Lifelong insulin therapy is required for T1D disease management.
Constant vigilance is necessary to manage fluctuations in blood glucose levels and avoid hospitalization.
A 10-15 year decrease in life expectancy occurs on average in T1D patients.
Long-term T1D health complications include risks of heart disease, kidney failure and vision loss.
The root cause of T1D is not addressed – Available therapies do not address the underlying autoimmune disease pathology.

The Facts

T1D impacts a significant number of people

> 9.5 million globally

T1D is one of the
fastest-growing
chronic diseases

> 500,000 new global patients each year

The ultimate goal for patients is a disease-modifying therapy that can slow, halt, or even reverse disease progression.

Zag Bio Solution

Beyond insulin, toward lasting disease modification

Our lead program, ZAG-101, a first-in-class, disease-modifying therapy, is in development for people with Type 1 diabetes or at high risk of developing the disease, with the goal of restoring immune tolerance and preventing autoimmunity. 

ZAG-101 has now advanced to the clinic. We initially plan to enroll patients with newly diagnosed T1D in our clinical studies of ZAG-101. Ultimately, we aim to treat earlier to prevent the onset of symptomatic disease.

By engaging the body’s natural process to restore balance to the immune system, ZAG-101 has the potential to fundamentally change the treatment paradigm for T1D.

Zag’s therapy delivers new instructions.

Our bifunctional antibodies deliver pancreatic beta-cell antigens to specialized antigen-presenting cells in the thymus, where they encounter developing immune cells.

Immune cells learn tolerance.

Developing immune cells are trained to recognize the pancreatic beta-cell antigen, generating a new population of antigen-specific regulatory T cells (Tregs).

Immune tolerance is restored at the site of disease.

Antigen-specific Tregs leave the thymus and travel to the pancreas where they restore immune tolerance and halt the autoimmune attack on beta cells, potentially preserving their ability to produce insulin.

 

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