Compound Information | SONAR Target prediction |
Name: | AMANTADINE HYDROCHLORIDE |
Unique Identifier: | SPE01500110 |
MolClass: | Checkout models in ver1.5 and ver1.0 |
Molecular Formula: | |
Molecular Weight: | 169.566 g/mol |
X log p: | -0.732 (online calculus) |
Lipinksi Failures | 0 |
TPSA | 0 |
Hydrogen Bond Donor Count: | 0 |
Hydrogen Bond Acceptors Count: | 1 |
Rotatable Bond Count: | 0 |
Canonical Smiles: | Cl.NC12CC3CC(CC(C3)C1)C2 |
Source: | synthetic |
Therapeutics: | antiviral, antiparkinsonian; treatment of drug-induced extrapyrimidal reactions |
Generic_name: | Memantine |
Chemical_iupac_name: | 3,5-dimethyladamantan-1-amine |
Drug_type: | Approved Drug |
Pharmgkb_id: | PA10364 |
Kegg_compound_id: | C13736 |
Drugbank_id: | APRD00221 |
Melting_point: | 258 oC (HCl salt) |
H2o_solubility: | 35 mg/mL (HCl salt), 0.9 mg/mL for free base |
Logp: | 2.197 |
Cas_registry_number: | 19982-08-2 |
Drug_category: | Dopamine Agents; Antiparkinson Agents; Antidyskinetics; Excitatory Amino Acid Antagonists; Central Nervous System Agents; ATC:N06DX01 |
Indication: | For the treatment of moderate to severe dementia of the Alzheimer-s type. |
Pharmacology: | Memantine, an amantadine derivative, is an NMDA receptor antagonist used in the treatment of Alzheimer-s disease. It differs from traditional agents used in Alzheimer-s disease by acting on glutamatergic neurotransmission, rather than cholinergic. There is some evidence that dysfunction of glutamatergic neurotransmission, manifested as neuronal excitotoxicity, is involved in the aetiology of Alzheimer-s disease (Cacabelos et al., 1999). As such, targeting the glutamatergic system, specifically NMDA receptors, was a novel approach to treatment in view of the limited efficacy of existing drugs targeting the cholinergic system. A systematic review of randomised controlled trials found that memantine has a positive effect on cognition, mood, behaviour, and the ability to perform daily activities. There is no evidence that memantine prevents or slows neurodegeneration in patients with Alzheimer-s disease. |
Mechanism_of_action: | 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. |
Organisms_affected: | Humans and other mammals |