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Updated: Jun 21, 2026

Ferric Chloride-induced Murine Thrombosis Models
Published on: September 5, 2016
Antitumor effect of dipyridamole mediated by inhibiting the interaction between platelets and tumor cells
Jie Xue1,2, Jianzhao Deng3, Hongwei Qin1
1Department of Blood Transfusion, The Central Hospital of Qingdao Jiaozhou, 99 Yunxi River South Road, Jiaozhou City, Qingdao, 266300, Shandong, China.
Dipyridamole is a well-known antithrombotic and a vasodilator. It is used to treat cerebrovascular and cardiovascular diseases owing to its antiplatelet effects. Platelets play a key role in thrombosis and hemostasis, and after cancer cells enter the bloodstream, they interact with these cells to protect them and promote metastasis. Dipyridamole inhibits tumor progression by blocking platelet aggregation and platelet-mediated Epithelial-to-mesenchymal transition (EMT) via targeting the extracellular signal-regulated kinase (ERK)-mitogen-activated protein kinases (MAPK) signaling pathway, further highlighting its potential antitumor properties. However, studies on the anti-tumor mechanisms of dipyridamole are currently limited and incomplete. In this review, we summarize the pathways through which dipyridamole disrupts platelet-tumor cell interactions and exerts antitumor effects, aiming to inform the development of novel anticancer therapies.
Dipyridamole is a well-known antithrombotic and a vasodilator. It is used to treat cerebrovascular and cardiovascular diseases owing to its antiplatelet effects. Platelets play a key role in thrombosis and hemostasis, and after cancer cells enter the bloodstream, they interact with these cells to protect them and promote metastasis. Dipyridamole inhibits tumor progression by blocking platelet aggregation and platelet-mediated Epithelial-to-mesenchymal transition (EMT) via targeting the extracellular signal-regulated kinase (ERK)-mitogen-activated protein kinases (MAPK) signaling pathway, further highlighting its potential antitumor properties. However, studies on the anti-tumor mechanisms of dipyridamole are currently limited and incomplete. In this review, we summarize the pathways through which dipyridamole disrupts platelet-tumor cell interactions and exerts antitumor effects, aiming to inform the development of novel anticancer therapies.
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