"DIBAIT": a Novel Small Peptide For Type 2 Diabetes Treatment
Di-Bait Project ID : 7-2015-3167
Summary of the technology
Project ID : 7-2015-3167
Description of the technology
Based on a provocative working hypothesis, we most probably identified the molecular origin of insulin resistance (IR). Systemic IR is induced via post-translational modification (PTM) of liver key regulatory proteins. We have discovered that hepatic futile utilization of the PTM-inducing residue, resulted in the abrogation of IR and correction of the glycemic-state, in type-2-diabetes (T2D) mouse model. We further found a way to achieve this glycemic control via the utilization of novel small molecules that operate through well-defined MoA. These novel small molecules are orally bioavailable and has nice safety profile.
Providing a cure to T2D, as opposed to symptomatic treatment, by nullifying the vicious circle that starts with peripheral IR, as a result of fatty liver, and ends up as full-blown type-2-diabetes (T2D).
We are finishing now the process of drug-candidate selection and be ready in a few months to move to drug-development phase. A collaboration with major Pharma Company can help accelerating this process in terms of CMC, covering regulatory aspect etc. in order to bring an effective therapy to hundreds of millions of T2D patients around the world