1.0 2009-07-21 20:28:14 UTC 2026-05-14 16:56:35 UTC T3D2967 Memantine SmallMolecule Memantine (C12H21N) is an exogenous organic compound with an average molecular weight of 179.30 g/mol. At room temperature, it exists as a solid. Memantine belongs to the amines, a subclass of organonitrogen compounds within the organic compounds. This compound acts as an NMDA receptor antagonist and a dopaminergic agent. Its biological roles and applications include use as an antiparkinson drug, a neuroprotective agent, and an antidepressant. Memantine exerts its action through uncompetitive NMDA receptor antagonism, binding preferentially to the NMDA receptor-operated cation channels. It targets several proteins, including the D(2) dopamine receptor (DRD2), the Alpha-7 nicotinic cholinergic receptor subunit (CHRNA7), the antagonist/binder of 5-hydroxytryptamine receptor 3A (HTR3A), and glutamate receptor ionotropic NMDA 1 (GRIN1), 2A (GRIN2A), 2B (GRIN2B), and 3A (GRIN3A). Studies suggest that memantine binds more effectively than Mg2+ ions at the NMDA receptor. In the brain of demented patients, prolonged increased levels of glutamate can counter the voltage-dependent block of NMDA receptors by Mg2+ ions, allowing continuous influx of Ca2+ ions into cells and leading to neuronal degeneration. Memantine is recorded in 11 sources, including anti-dementia drugs within healthcare, pharmaceuticals, and veterinary products. Other sources include food preservation in food processing and cookware, floors in building and construction, soap detergents and smoking requisites in household cleaning and consumer products, and electrical and electronic equipment such as magnets, radio transmission systems, and electrically stimulated smoking devices. The recorded exposure route for this compound is oral. Drug Synthetic Toxin Organic Compound Amine Drug Central Nervous System Agent Antiparkinson Agent Dopamine Agent Excitatory Amino Acid Antagonist Antidyskinetic Metabolite Synthetic Compound Human Neurotoxin 1,3-Dimethyl-5-adamantanamine 1-Amino-3,5-dimethyladamantane 3,5-Dimethyl-1-adamantanamine 3,5-Dimethyl-1-aminoadamantane 3,5-Dimethyltricyclo(3.3.1.1(3,7))decan-1-amine Abixa Akatinol Axura Ebixa Memantina Memantinum Memox Namenda C12H21N 179.3018 179.167399677 3,5-dimethyladamantan-1-amine memantine 19982-08-2 CC12CC3CC(C)(C1)CC(N)(C3)C2 InChI=1S/C12H21N/c1-10-3-9-4-11(2,6-10)8-12(13,5-9)7-10/h9H,3-8,13H2,1-2H3 BUGYDGFZZOZRHP-UHFFFAOYSA-N Organic compounds Organic nitrogen compounds Organonitrogen compounds Amines Monoalkylamines Hydrocarbon derivatives Organopnictogen compounds Aliphatic homopolycyclic compound Hydrocarbon derivative Organopnictogen compound Primary aliphatic amine Aliphatic homopolycyclic compounds adamantanes primary aliphatic amine Detected and Not Quantified Exogenous Membrane Memantine Action Pathway SMP0126204 Memantine Drug Metabolism Action Pathway SMP0143469 Solid White powder. melting_point 258°C solubility 35 mg/mL (HCl salt), 0.9 mg/mL for free base logp 3.28 logp 3.31 ALOGPS logs -3.60 ALOGPS solubility 4.55e-02 g/l ALOGPS logp 2.07 ChemAxon pka_strongest_basic 10.7 ChemAxon iupac 3,5-dimethyladamantan-1-amine ChemAxon average_mass 179.3018 ChemAxon mono_mass 179.167399677 ChemAxon smiles CC12CC3CC(C)(C1)CC(N)(C3)C2 ChemAxon formula C12H21N ChemAxon inchi InChI=1S/C12H21N/c1-10-3-9-4-11(2,6-10)8-12(13,5-9)7-10/h9H,3-8,13H2,1-2H3 ChemAxon inchikey BUGYDGFZZOZRHP-UHFFFAOYSA-N ChemAxon polar_surface_area 26.02 ChemAxon refractivity 54.49 ChemAxon polarizability 21.82 ChemAxon rotatable_bond_count 0 ChemAxon acceptor_count 1 ChemAxon donor_count 1 ChemAxon physiological_charge 1 ChemAxon formal_charge 0 ChemAxon Well absorbed orally with a bioavailability of approximately 100%. Peak plasma concentrations are reached in 3-7 hours. Food has no effect on absorption. 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 gamma-aminobutyric acid (GABA), benzodiazepine, dopamine, adrenergic, histamine, or glycine receptors or for voltage-dependent calcium, sodium, or potassium channels. Excreted largely unchanged. About 20% is metabolized to 1-amino-3-hydroxymethyl-5-methyl-adamantane and 3-amino-1-hydroxy-5,7-dimethyl-adamantane. Route of Elimination: 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. Half Life: 60-100 hours No indication of carcinogenicity to humans (not listed by IARC). For the treatment of moderate to severe dementia of the Alzheimer's type. #<HealthEffect::ActiveRecord_Associations_CollectionProxy:0x00007f722724c8b8> 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. As in any cases of overdose, general supportive measures should be utilized, and treatment should be symptomatic. Elimination of memantine can be enhanced by acidification of urine. (L1712) DB01043 HMDB15177 4054 CHEMBL807 3914 C13736 64312 Memantine Memantine 10029935 14530799 16906789 11026482 11403963 Drugs.com: http://www.drugs.com/cons/Memantine.html RxList: The Internet Drug Index (2009).: http://www.rxlist.com/ BE0000760 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 and ultimately 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. IC50 5.6 uM BindingDB 50062599 BE0000417 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 and ultimately 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. IC50 5.5 uM BindingDB 50062599 BE0000641 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 and ultimately 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. BE0000365 IC50 9.52 uM BindingDB 50062599 BE0000311 BE0003438 BE0000756 BE0003648 IC50 27.2 uM BindingDB 50062599 BE0002341 BE0000396 BE0000534 BE0000454 BE0003596 BE0003599 BE0000795 BE0002344 BE0003592 BE0002345 BE0000471 BE0000523 BE0000381 BE0002346 BE0000478 BE0003595 BE0000764 BE0003593 BE0003594 BE0003597