ZAG-101 in Type 1 Diabetes
Type 1 diabetes:
Decades of treatment without cure
Type 1 diabetes (T1D) is a well-characterized, chronic autoimmune disease where the immune system attacks and destroys the insulin-producing beta cells in the pancreas. For decades, the standard of care has been lifelong insulin therapy to help regulate blood glucose levels in people living with T1D.
Improving the status quo
for T1D patients
Even with recent improvements in glucose monitoring and insulin administration technologies, the underlying autoimmune pathology of T1D remains untreated.
The Facts
Number of people
living with T1D
T1D is one of the
fastest-growing
chronic diseases
The ultimate goal for patients is a disease-modifying therapy that can slow, halt, or even reverse disease progression.
Zag Solution
Beyond insulin, toward lasting disease modification
T1D patients still have functional beta cells at the time of diagnosis or before symptom onset, and our therapeutic approach aims to preserve functional beta cells to have a transformative impact on patients’ lives.
Our lead program is ZAG-101, a first-in-class, disease-modifying therapy for patients newly diagnosed with T1D or at high risk of developing the disease, with the goal of restoring immune tolerance and preventing autoimmunity.
Zag Bio is advancing ZAG-101 for Type 1 diabetes. By directly harnessing the body’s natural tolerance mechanisms, ZAG-101 has the potential to fundamentally change the treatment paradigm for T1D.
Thymus-Targeted Therapy
ZAG-101 is a bifunctional antibody that delivers pancreatic beta cell antigens to the thymus.
Immune Cells Learn Tolerance
By targeting thymic antigen-presenting cells (APCs), ZAG-101 is designed to reestablish central T cell tolerance, driving the expansion of antigen-specific regulatory T cells (Tregs) that migrate to the pancreas, protect β-cells, reduce inflammation, and promote tissue repair.
ZAG-101 Restores Local Immune Tolerance at the Pancreas
Harnessing the natural mechanism in the thymus, ZAG-101 trains and expands antigen-specific thymic Tregs that exit the thymus and protect beta cells from destruction in the pancreas, potentially preserving their ability to produce insulin.
As the first therapeutic approach to selectively deliver antigen to the thymus, ZAG-101 translates decades of proof-of-concept research—direct injection or lentiviral delivery of insulin to thymic APCs—that have demonstrated predictable shifts in regulatory T cell (Treg) and effector T cell (Teff) populations and restored glucose regulation in animal models of diabetes.
We plan to initially 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. We are currently completing IND-enabling studies for ZAG-101 and we plan to initiate clinical studies in T1D patients in the near future.
