@article {Heyn443, author = {H Heyn and D J McCarthy and S H Curry and M S Eisman and M W Anders}, title = {Brain uptake and biotransformation of remacemide hydrochloride, a novel anticonvulsant.}, volume = {22}, number = {3}, pages = {443--446}, year = {1994}, publisher = {American Society for Pharmacology and Experimental Therapeutics}, abstract = {The brain uptake and biotransformation of remacemide hydrochloride [(+/-)-2-amino-N-(1-methyl-1,2-diphenylethyl)acetamide monohydrochloride; FPL 12924AA] were studied in the rat. The brain uptake indices (BUI) for remacemide and its pharmacologically active metabolite FPL12495 [(+/-)-1-methyl-1,2-diphenylethylamine monohydrochloride] were 51 and 130\%, respectively. The BUI of [14C] remacemide and [14C]FPL12495 were not affected by increasing amounts of unlabeled remacemide or FPL12495, respectively. Likewise, the BUI of remacemide was not affected by dl-amphetamine or beta-phenethylamine. A mixture of [3H]remacemide hydrochloride (3H label in the glycine moiety) and [14C]remacemide hydrochloride (14C label in 1,2-diphenyl-2-aminopropane moiety) was administered by intracarotid injection. The ratio of 14C/3H in the brain was equal to that in the injection mixture, indicating that remacemide enters the brain intact. HPLC analysis of brain extracts of rats given [14C] remacemide hydrochloride by intracarotid injection revealed that 97.8 +/- 0.2\% (mean +/- SD) of the radioactivity was present as remacemide, whereas 1.9 +/- 0.2\% of the radioactivity was present as FPL12495. Finally, in vitro studies revealed that remacemide is hydrolyzed by whole-brain homogenates to the pharmacologically active metabolite FPL12495. Data indicate that remacemide enters the brain by passive diffusion and undergoes deglycination at the blood-brain barrier or within the brain to give FPL12495.}, issn = {0090-9556}, URL = {https://dmd.aspetjournals.org/content/22/3/443}, eprint = {https://dmd.aspetjournals.org/content/22/3/443.full.pdf}, journal = {Drug Metabolism and Disposition} }