Thirty-three years.
That is how long the patients in this trial had, on average, been managing Type 1 diabetes before they entered the programme at UChicago Medicine. Thirty-three years of calculating insulin doses, monitoring blood glucose, adjusting for meals and exercise and stress and illness. Thirty-three years of a condition that never sleeps.
Then, 10 out of 10 of them became insulin-free.
**The Result**
The trial, led by Dr. Piotr Witkowski at UChicago Medicine's Pancreas and Islet Transplant Program, tested a new approach to islet cell transplantation. Islet cells — the insulin-producing clusters in the pancreas — were transplanted from a donor into patients with T1D. The key difference: instead of the standard calcineurin inhibitor immunosuppression that has historically been used (and which is toxic to islet cells over time), patients received **tegoprubart** — an anti-CD40L monoclonal antibody developed by Eledon Pharmaceuticals.
The results presented at the **ATTD 2026 conference** in March:
✅ **10 out of 10 evaluable patients** achieved insulin independence ✅ **HbA1c below 6.0%** in all patients (mean approximately 5.35%) — well into the normal range ✅ **Zero episodes of transplant rejection** ✅ **Zero de novo donor-specific antibodies** (an early sign of immune attack) ✅ **Well-tolerated** — no nephrotoxicity, no hypertension, no neurotoxicity
For context: traditional islet transplantation protocols have historically achieved insulin independence in approximately 40–50% of patients at one year. A 100% rate — with these patients — is not a number that has appeared in this field before.
**Why the Drug Matters**
The immune system is the fundamental obstacle in islet transplantation. T1D itself is caused by the immune system attacking the body's own insulin-producing cells. Transplanting new islet cells from a donor puts them in front of the same immune system that destroyed the originals — which will attack the transplanted cells too, unless suppressed.
Conventional immunosuppression (calcineurin inhibitors like tacrolimus and cyclosporine) can prevent rejection, but they're toxic to islet cells over time — the very cells they're meant to protect — and carry long-term risks of kidney damage and infection.
Tegoprubart works differently. It targets **CD40 ligand (CD40L)** — a specific molecular signal in the T-cell activation pathway. By blocking this one pathway, it prevents rejection without broadly suppressing the immune system. No damage to the islets. No kidney toxicity. Just targeted protection of the transplanted cells.
**Who This Could Help**
Islet transplantation requires a donor organ, surgical expertise, and ongoing immunosuppression — so it won't be a population-wide cure for the ~400 million people with T1D worldwide. But for patients with **brittle T1D** — where blood sugar control is exceptionally dangerous and unpredictable, where hypoglycaemic episodes are frequent and severe — it represents a genuine, practical path to freedom from insulin.
Breakthrough T1D (formerly JDRF), which funded the study, has already committed to a follow-on trial specifically for T1D patients with chronic kidney disease — a population historically excluded from islet transplantation because calcineurin inhibitors damage already-compromised kidneys. Tegoprubart's kidney-safe profile changes that calculation entirely.
Eledon Pharmaceuticals is working toward regulatory guidance on a market pathway for tegoprubart in islet transplantation, with FDA conversations anticipated later in 2026.
Thirty-three years. Then nothing. Just normal blood sugar, maintained by cells that are finally being allowed to do their job. 💉➡️✨
*Sources: Eledon Pharmaceuticals press release (March 16, 2026) · Breakthrough T1D (breakthrought1d.org) · ATTD 2026 Conference presentation · BioSpace · The Scientist · BioPharma Dive*
