Until law, GLP-1 drugs were used to treat diabetes, obesity and even the recent evidences suggest that it could as well be used to treat chronic kidney problems. There is yet another research, published in JAMA Psychiatry on February 25, titled Once-Weekly Semaglutide in Adults With Alcohol Use Disorder: A Randomized Clinical Trial that explores if GLP-1 receptor agonist semaglutide reduce alcohol consumption and cravings in adults with alcohol use disorder.

What Do Studies Say?

The research was conducted over a period of 9 weeks, where in the randomized clinical trial, the participants who were administered semaglutide, it led to reductions in some but not all measures of weekly consumptions. It also reduced weekly alcohol and craving related to placebo, and also led to a greater relative reduction in cigarettes per day.

The research also found that weekly injections of semaglutide, which is the active ingredient in weight loss drugs like Wegovy also helped reduce cravings in people with alcohol use disorder.

The lead author Christian Hendershot said that these findings will help in developing new approaches to treat alcoholism. "Two drugs currently approved to reduce alcohol consumption aren't widely used. The popularity of Ozempic and other GLP-1 receptor agonists increases the chances of broad adoption of these treatments for alcohol use disorder," said Hendershot in news release by the University of Southern California's Institute for Addiction Research, where he is the director.

The study is government-funded research and was funded by the National Institute on Alcohol Abuse and Alcoholism, part of the National Institutes of Health.

How Was The Study Conducted?

The study was small, and took in account for only 48 adults over two months, thus experts say that it is not yet clear how safe these drugs are for people who do not need to lose weight. Though the results do add up with the evidence form animal studies on drugs like Ozempic and Wegovy on how it helps manage cravings, not just for food, but also for tobacco and alcohol. Scientists are also studying these drugs on smokers, people with opioid addiction and cocaine users.

Co-author Dr Klara Klein of the University of North Carolina at Chapel Hill who treats people with obesity and diabetes said, "This is such promising data. And we need more of it. We frequently will hear that once people start these medications that their desire to drink is very reduced, if not completely abolished."

Why Does It Work So Well Against Alcoholism?

The GLP-1 receptor agonists work by mimicking hormones GLP-1 in the gut and brain that regulates appetite and feelings of fullness. This response is what helps one lose weight, and what helps one curb their craving for alcohol. These drugs that mimic the functioning of your brain, which is responsible to tell your body when to stop consuming, are the same hormones that tell your body about other kinds of consumptions, including alcohol. Therefore by consuming the weight loss drugs one can treat alcohol use disorder.

However, the researchers have pointed out on the limited data on the research and have suggested to continue using the three approved drugs by the National Institute on Alcohol Abuse and Alcoholism and Substance Abuse and Mental Health Services Administration, namely, Disulfiram, Naltrexone, and Acamprosate to treat alcohol use disorder until large studies confirm these findings.

The US Food and Drug Administration (FDA) recently approved the first drug for Alexander disease, a rare and progressive neurological disorder. Alexander disease is marked by symptoms like seizures, slow development, muscle weakness, difficulty in walking and problems with speech and swallowing.

The FDA approved Zanvastro (zilganersen) for children and adults afflicted with Alexander disease. Being the first approved treatment for the condition, the drug is designed to directly target the abnormal protein buildup, one of the major factors that drives the disease.

Talking about the landmark drug, Emily Freilich, MD, Director of the Division of Neurology I at the FDA’s Center for Drug Evaluation and Research said, “For patients with Alexander disease and their families, there have been no approved treatment options, only supportive care while the disease progresses. Today’s approval is a landmark moment for this community, offering the first therapy that addresses the underlying cause of this rare and serious disease.”

What Is Alexander Disease?

According to the FDA, Alexander disease is extremely rare as it affects fewer than one in a million people. Alexander disease is a rare, genetic neurodegenerative disorder that is caused due to mutations in the GFAP gene. GFAP gene promotes the production of glial fibrillary acidic protein, a type of protein found in the central nervous system.

GFAP is found primarily in astrocytes, a type of specialised cells in the brain and spinal cord that support and protect nerve cells.

