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T0080 is a potent, selective, and central nervous system (CNS)-penetrating small-molecule antagonist of formyl peptide receptor 1 (FPR1). Developed by researchers at Tianjin Medical University General Hospital and Beijing Tiantan Hospital, T0080 blocks FPR1 signaling, which is activated by mitochondrial formyl peptides (mtFPs) and drives neuroinflammation and neurodegeneration. In preclinical models of multiple sclerosis (MS), such as experimental autoimmune encephalomyelitis (EAE) and cuprizone-induced demyelination, T0080 reduces microglial activation, mitochondrial dysfunction, axonal loss, and neuronal apoptosis. Additionally, T0080 has demonstrated efficacy in mitigating ischemic stroke-associated hemorrhagic transformation and atherosclerosis by reducing macrophage-mediated inflammation and vascular damage.
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