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Preclinical research has centered on three primary areas: Lipolysis Stimulation: AOD-9604 has been shown in rodent models to stimulate lipolysis via beta-adrenergic receptor pathways, particularly in visceral adipose tissue, without systemic growth-hormone-like signaling

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This metabolic reprogramming, characterized by abnormal activation of glycolysis and mitochondrial dysfunction, ultimately determines the fate and function of immune cells, leading to the occurrence and development of lung injury

Thereby, even if lipid peroxidation per se is insufficient to cause cell death, it may be considered as evidence for oxidative stress that contribute to liver injury

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