In Alexander disease, abnormal GFAP accumulates inside these cells. This leads to formation of cumulative protein called Rosenthal fibres. This disrupts the normal function of astrocytes and ultimately damages the nervous system.

In simple terms, the issue is not that the brain suddenly loses a particular protein. It is that a genetically altered version of GFAP is produced and progressively accumulates where it should not. This is why Alexander disease is considered an astrogliopathy, a disorder which is primarily driven by astrocyte dysfunction.

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Symptoms Of Alexander Disease

The disease can present very differently depending on the timing of its onset. In infants and young children, it can cause delay in development, loss of previously acquired essential skills, seizures, unusually large head, muscle weakness, feeding difficulties and problems with movement. Some severe early-onset cases may progress rapidly.

Juvenile and adult forms can be slower and may involve speech and swallowing difficulties, abnormal way of walking, muscle stiffness, poor coordination, weakness, breathing or sleep problems and autonomic dysfunction.

As symptoms of Alexander disease may overlap with many other neurological disorders, its diagnosis remains challenging. Doctors typically diagnose it by combining key findings in brain MRI with genetic testing for a disease-causing GFAP variant.

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What Makes The New Drug Different?

Until now, the treatment for Alexander Disease has largely focused on managing individual symptoms, like seizures, feeding problems and difficulties with movement, speech or swallowing.

Taking a different approach, Zanvastro, a type of RNA-targeted medicine is designed to reduce production of the abnormal GFAP protein.

Its goal is to lower the amount of disease-driving protein before it can continue accumulating and damaging astrocytes. The drug is administered once every three months as an injection into the spinal canal.

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Zanvastro's FDA Approval

The FDA's approval arrived after a controlled study involving 49 patients aged two and older, along with an open-label substudy involving four children younger than two.

Among patients aged five and older who already had walking difficulties, those receiving Zanvastro had significantly better walking speed after 61 weeks than others.

For children aged two to four, researchers used broader measures of motor development because walking speed alone is not a reliable measure at that age. Those children showed improvement in motor skills, while the control group declined.

The most common side effects included vomiting, back pain, cough, headache and post-lumbar-puncture syndrome. The FDA also warned that aseptic meningitis has been reported.

Alexander disease has long been a condition in which doctors treated complications but had no approved therapy that aimed at the biological process causing the disease.

Zanvastro does not reverse genetic mutations themselves. Instead, it targets one of the consequences of those mutations by reducing production of abnormal GFAP.

As Ionis Pharmaceuticals CEO Brett P. Monia said following the approval, the treatment allows the field to move “beyond managing individual manifestations of the disease to addressing its underlying biology.”

Creating a new senior position to focus entirely on technology and artificial intelligence, the US Food and Drug Administration (FDA) has just got its first AI chief. The move could change how the agency evaluates medicines, pharmaceutical products and new technologies in the healthcare sector.

On September 8, the US Department of Health and Human Services (HHS) announced that Jared Seehafer, M.S. will be FDA’s first Deputy Commissioner for Technology and Artificial Intelligence. The newly formed role puts AI and technology directly into the agency’s senior leadership structure.

Seehafer has around two decades of experience working at the intersection of software, AI and FDA-regulated medical technology.

As deputy commissioner, he will be the FDA’s senior leader for technology, software and AI and will help establish an agency-wide strategy for their use.

Why Does The US FDA Need An AI Chief?

From identifying potential drug candidates to analysing clinical-trial data and developing medical devices, the use of AI is increasing rapidly across pharmaceutical and healthcare industries.

But, for regulators, AI presents a different challenge. The FDA must determine whether AI-generated or AI-assisted evidence is reliable enough to support decisions about the safety and effectiveness of a product.

The agency has already begun moving in this direction. In May 2026, the FDA issued draft guidance on the use of artificial intelligence to generate information or data intended to support regulatory decision-making for drugs and biological products.

The FDA has also been exploring AI and cloud-based approaches to make clinical trials more efficient, including a pilot focused on early-phase trials.

