Key result
Absence or inhibition of PI3Kα resulted in a significant decrease in thrombus size and an increased time to arterial occlusion in mouse models, without modifying bleeding time.
Population
Mice selectively deficient in p110α in the megakaryocyte lineage and in vitro/ex vivo platelet models
Comparison
PI3Kα deficiency or isoform-selective PI3Kα… vs Wild-type mice or uninhibited controls
Design
Preclinical
Authors
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PI3Kα inhibition may offer antithrombotic benefit without bleeding liability in mice; leaves open translation to human therapy.
PI3Kα inhibition reduces arterial thrombosis in mouse models without increasing bleeding time, suggesting it may be a safe therapeutic target.
Laurent et al. (2018) studied Arterial thrombosis. PI3Kα inhibition or deficiency vs. Control/Wild-type was evaluated on Thrombus size and time to arterial occlusion. Absence or inhibition of PI3Kα resulted in a significant decrease in thrombus size and an increased time to arterial occlusion in mouse models, without modifying bleeding time.
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