Soman stands as a prominent nerve agent in preclinical investigations focusing on neuroprotection. Analogous to its organophosphorus counterparts, soman manifests heightened toxicity through cholinesterase inhibition, instigating a consequential cholinergic crisis. Its pronounced capacity to phosphonylate the catalytic serine of acetylcholinesterase (AChE) triggers the aging reaction, hindering AChE reactivation. Consequently, the development of effective antidotes for soman emerges as a challenge. While acute effects of soman exposure, with high doses, have been extensively scrutinized, there remains a limited exploration of the long-term repercussions following a single exposure to sub-lethal doses of soman. Our recent identification of a promising neuroprotective countermeasure, efficient in preclinical models exposed to VX or a sarin surrogate, has strengthened our intention to investigate its effectiveness in a more challenging model utilizing sub-lethal doses of soman. In order to characterize this innovative preclinical model, Swiss male mice were individually exposed to a single sub-lethal dose of soman (0.3; 0.5 or 0.9 DL50). Intoxication symptoms were assessed during the first hour post-soman exposure, while alterations in cerebral electrical activity induced by different soman doses were simultaneously evaluated through electrocorticography. Subsequently, a comprehensive assessment up to 1-month, examined AChE levels, inflammation, and hormonal changes across various brain regions, blood samples, and organs. This research provides crucial insights into both immediate and prolonged effects of soman exposure. Furthermore, the soman exposure model will be used to validate the efficacy of a neuroprotective countermeasure, opening avenues for further exploration and potential clinical applications.