Key result
Cyproheptadine and pizotifen significantly prolonged the time to thrombotic occlusion in mice compared to vehicle (787.4 sec and 1199 sec vs 375.3 sec, respectively), demonstrating their potential as antiplatelet agents.
Why the study?
Do cyproheptadine and pizotifen inhibit serotonin-enhanced platelet function and thrombosis in preclinical models?
Do cyproheptadine and pizotifen inhibit serotonin-enhanced platelet function and thrombosis in preclinical models?
Absolute Event Rate: 787.4% vs 375.3%
p-value: p=<0.0001
The antidepressant 5-HT2A antagonists cyproheptadine and pizotifen exert antiplatelet and thromboprotective effects comparable to clopidogrel, but may interfere with normal hemostasis.
Should not inform clinical antiplatelet use; leaves open translation of these agents to human thrombosis trials.
There is considerable interest in defining new agents or targets for antithrombotic purposes. The 5-HT2A receptor is a G-protein coupled receptor (GPCR) expressed on many cell types, and a known therapeutic target for many disease states. This serotonin receptor is also known to regulate platelet function. Thus, in our FDA-approved drug repurposing efforts, we investigated the antiplatelet activity of cyproheptadine and pizotifen, two antidepressant 5-HT2A Receptor antagonists. Our results revealed that cyproheptadine and pizotifen reversed serotonin-enhanced ADP-induced platelet aggregation in vitro and ex vivo. And the inhibitory effects of these two agents were found to be similar to that of EMD 281014, a 5-HT2A Receptor antagonist under development. In separate experiments, our studies revealed that these 5-HT2A receptor antagonists have the capacity to reduce serotonin-enhanced ADP-induced elevation in intracellular calcium levels and tyrosine phosphorylation. Using flow cytometry, we also observed that cyproheptadine, pizotifen, and EMD 281014 inhibited serotonin-enhanced ADP-induced phosphatidylserine (PS) exposure, P-selectin expression, and glycoprotein IIb-IIIa activation. Furthermore, using a carotid artery thrombosis model, these agents prolonged the time for thrombotic occlusion in mice in vivo. Finally, the tail-bleeding time was investigated to assess the effect of cyproheptadine and pizotifen on hemostasis. Our findings indicated prolonged bleeding time in both cyproheptadine- and pizotifen-treated mice. Notably, the increases in occlusion and bleeding times associated with these two agents were comparable to that of EMD 281014, and to clopidogrel, a commonly used antiplatelet drug, again, in a fashion comparable to clopidogrel and EMD 281014. Collectively, our data indicate that the antidepressant 5-HT2A antagonists, cyproheptadine and pizotifen do exert antiplatelet and thromboprotective effects, but similar to clopidogrel and EMD 281014, their use may interfere with normal hemostasis.
No takes yet. Share an insight, caveat, or question.
Lin et al. (2014) studied Thrombosis and Platelet Aggregation. Cyproheptadine and Pizotifen vs. Vehicle was evaluated on Time to vessel occlusion in a carotid artery injury-induced thrombosis model in mice (seconds) (p=<0.0001). Cyproheptadine and pizotifen significantly prolonged the time to thrombotic occlusion in mice compared to vehicle (787.4 sec and 1199 sec vs 375.3 sec, respectively), demonstrating their potential as antiplatelet agents.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: