. . "Side effects include pain, abnormal crying, leg pain, fever, increased apetite. Adverse drug reactions include: dizziness, confusion, headache, hallucinations, tiredness. Less common side effects include: vomiting, anxiety, hypertonia, cystitis, and increased libido. Doses of up to 400 mg have been tolerated."@en . . . . . "Well absorbed orally with a bioavailability of approximately 100%. Peak plasma concentrations are reached in 3-7 hours. Food has no effect on absorption."@en . . . . . . . . . . . . "1,3-Dimethyl-5-adamantanamine"@en . . "Memantine is an amantadine derivative with low to moderate-affinity for NMDA receptors. It is a noncompetitive NMDA receptor antagonist that binds preferentially to NMDA receptor-operated cation channels. It blocks the effects of excessive levels of glutamate that may lead to neuronal dysfunction. It is under investigation for the treatment of Alzheimer's disease, but there has been no clinical support for the prevention or slowing of disease progression."@en . "For the treatment of moderate to severe dementia of the Alzheimer's type."@en . "Memantine exerts its action through uncompetitive NMDA receptor antagonism, binding preferentially to the NMDA receptor-operated cation channels. Prolonged increased levels of glutamate in the brain of demented patients are sufficient to counter the voltage-dependent block of NMDA receptors by Mg²⁺ ions and allow continuous influx of Ca²⁺ ions into cells, ultimately resulting in neuronal degeneration. Studies suggest that memantine binds more effectively than Mg²⁺ ions at the NMDA receptor, and thereby effectively blocks this prolonged influx of Ca²⁺ ions through the NMDA channel whilst preserving the transient physiological activation of the channels by higher concentrations of synaptically released glutamate. Thus memantine protects against chronically elevated concentrations of glutamate. Memantine also has antagonistic activity at the type 3 serotonergic (5-HT₃) receptor with a potency that is similar to that at the NMDA receptor, and lower antagonistic activity at the nicotinic acetylcholine receptor. This drug has no affinity for \u03B3-aminobutyric acid (GABA), benzodiazepine, dopamine, adrenergic, histamine, or glycine receptors or for voltage-dependent calcium, sodium, or potassium channels."@en . "1-Amino-3,5-dimethyladamantane"@en . " "@en . . . "Take without regard to meals."@en . . "Humans and other mammals"@en . . "3,5-Dimethyl-1-aminoadamantane"@en . "Memantine"@en . "\"DrugSyn.org\":http://www.drugsyn.org/Memantine.htm"@en . . . . . . . . "3,5-Dimethyl-1-adamantanamine"@en . . . . . . . "60-100 hours"@en . "Memantina"@en . "* 9 to 11 L/kg"@en . . . . . . . . . . . . . . . . . "3,5-Dimethyltricyclo(3.3.1.1(3,7))decan-1-amine"@en . "19982-08-2"@en . "# Cacabelos R, Takeda M, Winblad B: The glutamatergic system and neurodegeneration in dementia: preventive strategies in Alzheimer's disease. Int J Geriatr Psychiatry. 1999 Jan;14(1):3-47. \"Pubmed\":http://www.ncbi.nlm.nih.gov/pubmed/10029935 # Rogawski MA, Wenk GL: The neuropharmacological basis for the use of memantine in the treatment of Alzheimer's disease. CNS Drug Rev. 2003 Fall;9(3):275-308. \"Pubmed\":http://www.ncbi.nlm.nih.gov/pubmed/14530799 # Robinson DM, Keating GM: Memantine: a review of its use in Alzheimer's disease. Drugs. 2006;66(11):1515-34. \"Pubmed\":http://www.ncbi.nlm.nih.gov/pubmed/16906789 # Rogawski MA: Low affinity channel blocking (uncompetitive) NMDA receptor antagonists as therapeutic agents--toward an understanding of their favorable tolerability. Amino Acids. 2000;19(1):133-49. \"Pubmed\":http://www.ncbi.nlm.nih.gov/pubmed/11026482 # Rammes G, Rupprecht R, Ferrari U, Zieglgansberger W, Parsons CG: The N-methyl-D-aspartate receptor channel blockers memantine, MRZ 2/579 and other amino-alkyl-cyclohexanes antagonise 5-HT(3) receptor currents in cultured HEK-293 and N1E-115 cell systems in a non-competitive manner. Neurosci Lett. 2001 Jun 22;306(1-2):81-4. \"Pubmed\":http://www.ncbi.nlm.nih.gov/pubmed/11403963"@en . . . . . "Memantine"@en . . . "approved"@en . . . . . . . . . "45%"@en . . "Memantinum"@en . "investigational"@en . " "@en . "Memantine undergoes partial hepatic metabolism. About 48% of administered drug is excreted unchanged in urine; the remainder is converted primarily to three polar metabolites which possess minimal NMDA receptor antagonistic activity: the N-glucuronide conjugate, 6-hydroxy memantine, and 1-nitroso-deaminated memantine. It is excreted predominantly in the urine, unchanged."@en . . . . . . .