For families facing a novel diagnosis of type 1 diabetes, the immediate aftermath is often a race against time. There is a fleeting window—known as the “honeymoon phase”—where the body still produces some of its own insulin, offering a critical opportunity to intervene before the disease reaches its full onset.
New research suggests that an inexpensive, decades-old drug typically reserved for organ transplant surgeries may be able to extend this window, effectively slowing the progression of type 1 diabetes in newly diagnosed patients. The study, published Sept. 27 in the journal The Lancet, found that a low dose of an immune-suppressing medication can preserve insulin-producing beta cells with significantly fewer side effects than higher doses.
The medication, known as polyclonal antithymocyte globulin (ATG), works by modulating the immune system to prevent it from destroying the beta cells in the pancreas. In type 1 diabetes, the immune system mistakenly attacks these cells, which are responsible for producing insulin—the hormone that allows glucose to enter cells for energy. When these cells are lost, glucose builds up in the bloodstream, leading to the lifelong requirement for external insulin therapy.
By intervening early, clinicians hope to maintain residual beta cell function, which is linked to a reduced risk of long-term complications, including heart and kidney disease.
Finding the “Sweet Spot” for Dosage
While previous studies had already indicated that high doses of ATG could reduce beta cell loss, the intensity of the treatment often came with severe immune reactions. The latest trial sought to identify the lowest effective dose to develop the treatment safer, particularly for children.
The study followed 117 participants between the ages of 5 and 25 who had been diagnosed with type 1 diabetes within nine weeks of the trial’s start. Researchers tested three different dosage levels: a high dose (2.5 mg/kg), an intermediate dose (1.5 mg/kg), and a low dose (0.5 mg/kg) of ATG.
The results showed that the lowest dose was remarkably effective, preserving beta cell function for a full year. Lead study author Dr. Chantal Mathieu, an endocrinologist at the University Hospital Gasthuisberg Leuven in Belgium, noted that the beneficial effect was most pronounced in the youngest children.
This finding is particularly significant since children between ages 5 and 11 typically experience a rapid decline in beta cell function following diagnosis, which leads to a sharp increase in their insulin requirements. By slowing this decline, doctors may be able to provide these children with a “smoother ride” into the management of their condition.
Balancing Efficacy and Side Effects
The primary hurdle with ATG has always been its origin. Because the drug is produced using cells from rabbits and horses, the human immune system can react to these foreign proteins, causing a condition known as serum sickness.
The study highlighted a stark difference in safety between the high and low dosages. Serum sickness impacted 82% of participants in the high-dose group, compared to only 32% in the low-dose group. The low-dose group saw a lower incidence of cytokine release syndrome—a runaway inflammatory response characterized by fever, nausea, and muscle pain—affecting 24% of participants compared to 33% in the high-dose group.
Beyond the clinical outcomes, ATG offers a practical advantage: it is widely available and inexpensive. For families struggling with the sudden financial and emotional burden of a diabetes diagnosis, a low-cost treatment option could significantly increase accessibility.
How ATG Compares to Other Therapies
ATG is not the only medication showing promise in the effort to delay the progression of type 1 diabetes, but it fills a different niche than current alternatives. For instance, Teplizumab (brand name Tzield) is approved for those in “stage 2” diabetes—people who have antibodies and abnormal blood sugar but still have most of their beta cells. However, because few people are diagnosed at this early stage, Tzield’s reach is limited.
Other options, such as the rheumatoid arthritis drug Baricitinib (Olumiant), require continuous administration to be effective and have not yet been extensively tested in children.
| Medication | Primary Target/Stage | Administration | Key Constraint |
|---|---|---|---|
| ATG | Newly diagnosed (Honeymoon phase) | Short-term infusion | Risk of serum sickness |
| Teplizumab | Stage 2 (Pre-symptomatic) | 14-day infusion | Limited early diagnosis |
| Baricitinib | Disease progression | Continuous apply | Untested in children |
The Next Generation: Gene-Edited Antibodies
While the low-dose ATG results are encouraging, researchers are already working to eliminate the drug’s most troublesome side effects. A new version of the drug, called SAB-142, is currently being developed by SAB BIO.
Unlike traditional ATG, SAB-142 is produced in cows that have been genetically modified to produce human antibodies. Dr. Michael Haller, chief of pediatric endocrinology at the University of Florida’s Diabetes Institute, explained that because these antibodies are human-derived, they are theoretically less likely to trigger serum sickness or be blocked by the patient’s own immune system.
A clinical trial for SAB-142 in newly diagnosed type 1 diabetes patients is expected to begin in late 2024 or early 2025. Many experts, including Yale endocrinologist Dr. Jennifer Sherr, suggest that the future of T1D treatment may not rely on a single “silver bullet” drug, but rather a multi-agent approach that combines different therapies to stop the autoimmune attack entirely.
This article is for informational purposes only and is not meant to offer medical advice.
The upcoming trials for SAB-142 will serve as the next major checkpoint in determining whether humanized antibodies can provide the same beta-cell preservation as ATG without the associated immune risks.
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