Our group investigates the complex signalling pathways that regulate platelet activation and thrombus formation, with a particular focus on how dysregulated signalling contributes to platelet hyperactivity in cardiovascular disease. A central aspect of our work is the design, synthesis, and evaluation of proteolysis-targeting chimeras (PROTACs) as powerful tools to study and manipulate platelet signalling. PROTACs function by recruiting a target protein to an E3 ubiquitin ligase, leading to its ubiquitination and subsequent degradation by the proteasome. This mechanism allows for the complete and selective removal of specific proteins from the cell, rather than simply inhibiting their activity, offering unique advantages in dissecting complex signalling networks. Applying this technology to platelets, anucleate cells with limited protein synthesis, provides an exciting opportunity to study protein turnover and pathway regulation in a system where traditional genetic tools are not feasible. We are particularly interested in using PROTACs to target key signalling mediators such as Bruton's tyrosine kinase (BTK), which plays a central role in GPVI and CLEC-2 pathways. By combining chemical biology with platelet physiology, our goal is to uncover new insights into platelet signalling and to develop innovative anti-platelet therapies that can prevent thrombosis without increasing bleeding risk.