Novel coumarin derivatives B and C demonstrated potential as multitarget antiplatelet agents by antagonizing α2-adrenergic, GPVI collagen, and P2Y12 ADP receptors in silico.
Do novel multitarget coumarins inhibit platelet aggregation in vitro and in silico?
Novel coumarin derivatives demonstrate potential as multitarget antiplatelet agents by simultaneously inhibiting multiple platelet aggregation pathways in preclinical models.
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Novel pharmacological approaches advocate developing multitarget drugs, that is, molecules capable of simultaneously acting on two or more pharmacological targets to produce synergistic effects from a single compound in each disease. This strategy may help reduce required doses and prevent drug–drug interactions typically associated with polypharmacy. Coumarins are natural products with diverse pharmacological activities, including antioxidant, anti-inflammatory, anticancer, neuroprotective, cardioprotective, and antithrombotic effects. The pleiotropic actions of these molecules suggest that modifying the coumarin structure could yield new multi-target antiplatelet agents with greater efficacy and safety than those currently available in clinical practice. In this work, we began with a theoretical approach using molecular docking and designed three coumarins that simultaneously inhibited platelet aggregation induced by epinephrine, collagen, and ADP. Experimentally, we evaluated the structure activity relationship of three coumarins: (A) 6,7-dimethoxy-3-(1H-pyrrol-1-yl)-2H-chromen-2-one, (B) 7,8-dimethoxy-3-(1H-pyrrol-1-yl)-2H-chromen-2-one, and (C) 3-(1H-imidazol-1-yl)-6,7-dimethoxy-2H-chromen-2-one. In silico studies suggest that compounds B and C may exhibit antagonistic interactions at the α2-adrenergic, GPVI collagen, and P2Y12 ADP receptors. Additionally, molecular docking indicates essential interactions between the compounds and the GPIIb/IIIa fibrinogen receptor.
Ramírez-Camacho et al. (Tue,) reported a other. Novel coumarin derivatives B and C demonstrated potential as multitarget antiplatelet agents by antagonizing α2-adrenergic, GPVI collagen, and P2Y12 ADP receptors in silico.
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