insomnia, which are among the most common conditions during pregnancy.
Previous studies have examined the short term safety of benzodiazepine and Z-hypnotic use in pregnancy, but evidence on their psychiatric and neurodevelopment effects in children remains scarce.
To fill this evidence gap, researchers used South Korea’s National Health Information Database to track nearly 3.8 million children born between 2010 and 2022.
Pregnancies exposed to benzodiazepines or Z-hypnotics were compared with unexposed pregnancies and with women who had used these drugs before but not during pregnancy (past users).
Twelve specific neurodevelopmental and general psychiatric disorders were assessed, including substance use disorder, schizophrenia, personality disorder, intellectual disability, autism, ADHD, and behavioural disorder.
Factors, such as mother’s age, income, underlying conditions and other medication use were also taken into account.
Among the 3 809 949 children, 94,482 (2.5%) were exposed to benzodiazepines or Z-hypnotics during pregnancy, 3 715 467 were unexposed, and 147 307 were born to past users.
During the tracking period of up to 14 years, a total of 10 060, 311 997, and 15 645 events occurred in the exposed, unexposed, and past user groups, respectively.
Overall, rates of psychiatric disorders were slightly higher (19.2%) in exposed children compared with 13.8% in unexposed children and 16.5% in the past user group.
However, these associations were no longer significant when the researchers used sibling analysis to disentangle drug effects from shared family, genetic, and environmental factors, and no increased risk was found for individual psychiatric disorders.
Further analyses were generally consistent with the main findings, although some estimates, such as exposure in early and late pregnancy, and longer durations of Z-hypnotic use specifically, remained modestly elevated in certain groups.
This is an observational study, so can’t establish cause and effect, and the researchers acknowledge that a prescription may not always reflect actual ingestion and their follow-up period may be insufficient to capture late onset conditions such as schizophrenia or personality disorders. What’s more, this study was not designed to assess the overall safety of these drugs but specific psychiatric outcomes in children.
However, use of a large, nationally representative database and rigorous methods to overcome confounding suggest the results withstand scrutiny.
As such, they say this study suggests “no substantial evidence that prenatal exposure to benzodiazepines or Z-hypnotics increases the risk of psychiatric disorders in children.”
Although these findings provide reassurance about neuropsychiatric safety, further research is needed to clarify the modest elevations seen in some analyses and help inform discussions when considering sedative therapy in pregnancy, they add.
In a linked editorial, researchers agree that this evidence is reassuring, but this does not mean that sedatives should be prescribed without caution.
Clinicians should be mindful of signals around prolonged use and late pregnancy exposure, while also balancing the risks of untreated maternal psychiatric illness, they write.
However, they conclude that this study “offers a compelling example of how observational research can generate reliable estimates of prenatal drug safety.
Hantaviruses are not new. They have circulated for decades in rodent populations, particularly in rats and mice. Humans can become infected if they are bitten or scratched by a rodent or by inhaling aerosolised particles. These are tiny bits of rodent urine, faeces or saliva floating through the air that are contaminated by the virus.
Infections between humans can be prevented by closely observing people who were exposed and isolating those who are sick. This limits the risk of further spread, as transmission generally requires close contact.
However, as an interdisciplinary group of scientists working on emerging infectious diseases, we argue that hantaviruses might pose a much bigger threat to African countries than currently known. We are concerned for three reasons.
Firstly, diagnostic testing capacity across much of the African continent remains limited. This is a real issue. In many rural settings, under-resourced diagnostic services may overlook sporadic cases. This may allow hantaviruses to spread without anyone noticing. Our medical expertise tells us that larger outbreaks are likely to be recognised eventually. But these delays in diagnosing the cases will slow down effective control measures.
Secondly, monitoring systems are lacking and likely to miss infections in wildlife and in human beings.
Thirdly, climate change and accelerating changes to the way land is used could increase the risk of spread of hantaviruses from animals to people. This is because global change may increase rodent populations and bring rats and mice into closer contact with humans.
For example, modelling studies in the Americas found broad zones with enzootic circulation (where an animal community always carries a certain disease). This is because many rodent species tend to live across a wide variety of environments where humans are also found. As human and rodent populations increase, the likelihood of encounters also increases. Some rodent species flourish in habitats shaped by humans or even in buildings. This poses a high risk for transmission of pathogens.
As a typical zoonosis (animal disease that spreads to humans), hantaviruses must be seen as a One Health issue. One Health is an approach that understands and takes into account the close connection between human, animal and ecosystem health. Hantaviruses cannot simply be seen as a clinical management or infection control issue.
It is really important that African governments set up better monitoring of wildlife so that they can detect when and where animal viruses like this are likely to spill over into the human population. This will help stop larger outbreaks of hantavirus, which can be deadly.
