Blood-brain penetration of 5-hydroxytryptamine derivatives

Bioorganic & Medicinal Chemistry Letters
1994.0

Abstract

Glycosyl phosphate derivatives of N-acetyl-5-hydroxytryptamine were synthesized from 2-deoxy-Dglucose, D-glucose and D-mannose. These brain transport vectors for the precursor of melatonin were tested for locomotion on mice : with intracerebral and peripheral administrations, the prodrugs exhibited an inhibitory effect, whereas the same effect was observed for melatonin or its precursor onlywith an izv injection. The blood brain barrier (BBB) protects the brain against toxic effects of compounds produced at the periphery and also constitutes a serious limitation in the use of drugs directed towards cerebral targets. Among the various strategies proposed to improve the crossing of BBB by prodrugs (l-3), the use of glycosyl phosphotriester derivatives has been previously proposed (4) and we have recently shown that, in mice, the AZI delivery within the brain was markedly improved by using an oral dose of AZIglycosyl ester prodrug (5). In the present work, we developed the glycosyl phosphotriester transport system to N-acetyl-5 hydroxytryptamine 1 which is the immediate metabolic precursor of melatonin 2.Melatonin is a neural hormone which exerts numerous physiological effects in brain function including behavioral changes : food and fluid intake (6), sexual behavior (7-l l), sleep (12,13) and in particular locomotor activity (14-16). The clinical perspectives of this serotonin metabolite cover various fields such as aging process, cancer, epilepsy, seasonal affective disorder and circadian rhythmicity (17,18).The herein presented experiments studied the ability of N-acetyl-Shydroxytryptamine glycosyl phosphotriester derivatives to cross the BBB by measuring their functional cerebral effect on locomotion. This effect was compared to that of melatonin 2 itself, which exhibited a decreased locomotor activity with intracerebral injection of low doses (0.1-100 ng) (14), whereas a peripheral administration at high concentration (30 mg/kg) was shown to be inactive in mice (16).

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