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Cholesterol Drug May Weaken Ovarian Cancer’s Metastatic Defense

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1 month ago

May 12, 2026

The accumulation of fluid in the belly, known as ascites, is something that women with advanced ovarian cancer may know all too well. The results of research by a team at Duke University School of Medicine now suggest that, more than causing discomfort, this fluid may protect cancer cells from a form of cell death known as ferroptosis, helping cancer cells survive and spread. The studies also indicated that a decades-old cholesterol-lowering drug, bezafibrate, may be able to disrupt that protection.

The findings, derived through lab experiments and an analysis of patient samples, do not show that bezafibrate treats ovarian cancer. But they do suggest that changing the environment that cancer depends on could make it more vulnerable to existing cancer treatment.

“Doctors have mostly viewed ascites as a symptom rather than an active driver of disease,” said Jen-Tsan Chi, PhD, a professor in the department of molecular genetics and microbiology and co-leader of the Cancer Biology Program at the Duke Cancer Institute. “We’ve learned it gives cancer a survival advantage, which fills a major gap in understanding how ovarian cancer spreads.”

Chi is senior and corresponding author of the team’s published paper in Nature Communications, titled “Ascites protects against ferroptosis and enables the peritoneal growth of ovarian cancer.” In their paper, the authors concluded, “Our findings identify ascites as a key determinant of ferroptosis resistance in metastatic OVCA and highlight its role in promoting tumor survival and dissemination within the peritoneal cavity.”

The peritoneum is a frequent site of metastasis in ovarian cancer (OVCA), the authors explained, and this is often accompanied by the accumulation of ascites in the peritoneal cavity. And while ascites is observed in other diseases such as liver cirrhosis, it’s most often associated with metastatic OVCA. The fluid occurs in 90% of those with advanced ovarian cancer. Doctors will drain ascites to ease pain, improve mobility, and make breathing easier, which offers patients relief even if it doesn’t stop the disease.

“Due to the enrichment of cellular and acellular factors, the ascitic fluid is reported to harbor a growth-promoting and immune-evading environment for cancer cells and is thought to serve as a medium for cancer cell dissemination and tumor progression and metastasis,” the team continued. However, they noted, “Despite its prevalence, ascites and its role in the peritoneal growth of OVCA remain poorly understood.”

According to the newly reported study findings, ascites also acts as a shield, helping cancer cells evade a specific form of cell death called ferroptosis. Ferroptosis is a kind of cellular rusting. It happens when iron inside a cell reacts with certain fats, causing the cell membrane to break apart. Many metastatic cancer cells—those that float freely through the abdomen looking for new places to grow—are naturally vulnerable to this kind of damage. “… we and other groups have reported that detached and metastasizing OVCA cells are especially vulnerable to ferroptosis, a form of cell death characterized by iron dependency and an irreversible accumulation of lipid hydroperoxides,” the authors wrote.

The study in Nature Communications shows how they survive anyway. For their research, the scientists bathed cancer cell lines and patient-derived tumor cells in ascites collected from patients, and observed how they responded to ferroptosis triggers. “Nothing is currently known about how ascites may influence OVCA cells’ ferroptosis,” they noted. “Given the common occurrence of ascites with peritoneal metastasis, ascites may be crucial for the peritoneal spread of OVCA.”

From left, Duke University School of Medicine researchers Susan K. Murphy; Andrew Berchuck, MD; Yasaman Setayeshpour, PhD, and Jen-Tsan Ashley Chi, PhD, are studying how a common class of cholesterol drugs, called fibrates, can strip away a key defense used by ovarian cancer cells, making them more vulnerable to treatment. [Duke University School of Medicine/Mark Dolejs] — (From Left) Susan Murphy, Andrew Berchuck, Yasaman Setayeshpour, and Jen-Tsan Chi pose in the lab. Research accepted to Nature Communications led by Chi, professor in MGM, integrative immunology, and medicine, found that a cholesterol drug may make it harder for ovarian cancer cells to survive. In lab studies, fibrates weakened the protective effect of abdominal fluid that helps tumors resist a type of cell death, known as ferroptosis. Chi is also a professor of biomed engineering, cell biology and pharmacology and cancer biology and a member of DCI. [Mark Dolejs for Duke University School of Medicine]

The team found that the fluid protected cancer cells by changing how the cells store fats and control iron levels, effectively blocking cell death. The protection required only trace amounts. As little as 2% immersion shielded cancer cells from destruction, even though in patients these cells are entirely enveloped by the fluid.

