The Multitarget Synergistic Effect and Clinical Value of Edaravone Dexborneol in Neuroprotection for Acute Ischemic Stroke

Acute ischemic stroke (AIS), as the second leading cause of death worldwide, involves complex pathophysiological mechanisms including oxidative stress, inflammatory cascade reactions, and blood-brain barrier disruption [1]. Edaravone Dexborneol is a novel dual-effect neuroprotectant composed of the free radical scavenger edaravone and the anti-inflammatory component dexborneol in a 4:1 molar ratio [2]. Preclinical studies have shown that Edaravone Dexborneol can significantly reduce cerebral infarction volume, inhibit the formation of neutrophil extracellular traps, and improve blood-brain barrier permeability by protecting the neurovascular unit—a functional complex that maintains brain function, composed of neurons, vascular endothelial cells, astrocytes, and other components [3]. Its molecular mechanism is associated with regulating the dynamic balance of pro-inflammatory factors (IL-1β ↓ 46.8%, IL-6 ↓ 38.2%) and anti-inflammatory factors (IL-4 ↑ 2.1-fold, IL-10 ↑ 1.8-fold). The pivotal phase III TASTE clinical trial (NCT04119063) demonstrated that intravenous administration of Edaravone Dexborneol within 48 hours of onset significantly improved 90-day functional independence (mRS ≤ 1: 34.6% vs. 24.9%, OR = 1.59, 95%CI 1.21 - 2.08) compared with edaravone monotherapy, with no significant difference in adverse event rates (15.3% vs. 13.8%, P = 0.34). The TASTE-SL subgroup study confirmed that the sublingual preparation has a bioavailability of 82.4% ± 11.6% of intravenous administration, providing a new approach for prehospital emergency care. Future research should explore its synergistic effect with endovascular thrombectomy through multicenter randomized controlled trials (such as the OPTIMAL-AIS study) and clarify the neurovascular unit protection mechanism based on omics technologies. The multitarget regulatory characteristics of Edaravone Dexborneol provide a new paradigm for breaking through the bottleneck of neuroprotective therapy for AIS.