Type 1 diabetes (T1D) is the immune mediated form of diabetes that results from the body’s destruction of insulin producing pancreatic beta-cells. Immune cells, particularly T and B cells, contribute to the killing of insulin producing beta-cells. A lack of sufficient insulin production results, which prevents tissues from using glucose, leading to high blood sugars. Treatment is with life-long insulin administration by an insulin pump or multiple daily injections.  Genetic risk for T1D development is predisposed by the HLA-DQ8 gene. People with this gene are ~11x more likely to develop T1D than those that do not have the gene, and 50-60% of all patients with T1D have the HLA-DQ8 gene.

IMT’s approach to T1D is to develop a small molecule drug that effectively starves the autoimmune process by blocking the function of DQ8 bearing cells to activate T-lymphocytes. We completed a Phase 1b human study with an FDA-approved drug, L-methyldopa, that had been validated as a hit in our drug screening. Results of the study (Michels et al., ADA Annual Meeting, 2018) showed that DQ8 activity is significantly inhibited by the drug in antigen (insulin) presentation to T cells in adult patients with newly diagnosed type 1 diabetes. Moreover, the study demonstrated that the DQ8 inhibition extended to presentation of α-gliadin showing promise of this approach for treating celiac disease.

Our lead drug, IMT-002, occupies this peptide binding groove of DQ8 on the surface of antigen presenting cells to block the binding of insulin and other beta-cell proteins and subsequent activation of CD4 T-cells. When HLA-DQ8 is blocked, the immune system will no longer attack insulin producing beta-cells, thus modify the disease course to keep patients making their own insulin.


Autoimmune disease, with no current cure and diagnosed largely in children, in which insulin-producing beta cells are destroyed and patients are dependent life-long on injected or pumped insulin to survive.

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