“What surprised us was how selective this effect was,” said first author Yasaman Setayeshpour, a graduate student in molecular genetics and microbiology at Duke School of Medicine. “Ascites didn’t protect the cancer cells from other well-known types of cell death, like apoptosis or necrosis—it only blocked ferroptosis.

“To figure out why, we broke ascites down into major parts, like lipids, proteins, and small molecules, and tested what happened when each was removed. When we took the lipids out, the protective effect disappeared. That told us lipids are the key reason ascites helps these cancer cells survive,” Setayeshpour said.

The researchers also found an unexpected helper in the form of bezafibrate, an older type of cholesterol-lowering drug that is used to lower triglycerides by altering how the body processes fats. “The idea behind testing lipid-lowering drugs was to mimic what happens when lipids are removed from ascites,” Setayeshpour explained.

The studies showed that bezafibrate restored sensitivity to ferroptosis, but only when ascites was present. On its own, the drug did not trigger cell death, nor did it slow tumor growth in mice. The researchers found that the drug’s impact hinged on the cancer’s surroundings, in this case, the fat-rich fluid bathing the tumor. The studies showed that targeting this environment, using repurposed drugs like bezafibrate, could leave cancer cells more exposed to existing cancer treatments. “Given the intrinsic vulnerability of metastatic cancer cells to ferroptosis, these data suggest that ascites-mediated protection represents a critical mechanism supporting peritoneal survival,” the team noted. “Importantly, re-sensitization to ferroptosis by bezafibrate raises the possibility that therapeutic targeting of this pathway may limit peritoneal dissemination.”

Chi said the finding could have implications beyond ovarian cancer. Other cancers, including colorectal and pancreatic cancers, can also spread within the abdominal cavity. “These findings may also extend beyond ovarian cancer to other metastatic settings, including peritoneal colorectal cancer and pleural, brain, or spinal metastases,” the authors stated.

“This work shows how much the environment around a tumor matters,” Chi said. “Biological fluids like ascites don’t just give cancer cells a place to move. They actively help drive how cancer spreads.”

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STAT+: Trump administration revisits policy to close Medicare drug price negotiation loophole

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2 hours ago

June 12, 2026

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WASHINGTON — The Trump administration on Friday proposed to change a policy that is designed to prevent drugmakers from avoiding Medicare price negotiation by adding active ingredients to drugs.

The policy is part of an annual proposed rule that establishes the process that the Centers for Medicare and Medicaid Services uses to choose the next 20 drugs and biologics for price negotiation. Those drugs will be announced by Feb. 1, 2027, and their negotiated prices will take effect in 2029. The administration also considered a similar policy last year but put off a decision to study it further.

Medicare must wait seven to 11 years after a product is approved by the Food and Drug Administration before it can negotiate its price, depending on the type of medicine. Biologics that are typically administered in doctor offices get more time than drugs taken orally.

Continue to STAT+ to read the full story…

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Hantavirus One-Shot mRNA Vaccine Fully Protects in Syrian Hamster Model

Published

5 hours ago

June 12, 2026

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Last month, the Andes virus outbreak on a Dutch cruise ship departing from Argentina brought a transmission context for hantavirus, that was previously unprecedented, to the forefront. The Andes virus is the only member of the hantavirus family that is capable of efficient person-to-person spread through close contact with respiratory secretions. Other hantaviruses are typically spread through contact with infected rodents, making the Andes virus a much more significant public health threat.

While at sea, the outbreak spread among passengers and crew, infecting 13 people and killing three. The cruise passengers have since returned to their home countries, 23 in total. Because a person can carry the virus for weeks before showing any symptoms, health agencies are facing a complex challenge of identifying everyone who was exposed. There are currently no vaccines or preventive treatments approved for the virus; this travel-related outbreak brought the need for vaccine development to the forefront.

Researchers at The University of Texas Medical Branch (UTMB) had previously developed and tested two mRNA vaccines against intramuscular Andes virus challenge in golden Syrian hamsters (“1-methylpseudouridine-modified or non-modified mRNA modalities encoding the envelope glycoproteins, Gn and Gc, in a single open reading frame.”)

