The Oxford biotech will present new mouse data on MTRX31, a drug it says works on how cells use fuel rather than on appetite.
Fifteen minutes is all Xavier Jacq gets. On Wednesday, 30 September, in Milan, the chief scientific officer of MitoRx Therapeutics will stand up at the 62nd Annual Meeting of the European Association for the Study of Diabetes (EASD) and talk about a study in mice. It is a short slot for a drug that the company says works differently from the obesity medicines most people have heard of [1].
The meeting itself runs from 28 September to 2 October at the Allianz MiCo convention center in Milan, and Jacq’s talk is in Warsaw Hall. Its authors are listed as Jacq, Roberta Torregrossa, Rick Cousins, Norman Law and Jonathan Rees.
The drug is MTRX31, a small molecule from the Oxford-based biotech. Many of the best-known weight loss drugs work in part by dialing down appetite. MitoRx says MTRX31 is designed to reduce fat that has ended up in the wrong places by restoring healthy mitochondrial metabolism, without suppressing appetite. Mitochondria are the power plants inside our cells, where fuel gets burned for energy, and the company’s starting point is that in some people with obesity they stop doing that job well.
A specific slice of patients
MitoRx is aiming at what it calls high-risk obesity. By the company’s estimate, that describes about 25–40% of people with obesity. It comes with a recognizable set of features: fat packed around the organs (visceral fat), insulin resistance, fat that spills into tissues where it doesn’t belong, and mitochondria that aren’t working properly. You may have seen it called metabolically unhealthy obesity. A diabetes conference is a natural place to talk about it, given that insulin resistance sits right in the middle of the description.
Those patients, MitoRx points out, face a disproportionate risk of fatty liver disease, its more aggressive cousin steatohepatitis, type 2 diabetes and cardiovascular disease caused by clogged arteries. That list overlaps heavily with the conditions that eat into healthy years later in life.
Reading the talk title slowly
The title of the presentation gives away the mechanism if you read it slowly. MTRX31, it says, induces weight loss in diet-induced obesity (DIO) mice “by switching metabolism from fat to carbohydrate oxidation.” Oxidation just means burning. On a first read, that sounds backwards, since you would expect a weight loss drug to burn more fat, and it would be no surprise if that is where most of the questions in Milan land.
MitoRx describes what is happening as a reset of the balance between the two fuels. According to the company, that balance becomes attenuated in obesity, and MTRX31 restores it. Scientists call the body’s ability to swap between fuels metabolic flexibility. Picture a dimmer switch that has been stuck on one setting for years, and a drug that gets it moving again.
The release doesn’t go further on how, understandably saving the detail for the presentation. The new data will cover the drug’s mode of action, along with structural biology work that MitoRx says points to a single, well-characterized molecular target.
The mouse study was also run at thermoneutrality. That means housing the animals at a temperature where they don’t need to burn extra energy just to stay warm, which takes one variable off the table.
What MitoRx says the mice showed
In the DIO model, the release says, MTRX31 produced significant reductions in body weight and fat mass, preserved lean mass and improved metabolic parameters. MitoRx also says it delivered greater and more durable weight loss than tirzepatide, a widely used obesity drug, at the doses evaluated.
All of that comes from the company’s own announcement, and none of it comes with figures. Doses, timelines and the size of the difference will have to wait for the slides. Mouse results have a long history of not carrying over neatly to people, and a curtain-raiser press release is not a peer-reviewed paper.
The lean mass claim is the one worth watching. When people lose weight, some of what comes off can be muscle, and muscle is something most of us would like to hang on to as we get older. Durability matters too, given how often weight returns once treatment changes. If MTRX31’s preclinical profile held up in humans (a big if), it would speak to two things people want from weight loss beyond the number on the scale.
The longevity angle sits in the mitochondria themselves. Declining mitochondrial function is one of the most discussed features of aging biology, and MitoRx is testing whether nudging it back toward health can rebalance metabolism in a condition tied to so many age-related diseases. Whether it does anything of the sort in people is unknown.
A webcast of the presentation will be available to conference attendees through the EASD website after the event. MitoRx is based in Harwell, Oxford, with an additional laboratory in Babraham, Cambridge, and its release refers only to preclinical work, so human data remain to come.
