A Lesser-Known Neuroprotective Option: Esafosfine in Hypoxic Brain Injury
DOI:
https://doi.org/10.5281/zenodo.17251594Keywords:
Esafosfine, D-fructose-1,6-diphosphate, Neuroprotection, Hypoxic brain injury, Cerebral circulationAbstract
Esaphosfin (D-fructose-1,6-bisphosphate) is a metabolic modulator that supports intracellular energy pathways and has demonstrated neuroprotective effects in preclinical models of hypoxic-ischemic brain injury. In animal studies, Esaphosfin improved cerebral perfusion, reduced oxidative stress and apoptotic cell death, accelerated electroencephalographic recovery, and limited histological neuronal damage. Additionally, it exhibited anticonvulsant properties by attenuating epileptiform activity. Although clinical data remain limited, intravenous administration has been reported to be safe and well tolerated. Unlike conventional neuroprotective agents such as nimodipine, mannitol, and barbiturates, Esaphosfin exerts direct effects on cellular energy metabolism, offering potential advantages in perioperative and intensive care settings. These findings highlight the need for randomized controlled trials to comprehensively evaluate the efficacy and safety of Esaphosfin in clinical contexts.
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