Platelets are best known for their role in blood clotting but also play an important part in inflammation. They express purinergic receptors, which regulate their activation in both processes. We have discovered that the P2Y1 receptor controls platelet-driven inflammation while preserving normal clotting. This unique role makes P2Y1 an attractive therapeutic target for conditions such as chronic obstructive pulmonary disease (COPD), where inflammation contributes to disease progression.
Our group has designed selective P2Y1 antagonists that suppress inflammation without impairing haemostasis. In preclinical COPD models, these molecules reduced lung inflammation and prevented damage linked to excessive platelet activation. Our ongoing work focuses on optimising these compounds into orally available small-molecule drugs.
This project is conducted in collaboration with Professor Simon Pitchford at the Institute of Pharmaceutical Science, King’s College London, and is funded by the Medical Research Council. By selectively modulating platelet function, we aim to deliver safer and more effective anti-inflammatory therapies that address unmet needs in respiratory disease and beyond.