New treatment could lower liver fat, improve blood sugar control, and reduce cholesterol

A diagnosis of serious liver disease can feel like a slow countdown. Scar tissue builds quietly, the liver stiffens, and the risks climb toward cancer, heart attack, stroke, and even transplant. Now, researchers at McMaster University say a new drug candidate may be able to do what today’s care often cannot; stop liver scarring and even reverse it in preclinical studies.

The work was led by McMaster professor Greg Steinberg in collaboration with Espervita Therapeutics and researchers in the United States, France, and Australia. The team focused on liver fibrosis, a dangerous buildup of scar tissue that can follow metabolic dysfunction-associated steatohepatitis, also known as MASH. This condition often appears in people living with obesity or metabolic illness, including type 2 diabetes.

If the early findings hold up in humans, the research points toward a treatment that could lower liver fat, improve blood sugar control, reduce cholesterol, and address scarring at the same time. That combination targets a major gap in care, especially in Canada, where the researchers say no drugs are approved to treat MASH.

“Currently, we have no drugs approved in Canada to treat MASH,” said Steinberg, a professor in McMaster’s Department of Medicine and lead author of the research. “Right now, patients are typically prescribed a Mediterranean diet and some lifestyle and exercise recommendations, but no specific medical interventions have been approved in Canada. And while two therapies have recently received approved in the US and EU, these agents have only been shown to reduce fibrosis in only about one-third of patients.”

MASH sits at a harsh crossroads of metabolism and inflammation. It can start with fat buildup in the liver, then move toward tissue injury and scarring. Over time, fibrosis can change how the liver works and raise the odds of liver cancer.

The danger does not stay confined to the liver. Steinberg’s team notes that liver fibrosis can contribute to heart attack and stroke. Severe cases can end in transplantation. Yet many patients face a limited menu of options and long stretches of uncertainty.

Lifestyle changes can help some people. Diet and exercise may slow disease in certain cases. But Steinberg says the usual approach often fails to undo fibrosis that has already formed. The new drug candidate, according to the lab’s preclinical data, does more than slow damage; it appears to repair.

The drug candidate is called EVT0185. Espervita Therapeutics developed the compound; Steinberg is the company’s chief scientific officer, a shareholder, and a co-founder. Through a research partnership with McMaster University, scientists evaluated the compound in disease models and reported what they describe as strong curative and restorative effects.

In the study, researchers showed that EVT0185 can help control blood sugar levels, reduce cholesterol, and break down the fat buildup that drives fibrosis. Those outcomes matter because MASH often travels with diabetes and other metabolic problems, creating a cycle that is hard to interrupt.

The compound carries an unusual backstory. EVT0185 was first described as a potential liver cancer treatment after anti-tumor activity was detailed in a paper published in Nature. Steinberg says it still holds promise as a cancer therapy, but the new work suggests it may also have a role earlier in the disease pathway, before cancer develops.

“There’s a huge unmet need for agents that reduce liver fibrosis and also have a positive effect on blood glucose and cholesterol,” Steinberg said. “This drug candidate addresses a major therapeutic gap and has the potential to fundamentally change how we treat severe liver disease and, in turn, prevent liver cancer and other complications, including diabetes and heart disease.”

EVT0185 targets two enzymes Steinberg describes as critical for controlling fat synthesis and fat burning: ACLY and ACSS2. The research frames this dual targeting as a way to change how the body handles carbon, the building block that can end up stored as harmful fat.

Steinberg describes the effect as a “carbon release valve” in the body. Instead of allowing harmful material to pile up in the liver and bloodstream, the process diverts it out of the body through urine. In simple terms, the compound aims to stop the buildup at its source and redirect the overflow.

That matters because liver fibrosis does not happen in a vacuum. It grows from repeated injury and stress. If a therapy can reduce the drivers of that stress while also helping the body clear the excess, it may offer a path to both prevention and repair.

The results so far come from preclinical work. That stage is where researchers test a candidate in disease models to look for signs of benefit and to begin building a safety case. It is not the same as proving it works in people.

Even so, the timeline laid out by Steinberg suggests forward motion. He says EVT0185 is on track to enter clinical trials by 2027, pending a final slate of preclinical and toxicology work. Those steps matter because a drug must show it can be used safely before it can be tested broadly in human volunteers and patients.

For people living with MASH and late-stage fibrosis, that timeline can still feel far away. But it also offers something many patients lack: a clear sense that new options are moving through the pipeline, and that researchers are aiming for reversal, not just delay.

If EVT0185 continues to show strong results, it could reshape how clinicians approach severe liver disease tied to metabolic dysfunction. A therapy that reduces fibrosis while also improving blood sugar and cholesterol would fit the real lives of patients who often manage multiple related conditions at once. It could also shift care earlier, aiming to prevent liver cancer and other complications rather than only treating damage after it advances.

For research, the work highlights a strategy built around hitting two enzymes at the same time, instead of focusing on one pathway. That approach may guide other teams working on metabolic disease and fibrosis in different organs. The “carbon release valve” concept also offers a clear framework for studying how the body reroutes excess material under treatment, which could lead to new biomarkers and better ways to track response.

For public health, an effective anti-fibrosis drug could lower the need for transplants, reduce complications like heart attack and stroke linked to advanced liver disease, and improve quality of life for millions of people living with MASH.

Research findings are available online in the journal Cell Metabolism.

The original story "New treatment could lower liver fat, improve blood sugar control, and reduce cholesterol" is published in The Brighter Side of News.

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