Anti-Human CD3 (Teplizumab)

Type I diabetes is a chronic autoimmune disease that destroys insulin-producing beta-cells in the islets of Langerhans, leading to a dependence on exogenous insulin for survival1.

Teplizumab (TZIELD) is a humanized, anti-CD3ε IgG1κ monoclonal therapeutic that delays the onset of Stage 3 Type 1 diabetes1, 2.

CD3ε plays an essential role in T cell development and is part of the T cell-receptor CD3-complex, which acts as an external signal transducer3.

Defects in CD3ε cause immunodeficiency and have been linked to susceptibility to type I diabetes in women.

Teplizumab is an Fc receptor-nonbinding anti-CD3 antibody4 whose Fc region is mutated (L234A; L235A) to reduce effector functions2.

When Teplizumab is administered by intravenous infusion once daily for 14 consecutive days, it reduces the loss of beta-cell function1.

Teplizumab treatment modifies CD8+ T lymphocytes, which are thought to kill beta-cells, to display a partially exhausted phenotype associated with delayed disease progression1, 5.

Teplizumab delays the median onset of Stage 3 Type 1 diabetes by 2 years compared to placebo1, 2.

Additionally, the effects of treatment persist over time.

The median years to diabetes diagnosis after Teplizumab treatment is ~ 5 years compared to ~ 2 years in the placebo-treated group6.

In November 2022, the United States Food and Drug Administration approved Teplizumab injection to delay the onset of Stage 3 Type 1 diabetes in adults and pediatric patients aged 8 years and older who have Stage 2 Type 1 diabetes7.