The development of effective antiviral drugs is crucial in our preparation to fight future pandemic threats. The COVID-19 pandemic underscored the need for rapid development and wide availability of antiviral drugs. To address this need, DNDi joined with partners to progress the AI-driven Structure-enabled Antiviral Platform (ASAP) for antiviral drug discovery, one of the Antiviral Drug Discovery (AViDD) Centers for Pathogens of Pandemic Concern.

The ASAP platform uses artificial intelligence (AI) and structural-based design to enable rapid identification and optimization of small molecule compounds that can disrupt viral replication. The platform relies on X-crystallography fragment screening to identify the chemical starting points and molecular dynamics simulations to rapidly optimize lead compounds for high potency and pharmacokinetics. ASAP also employs deep mutational scanning (DMS) to gain insights into the potential for resistance development to allow prioritization of the virus protein targets.  

The goal of the ASAP platform is to accelerate the discovery and development of new, effective antiviral drugs that can be rapidly advanced through clinical trials and ultimately be made widely available. The platform’s flexibility and adaptability enable it to be applied to a wide range of viruses and viral families, including those that are currently neglected.

Project updates


The project continued work focused on the development of novel antiviral drugs targeting three viral families: flaviviruses, coronaviruses, and enteroviruses, including two programmes on coronaviruses progressing in lead optimization. The leading programme targeting MERS/SARS-CoV-2 MPro inhibitors is expected to select a shortlist of compounds that will progress to pre-clinical studies in early 2024. The second programme, focused on SARS-CoV-2 nsp3-Mac1 inhibitors, is undergoing further validation enabled by tool compounds developed by the project. Two additional programmes are in early-stage lead optimization, with the first targeting the enterovirus EV-D68 and EV-A71 3C proteases and the second targeting the dengue and Zika virus flavivirus NS2B/3 protease.