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Through the CREB/BDNF axis, Sem increases remyelination and overcomes demyelination, therefore can amend experimental autoimmune encephalomyelitis (EAE)-induced multiple sclerosis in mice (Sadek et al

Proposed explanations include: Tissue retention of peptide or active metabolites Persistent activation of signaling cascades beyond peptide clearance Potential for active metabolites with prolonged tissue residence Excretion Pathways Limited data on elimination routes indicates: Likely renal excretion of peptide fragments based on molecular weight and water solubility Potential hepatic contribution to metabolite clearance No evidence of accumulation in chronic dosing studies in rats and monkeys Degradation products eliminated without evidence of toxic metabolite formation The dramatic disconnect between three-minute plasma half-life and prolonged metabolic effects remains one of the most intriguing and poorly understood aspects of AOD-9604 pharmacology, requiring further mechanistic investigation

Sedky, A

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An overview of major safety and efficacy clinical trials is provided in Tables 1, 2, 3, and 4 to bring context to the mechanistic findings reported herein

Most users find these effects tolerable and transient