Provention Bio Inc. (NASDAQ:PRVB) has announced comprehensive follow up results from its vital TN-10 study, which is presented during the ADA’s 80th Scientific Session.
Teplizumab showing delay in onset insulin-dependent T1d
The data showed that a single teplizumab 14-day course demonstrated a significant delay in early insulin-dependent Type 1 diabetes patients. The delay in presymptomatic patients was significant by an average of around 3-years relative to placebo. Provention Bio had previously reported the new data from the “At-Risk” TN-10 trial with another year of the additional trial to the two-year average delay in the New England Journal of Medicine.
Tepliziumab is an anti-CD3 monoclonal antibody, and it is the company’s main drug candidate under development. The company is developing the drug for prevention or delay of insulin-dependent type 1 diabetes in presymptomatic patients. This is defined by the presence of more than two T1D related dysglycemia or autoantibodies.
T1D delayed up to 3 years with teplizumab treatment
TrialNet, a popular group of T1D researchers, conducted the study funded by the Nationa Institute of Diabetes and Digestive and Kidney Diseases. The company’s CEO, Ashleigh Palmer, indicated that the continuing early clinical-stage type 1 diabetes delay with just a single teplizumab was an important milestone. TID can now be delayed by around 3-years relative to placebo, which is great news for patients dealing with glucose monitoring, insulin dependency, and having lifestyle challenges. Palmer asserted that they understand the urgency of delaying early-stage T1D progression before beta cell loss. The CEO added that the company was committed to bringing teplizumab to T1D patients quickly.
More findings from the study indicated a decrease in the C-peptide levels in the control group. This is usually the measure of an individual’s insulin production, and the decrease underscores the effect of beta-cell destruction, which characterizes T1D. On the other hand, teplizumab stabilized and considerably reversed the decrease of C-peptides, which is an indication of delay in beta cell destruction and insulin production restoration in dysfunctional cells.
