Type 1 Diabetes (T1D) is an autoimmune disease in which the body attacks and destroys its own insulin-producing β-cells. It affects over 3 million people in the United States. For most T1D patients, it is extremely difficult to achieve normal glycemic control even with frequent blood glucose measurements, diet control, careful determination of insulin dosage, and multiple daily insulin injections. Considering the numerous approaches to reduce or eliminate the physical, emotional, psychological and economic hardships of T1D, arresting or reversing the disease before β-cell destruction is the most ideal but difficult solution to implement.

A number of proposed therapeutics have focused on targeting and destroying the T-cells that are ultimately responsible for attacking and killing β-cells. However, in recent years a pathogenic role for B cells has also emerged. B cells can take up islet antigens, present them to helper T cells, and differentiate into antibody secreting plasma cells which enhance antigen uptake by antigen-presenting cells ultimately leading to the activation of cytotoxic T cells for β-cell destruction. A number of non-obese (NOD) diabetic mouse studies and at least one human clinical trial have demonstrated the ability to slow, arrest, or even reverse T1D through B-cell depletion. However, generalized B-cell depletion may lead to significant off-target safety issues thus restricting the allowable treatment duration and limiting its application to a small subpopulation of T1D patients for whom the risk is justified based on the anticipated benefits. An ideal product and treatment regimen would destroy only T1D specific Bcells while sparing the healthy B-cells. The development of just such a product, targeting insulin-specific B cells, is the focus of Akston Biosciences.