YLF-466D effectively stimulates AMPK, as indicated by phosphorylation at Thr172, and this activation correlates with its capacity to suppress aggregation induced by various agonists such as thrombin, ADP, and collagen. This suggests that YLF-466D's antiaggregatory effects are broad, affecting multiple pathways leading to platelet activation, rather than being specific to any single platelet-activating agent. These effects, including the inhibition of platelet aggregation, are observed to be concentration-dependent, reaching optimal efficacy at 150 μM. The IC50 values for the inhibition of aggregation induced by thrombin, ADP, and collagen are approximately 84, 55, and 87 μM, respectively[1].
体外研究
YLF-466D effectively stimulates AMPK, as indicated by phosphorylation at Thr172, and this activation correlates with its capacity to suppress aggregation induced by various agonists such as thrombin, ADP, and collagen. This suggests that YLF-466D's antiaggregatory effects are broad, affecting multiple pathways leading to platelet activation, rather than being specific to any single platelet-activating agent. These effects, including the inhibition of platelet aggregation, are observed to be concentration-dependent, reaching optimal efficacy at 150 μM. The IC50 values for the inhibition of aggregation induced by thrombin, ADP, and collagen are approximately 84, 55, and 87 μM, respectively[1].
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