Precision therapeutics for type 1 diabetes
Type 1 diabetes begins in the islet. So does our therapy.
Islex Therapeutics is developing islet-targeted antibodies designed to concentrate therapeutic activity in the pancreas, where insulin-producing β-cells are lost.
The problem
Type 1 diabetes is two diseases at once
It is an autoimmune disease, and it is a disease of progressive β-cell loss. Most therapies in development address the first. Far fewer act on the β-cell itself.
An immune attack
The immune system learns to recognize proteins on insulin-producing β-cells and destroys them. Systemic immune modulation, the dominant strategy in the field, acts on that response throughout the body.
A cell under strain
β-cells carry an unusually heavy protein-folding burden. Under inflammatory stress they become both less functional and more visible to the immune system, which accelerates their own loss.
Prevalence, incidence and HbA1c figures: [SOURCE REQUIRED — add citation before publishing]
Our approach
A target that is almost exclusively β-cell
ZnT8 is a zinc transporter central to how β-cells make, store and release insulin. It is one of the most highly expressed and most β-cell–specific membrane proteins in the body, and it is one of the proteins the immune system learns to recognize in type 1 diabetes.
That combination is what makes it interesting to us. A molecule that binds ZnT8 goes where ZnT8 is, which is almost nowhere except the pancreatic islet.
ILX-101 mechanism
Bind
ILX-101 binds ZnT8 where it presents at the β-cell surface.
Internalize
The antibody–protein complex is drawn into the cell and trafficked to the endoplasmic reticulum.
Stabilize
In preclinical models, this is associated with reduced markers of ER stress and reduced antigen presentation on the β-cell surface.
Why this target
Human genetics points the same direction
People who carry loss-of-function mutations in SLC30A8, the gene encoding ZnT8, show substantially lower risk of type 2 diabetes. Individuals with complete loss of ZnT8 are otherwise phenotypically normal.
- An analysis of approximately 150,000 individuals across five ethnic groups found protein-truncating SLC30A8 mutations associated with reduced type 2 diabetes risk.
- An independent analysis of a South Asian genome registry of roughly 100,000 individuals, including loss-of-function homozygotes, identified SLC30A8 as the strongest genetic signal for type 2 diabetes protection among its significant hits.
Flannick et al., Nature Genetics, 2014. Lamarche et al., Diabetologia, 2025.
Backed by investors who know this disease
Our Series A brought together life-science and diabetes-focused investors alongside a scientific advisory board drawn from the leading centers in type 1 diabetes research.
ILX-101 and ILX-101-plus are investigational and have not been approved by the U.S. Food and Drug Administration or any other regulatory authority. Their safety and efficacy have not been established. Findings described on this site are from preclinical research and are not predictive of results in humans. This site is for general informational purposes and is not medical advice.