Key result
Tipiracil hydrochloride inhibits thrombosis without significant bleeding versus standard antiplatelets in preclinical models.
Why the study?
Most current anti-platelet drugs permanently inhibit platelet function and carry systemic side effects like thrombocytopenia and hemorrhage, prompting investigation into whether the specific thymidine phosphorylase inhibitor tipiracil hydrochloride is a safe anti-platelet drug.
Does tipiracil hydrochloride inhibit thrombosis without inducing significant bleeding in preclinical models?
Does tipiracil hydrochloride inhibit thrombosis without inducing significant bleeding in preclinical models?
Tipiracil hydrochloride, a specific TYMP inhibitor, shows promise as a novel, safe anti-platelet and anti-thrombotic agent in preclinical models.
Hypothesis-generating for tipiracil as a novel antiplatelet without bleeding; requires human trials before any clinical consideration.
Rationale Most of the current anti-platelet drugs inhibit platelet function permanently and have systemic side effects, including thrombocytopenia and hemorrhage. We previously found that thymidine phosphorylase (TYMP), a platelet cytoplasmic protein, facilitates multiple agonist induced platelet activation and enhances thrombosis. A specific TYMP inhibitor, namely, tipiracil hydrochloride (TPI), has been approved by the U.S. Food and Drug Administration for clinical use as an auxiliary drug making it possible to be repositioned as an anti-platelet medicine. Objective We aimed to test the hypothesis that TPI is a novel and safe anti-platelet drug by examining its role in platelet activation and thrombosis using both in vitro and in vivo studies. Methods and Results By co-expression of TYMP and Lyn or Lyn-SH3 domain tagged with glutathione S-transferase, we showed the direct evidence that TYMP binds to the SH3 domain in its partners. TYMP haplodeficiency is sufficient to inhibit thrombosis in vivo regardless of gender. TPI treatment rapidly inhibited collagen- and ADP-induced platelet aggregation, which copied the phenotype of TYMP deficient platelets. Under both normal and hyperlipidemic conditions, treating wild type (WT) mice with TPI via intraperitoneal injection, intravenous injection, or gavage feeding dramatically inhibited thrombosis without inducing significant bleeding. Even administered above the effective dose, TPI has a lower bleeding side effect compared to aspirin and clopidogrel. Most importantly, intravenously delivery of TPI alone or combined with tissue plasminogen activator dramatically inhibited the growth of developing thrombi. Dual administration of very low dose of aspirin and TPI also dramatically inhibited thrombosis without disturbing hemostasis. Conclusion This pharmacological study demonstrated that TYMP participates in multiple signaling pathways in platelet and plays a mechanistic role in regulating platelet activation and thrombosis. TPI, a specific TYMP inhibitor, would be a novel safe anti-platelet and anti-thrombosis medicine.
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Zulfiker et al. (2020) studied Thrombosis. Tipiracil Hydrochloride (TPI) vs. Vehicle/Saline, Aspirin, Clopidogrel was evaluated on Time to occlusive thrombus formation in FeCl3-induced carotid artery thrombosis model. Tipiracil hydrochloride dramatically inhibited platelet activation and in vivo thrombosis under normal and hyperlipidemic conditions without inducing significant bleeding compared to standard antiplatelets.
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