HeartBeat.bio and biotix.ai have entered into a strategic partnership centered around the identification and validation of new heart failure therapeutic targets.
By combining biotix.ai's causal genome mapping capacity with HeartBeat.bio's human-based Cardoid drug discovery platform, the pair will identify previously unrecognised genetic targets instrumental in heart failure.
Once biotix.ai's large-scale, Mendelian randomisation platform identifies these targets, HeartBeat.bio will validate them using its human-like in vitro assay that recapitulates key aspects of heart biology and disease.
Through this agreement, HeartBeat.bio will hold exclusive rights to the initiation of drug discovery programmes based on identified targets, as well as the opportunity to enter into third-party co-development partnerships.
This means that HeartBeat.bio will hold the intellectual property to all discovered targets, while biotix.ai will be eligible to receive payments and royalties related to the meeting of drug discovery milestones.
This discovery agreement comes at a time where heart failure impacts more than 30 million people — remaining one of the leading causes of death and hospitalisation worldwide.
Despite new therapeutic advances in recent years, many patients lack access to effective treatment options, underscoring the need for the identification and validation of novel therapeutic targets.
“Our mission is to transform the way heart failure is treated by combining our human-based drug discovery platform with cutting-edge AI technologies,” said Michael Krebs, CEO of HeartBeat.bio.
“This collaboration with biotx.ai allows us to explore the full potential of novel, genetically guided targets for therapeutic innovation.”
“biotx.ai is committed to turning complex biological data into actionable drug targets,” added Marco Schmidt, CEO of biotx.ai.
“Partnering with HeartBeat.bio enables us to bridge the gap from causal genes to functional validation in a highly relevant human model. Together, we aim to accelerate the development of disease-modifying therapies for heart failure.”
