Historically, proteins are the main biomolecules considered for small molecule drug design. More than 95% of current therapeutics have been developed to modulate protein targets. However, in recent years, certain RNAs have been identified as druggable targets, thereby opening the race to drug RNA with small molecules.
Our target-agnostic AI-based drug discovery platform generates small molecules that can interact with well-defined RNA structures and modulate downstream processes. We currently develop small molecules that can bind to the internal ribosome entry site (IRES) in the 5' untranslated region of the hepatitis C virus (HCV) RNA genome, which is responsible for the initiation of viral protein synthesis. Our AI-designed molecules are able to alter the structural features of a functional HCV RNA and have the ability to inhibit virus-mediated translation and replication.
Hepatitis C is an inflammation of the liver caused by the hepatitis C virus. The virus can cause both acute and chronic hepatitis, ranging in severity from a mild illness to a serious, lifelong illness including liver cirrhosis and cancer.
Globally, an estimated 58 million people have chronic hepatitis C virus infection, with about 1.5 million new infections occurring per year. In 2019, approximately 290 000 people died from hepatitis C, mostly from cirrhosis and hepatocellular carcinoma.
About 5% of patients do not succeed in eradicating HCV, largely due to antiviral drugs triggering strong drug selection favoring mutants that offer partial resistance to them. Thus, it is necessary to continue developing or improving the efficiency of antiviral drugs against HCV