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AI May Make Drug Approvals Faster

One of the biggest opportunities is using artificial intelligence to process large volumes of information that regulators already receive during drug development and review.

AI could eventually help regulators identify patterns in clinical-trial data, analyse safety aspects, review large regulatory submissions and support more efficient assessment of complex datasets in health and pharmaceutical sector.

But does faster automatically mean better? AI systems may produce incorrect outputs. So regulators need to understand how an algorithm reached a particular conclusion before relying on it for decisions that affect patients. That makes validation, transparency, data quality and human supervision critical in this area.

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The Future Of Drug Regulation

The appointment comes alongside several other leadership changes at the FDA. HHS also named Michael Davis as permanent director of the Center for Drug Evaluation and Research, Karim Mikhail as director of the Center for Biologics Evaluation and Research, and Bret Koplow as director of the Center for Tobacco Products.

The broader message from HHS is that the FDA wants to modernise its regulatory infrastructure while accelerating innovation.

“We are building an FDA that moves faster, demands excellence, and delivers results for the American people,” HHS Secretary Robert F. Kennedy Jr. said. “These leaders will drive the reforms needed to confront our nation’s most serious health challenges and strengthen American leadership in medical innovation.”

FDA Acting Commissioner Kyle Diamantas said the appointments were intended to help build the workforce and infrastructure needed to “accelerate innovative” work across the agency.

Small-cell lung cancer (SCLC) is one of the most aggressive forms of lung cancer. It tends to grow rapidly, spread early and often returns even after initially responding well to treatment.

A new drug combination from Amgen and AstraZeneca has shown a significant overall survival benefit in patients with extensive-stage small-cell lung cancer (ES-SCLC), offering a new way to delay the disease's return and progression.

On September 8, the companies said that the Phase III DeLLphi-305 trial found that combining Amgen's tarlatamab, marketed as Imdelltra, with AstraZeneca's durvalumab, marketed as Imfinzi, significantly improved overall survival compared with Imfinzi alone.

Small-Cell Lung Cancer Is Difficult To Treat

The cancer can initially respond well to chemotherapy, but that response often does not last for a long time.

Many tumours become resistant to treatment, allowing the disease to return and become harder to treat. Research has described recurrent SCLC as frequently resistant to further therapy.

This is particularly challenging disease goes in extensive stage, where the cancer has already spread beyond the lung. Even with current treatments, the median overall survival for ES-SCLC remains around one year.

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How Does The New Drug Combination Work?

The two medicines attack the cancer through different mechanisms. Durvalumab is an immune checkpoint inhibitor. It blocks PD-L1, a protein cancers can use to evade the immune system, helping immune cells recognise and attack cancer cells.

Tarlatamab is a bispecific T-cell engager. It is designed to attach to DLL3 on small-cell lung cancer cells and CD3 on T cells, effectively bringing immune cells into contact with the cancer cells so they can destroy them. DLL3 is found on the surface of SCLC cells in about 85%-96% of patients but is minimally expressed on healthy cells.

In the trial, 563 patients whose disease had not progressed after initial treatment with Imfinzi plus platinum chemotherapy and etoposide were randomly assigned to receive either the combination or Imfinzi alone as maintenance treatment.

The combination improved overall survival, progression-free survival and response rate. No new safety concerns were identified.

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Hope For Patients With SCLC

The significance of the findings lies in effectively controlling the cancer after initial treatment, when the disease is at the highest risk of returning.

Jacob Sands, MD, Associate Chief of the Lowe Center for Thoracic Oncology at Dana-Farber Cancer Institute, said: “Given the aggressive nature of small cell lung cancer, many patients quickly relapse on current therapy and never reach second-line treatment.” He added that the results suggest the potential to reshape the natural history of the disease.

Susan Galbraith, AstraZeneca's Executive Vice President of Oncology Haematology R&D, said the results showed an “unprecedented improvement in overall survival” for patients with this highly aggressive cancer.

The full trial data are yet to be presented at a medical meeting and will be submitted to regulatory authorities.