Pim kinase and the regulation of platelet function, thrombosis and haemostasis

Platelet driven thrombosis continues to account for high levels of mortality worldwide.

Despite the therapeutic benefits of current anti-platelet drugs such as aspirin and clopidogrel, these therapies are associated with variable patient outcomes and increased bleeding risk.

Safer, more efficacious clinical strategies, are therefore needed to combat thrombotic risk without increasing the risk of patient bleeding We have recently identified a kinase, Pim kinase, expressed in platelets and demonstrate its inhibition modulates platelet activation and thrombosis. More specifically our data indicates that Pim kinase selectively regulates Thromboxane A2 mediated platelet activation.

Biochemical, molecular biology and functional analyses will be used to determine the mechanism of action by which Pim kinase regulates platelet function.

We will use gene deletion and pharmacological approaches to dissect the precise sites of action with an aim of establishing the potential of repurposing Pim kinase inhibitors as anti-platelet and anti-thrombotic therapies.