| Compound Information | SONAR Target prediction |
| Name: | Amantadine hydrochloride |
| Unique Identifier: | LOPAC 00243 |
| MolClass: | Checkout models in ver1.5 and ver1.0 |
| Molecular Formula: | C10ClH18N |
| 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 |
| Class: | Dopamine |
| Action: | Releaser |
| 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 |
| Found: 24 nonactive as graph: single | with analogs | [1] << Back 1 2 3 4 5 6 7 8 9 10 Next >> [24] |
| Species: | 4932 |
| Condition: | DEP1 |
| Replicates: | 2 |
| Raw OD Value: r im | 0.7038±0.00700036 |
| Normalized OD Score: sc h | 0.9881±0.012372 |
| Z-Score: | -0.5019±0.530282 |
| p-Value: | 0.639804 |
| Z-Factor: | -61.0339 |
| Fitness Defect: | 0.4466 |
| Bioactivity Statement: | Nonactive |
| ps |
| DBLink | Rows returned: 653 | [1] << Back 101 102 103 104 105 106 107 108 109 Next >> [109] |
| 7170481 | [(1S,2R,4S)-1,7,7-trimethylnorbornan-2-yl]azanium |
| 7170956 | [(1S,2S,4R)-1,3,3-trimethylnorbornan-2-yl]azanium |
| 7170957 | (1S,2S,4R)-1,3,3-trimethylnorbornan-2-amine |
| 7173891 | [(1R,2R,4S)-1,3,3-trimethylnorbornan-2-yl]azanium |
| 7173892 | (1R,2R,4S)-1,3,3-trimethylnorbornan-2-amine |
| 7177099 | [(1R,2R,5R)-5-methyl-2-propan-2-yl-cyclohexyl]azanium |
| internal high similarity DBLink | Rows returned: 12 | 1 2 Next >> |
| BTB 10381 | 1.0000 |
| SPE01500110 | 1.0000 |
| RJC 04000 | 1.0000 |
| RH 01534 | 1.0000 |
| RDP 00128 | 1.0000 |
| LOPAC 00377 | 1.0000 |
| active | Cluster 6660 | Additional Members: 3 | Rows returned: 0 |
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