Adult T-biphenotypic acute leukaemia: clinical and biological features and outcome.

UNLABELLED: Multiple sclerosis is a debilitating demyelinating progressive neurodegenerative disease, that eventually leads to the death of patients. Transcriptomic patient dataset analysis revealed marked alterations in P2Y12 expression in microglia from individuals with Multiple Sclerosis. Absorption, Distribution, Metabolism, and Excretion (ADME) profiling highlighted clopidogrel, a P2Y12 inhibitor, as a potentially promising treatment option for advanced stages of the disease. Our previous invitro studies using N9 microglial cells showed that, clopidogrel effectively mitigated TNF-α mediated inflammatory response and chemotaxis. We employed targeted metabolomic analysis of healthy, cuprizone-fed, clopidogrel-treated, and clopidogrel-treated cuprizone-fed mice to understand the metabolic modulation associated with clopidogrel treatment. Our analysis reveals that cuprizone-fed mice show deregulation of metabolic pathways important for lipid, oxidative stress, and biotin metabolism. Notably, clopidogrel modulates metabolic pathways in cuprizone-fed mice particularly involved in lipid, biotin and myelin biosynthesis. Taken together, our earlier findings with N9 microglial cells and current results from the cuprizone-fed mice model suggest clopidogrel as a potential therapeutic agent in Multiple Sclerosis.

SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s13205-026-04715-0.