For anyone who’s watched a loved one—or themselves—navigate the daily grind of type 1 diabetes, the diagnosis feels like a door slamming shut. The immune system, for reasons still not fully understood, turns on the pancreas and begins destroying the beta cells that make insulin. Once that process starts, there’s been no way to stop it. Until now, maybe.

A child with type 1 diabetes checks their blood sugar levels, a routine that could change if early intervention therapies prove effective. (Image: New Atlas)


In a new study published in The Lancet and presented at the 2025 European Association for the Study of Diabetes (EASD) Annual Meeting in Vienna, researchers from UZ Leuven in Belgium tested whether an existing immune-suppressing drug called antithymocyte globulin (ATG) could slow that destruction. ATG isn’t new—it’s been used for years to help transplant patients avoid organ rejection. But this time, scientists gave it a new mission: protect the pancreas in young people just diagnosed with type 1 diabetes.

The trial enrolled 117 participants between the ages of 5 and 25, all diagnosed within the past three to nine weeks. That early window matters. It’s when some beta cells are still hanging on, still producing insulin. The goal was to see if ATG could help keep those cells alive longer.

Participants were randomly assigned to receive one of four doses of ATG—or a placebo—via a two-day IV infusion. The researchers then tracked how much insulin their bodies could still make after 12 months, using a test called the mixed-meal tolerance test, which measures C-peptide levels. (C-peptide is a byproduct released when the pancreas makes insulin, so it’s a reliable marker of how well the pancreas is still working.)

The results? Promising, with a caveat. The highest dose—2.5 mg/kg—was the most effective at preserving beta cell function. But it also came with a steep cost: 82% of those patients experienced serum sickness, and 33% developed cytokine release syndrome, both immune-related side effects. That’s a tough trade-off, especially for kids and teens.

The sweet spot, it turns out, might be a lower dose. The 0.5 mg/kg group also showed significant preservation of insulin production, but with far fewer side effects—just 24% experienced serum sickness, and 32% had cytokine release syndrome. No deaths or lasting harm were reported across any group.

This matters because it’s the first time a therapy has shown real potential to change the course of type 1 diabetes after diagnosis—not just manage blood sugar levels. That’s a seismic shift. It means that instead of resigning to a lifetime of insulin injections and glucose monitoring, newly diagnosed patients might have a chance to hold onto some natural insulin production for longer. That could translate to fewer complications, better blood sugar control, and a higher quality of life.

It also signals a broader trend in medicine: the repurposing of old drugs for new uses. ATG is already on the market, which could fast-track its path to approval for this new indication. And because it’s not a brand-new pharmaceutical, it may be more affordable than cutting-edge biologics.

Still, questions remain. How long does the protective effect last? Could repeated doses extend the benefit? And how early is early enough to intervene?

For now, this study opens a hopeful chapter in diabetes care. If further trials confirm these results, we could be looking at the first real disease-modifying therapy for type 1 diabetes—a breakthrough decades in the making.