When tested in the Syrian hamster model, both mRNA vaccines were efficacious in hamsters using a two-dose regimen. Recognizing that a fast-moving international outbreak doesn’t allow time for patients to wait weeks between shots, the team retested the vaccines to determine whether a single dose would be effective.

Now, a new report shares the finding that the vaccine provided full protection against the Andes hantavirus after a single dose.

This work is published in The Lancet in the paper, “Single-dose mRNA vaccines against Andes hantavirus.”

Alexander Bukreyev, PhD, head of the Laboratory of Viral Pathogenesis and Vaccine Development at UTMB, said that the group is working to fast-track these single-dose vaccines into human clinical trials.

The results exceeded expectations. When testing the vaccines in an animal model that mimics human disease, the scientists found that a single shot provided 100% protection against a lethal dose of the virus. Even when the researchers significantly lowered the dosage to a fraction of the original amount, the results remained definitive.

“Every vaccinated animal remained completely healthy and showed no symptoms or weight loss,” said Michelle Meyer, PhD, senior scientist in the Bukreyev Laboratory. “When we looked at the tissues from the vaccinated animals a month after infection, the virus was entirely gone. The vaccines triggered a powerful immune response, creating protective antibodies in as little as 14 days.”

Because the Andes virus can take a relatively long time to make a human severely ill, these fast-acting vaccines could serve a dual purpose, possibly functioning as an emergency tool for people who have already been exposed.

“If given quickly to high-risk contacts during an outbreak, such as the Andes virus situation on the cruise ship, the vaccines could theoretically jump-start their immune systems fast enough to intercept the virus—stopping it from replicating and preventing them from getting sick or spreading it further,” Bukreyev said.

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SonoThera Raises $125M to Develop Ultrasound-Mediated Genetic Medicines

Published

6 hours ago

June 12, 2026

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Biotechnology company SonoThera has raised $125 million in an oversubscribed Series B financing round. The financing was led by Vida Ventures, with participation from ARK Invest, CureDuchenne Ventures, Leaps by Bayer, Otsuka Pharmaceutical, SymBiosis, UCB Ventures SA, Vivo Capital, and existing investors ARCH Venture Partners, Alexandria Venture Investments, Duquesne Family Office, Illumina Ventures, Johnson & Johnson Innovation – JJDC, Medical Excellence Capital, RA Capital, and Vertex Ventures HC.

SonoThera will use the funds to advance its lead programs in Duchenne muscular dystrophy (DMD) and autosomal dominant polycystic kidney disease (ADPKD) in the clinic. The funds will also support efforts to expand its pipeline of targeted redosable genetic medicines across multiple organ systems and scale its proprietary platform technologies for safe, targeted therapy delivery.

The company’s platform combines a proprietary ultrasound-mediated delivery technology dubbed RIPPLE, with a payload engineering platform dubbed PORE. The platforms are designed to support the development of DNA and RNA therapeutics, gene editing, and gene silencing approaches. SonoThera is using its tech to develop genetic medicines that it claims will address key limitations of conventional gene therapies including delivery challenges, payload size constraints, immune responses, safety events, and difficulties with redosing.

As Kenneth Greenberd, PhD, SonoThera’s co-founder and CEO, stated “we founded SonoThera to take a fundamentally different approach, with a platform designed to broaden the therapeutic possibilities of the field. We believe our technology has the potential to expand the range of diseases addressable by genetic medicines while enabling more precise, durable, safer, and repeatable therapies for patients.”

SonoThera has already demonstrated the targeted delivery and expression capabilities of its platform across multiple tissues, including skeletal muscle, heart, liver, kidney, adipose, and brain. It has also shown that it can deliver large payloads such as full-length dystrophin for DMD and RNA-based payloads for gene silencing applications in preclinical studies.

The company expects to initiate its first clinical trial in DMD in 2027.

Commenting on the financing, Rajul Jain, MD, managing director at Vida Ventures, said “we believe SonoThera, with its RIPPLE delivery and PORE payload engineering technologies, has the potential to unlock opportunities in diseases with significant unmet need that have been previously inaccessible to other genetic medicine approaches.”

In connection with the financing, Jain and Rakhshita Dhar, MS, vice president & head of Healthcare Venture Investments at Leaps by Bayer, have joined SonoThera’s Board of Directors.

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