Weak surveillance may be allowing hantaviruses to spread unnoticed
In Africa, scientists have discovered several hantaviruses, including Sangassou virus in Guinea in small mammal species, such as rodents. More recently, hantaviruses were found in shrews and bats too – not just in rats and mice as previously thought.
The fact that hantaviruses may circulate in a much wider range of animals and environments than scientists originally realised makes their ecology and potential spillover risk into humans more complex.
One of the current problems facing Africa is that there hasn’t been enough research into the ecology of hantaviruses and which animals host them. There are very few genetic sequences available that would allow scientists to analyse interactions between viruses and hosts and the possible risk this poses to humans.
Combined with limited monitoring of the disease, Africa is experiencing a hantavirus surveillance gap. This gap needs to be closed because hantavirus infections and disease may be more widespread than many health systems assume.
Climate change and land use
Climate and land-use change influence rodent populations which host hantaviruses, and increase human-rodent contact. Hantavirus boomed in the US between 1993 and 1995 because El Niño brought very heavy rains and warmer winters, which led to a bumper crop in seeds that rodents eat. This improved nutrition led to a massive increase in rodent numbers. Outbreaks elsewhere have likewise been linked to weather phenomena.
More rodents means more of them seeking food and shelter in the vicinity of humans. More competition for resources leads to more aggressive behaviour between animals and biting transmits the virus. Because El Niño episodes are predicted to become more frequent and intense in future, hantaviruses are likely to affect African countries more and more.
In Africa, land-use change is likely to play an increasingly important role in hantavirus ecology and emergence, as was the case with Lassa fever (another virus spread by rodents) in Nigeria and Guinea. Deforestation, agricultural expansion, mining activities, road construction and urban growth are transforming natural habitats across many regions of the continent. These environmental changes can force populations of rodents, shrews and bats to move into farms, villages, peri-urban settings and water sources used by people.
When humans expand into previously undisturbed habitats in search of land, food, or economic opportunity, this also creates a new opportunity (known as an ecological interface) where hantaviruses and other zoonotic pathogens may circulate more easily between wildlife reservoirs and humans.
What needs to happen next
When people and wildlife come into close contact, viruses like Andes can jump from animals and begin transmitting between humans. Hantaviruses can cause severe human disease and this is likely far more widespread than currently recognised.
Fortunately, the risk of Andes hantavirus spreading beyond the cruise ship passengers and crew and their close contacts is small. But Sars coronavirus and monkeypox virus are recent examples that some zoonotic viruses have the potential to spread rapidly and widely among humans.
Virological and ecological studies of wildlife reservoirs and surveillance of possible hantavirus infection and disease in humans in endemic regions are needed. This requires specialised diagnostic tools combined with samples from rodents in areas where humans have disturbed their habitat and have since experienced unexplained febrile illness (acute high fevers).
Once there is firm evidence of human disease, scientists and medical professionals will be able to argue for the widespread use of diagnostic tests. The results of these tests will determine how much of a threat the virus poses to human health.
Genetic sequencing and data-sharing partnerships can then help connect animal, environmental and human signals into a clearer picture of risk.
The greatest gap currently may be the failure to identify where, how, and under which environmental conditions spillover events occur before outbreaks emerge.
Strengthening surveillance to identify high-risk interfaces, emerging transmission zones, and drivers of spillover is therefore essential to anticipate potentially pathogenic African hantaviruses before larger outbreaks occur.
Researchers at WashU Medicine and collaborating institutions have developed a novel computational tool that can accurately identify a genetic problem in a gene called RFC1 that is linked to certain forms of peripheral neuropathy. Peripheral neuropathy is one of the most common neurological disorders and can cause pain, sensory loss, imbalance and weakness. It affects 12–20% of all people in the U.S. and can affect up to 30% of adults over age 65. The new research is published in Annals of Neurology.
The disease-causing change, known as an RFC1 repeat expansion, has been associated with neuropathy, but its role across the broader spectrum of patients with unexplained, or “idiopathic,” neuropathy has remained unclear. One reason is that these repeat expansions — in which the set of DNA “letters” AAGGG is repeated many more times than normal — are difficult to detect using standard genetic testing methods.
The research team led by senior author Sheng Chih (Peter) Jin, an assistant professor of genetics and of pediatrics, and first author Zitian Tang, a graduate student in Jin’s lab, set out to bridge this technical gap by developing a new computational pipeline coupled with machine learning that can reliably identify and classify repeat expansions from genome sequencing data. Using this approach, they found that RFC1 repeat expansions may account for more than 2% of cases of idiopathic peripheral neuropathy.
The new tool offers a more affordable and reliable way to look for this extremely complex genetic variation in both clinical and research settings. The finding also supports broader genetic testing for people with unexplained peripheral neuropathy, including those who have muscle weakness as well as sensory symptoms. The team has made the tool public on GitHub, which could help expand testing to help more patients receive an accurate diagnosis and give families clearer information about the genetic causes of their condition.
