| Identification | Back Directory | [Name]
ALPHA-(4-CHLOROPHENYL)-4-[(4-FLUOROPHENYL)METHYL]-1-PIPERIDINEETHANOL | [CAS]
119431-25-3 | [Synonyms]
SL 820715
ELIPRODIL
1-(4-broMophenyl)-2-(4-(4-fluorobenzyl)piperidin-1-yl)ethanol
α-(4-Chlorophenyl)-4-[(4-fluorophenyl)Methyl]-1-piperidineethanol
1-(4-chlorophenyl)-2-(4-(4-fluorobenzyl)piperidin-1-yl)ethan-1-ol
α-(4-chlorophenyl)-4-[(4-fluorophenyl)methyl]-1-piperidineethanol
(+-)-alpha-(p-Chlorophenyl)-4-(p-fluorobenzyl)-1-piperidineethanol
1-Piperidineethanol, α-(4-chlorophenyl)-4-[(4-fluorophenyl)methyl]-
ALPHA-(4-CHLOROPHENYL)-4-[(4-FLUOROPHENYL)METHYL]-1-PIPERIDINEETHANOL
SL 820715, α-(4-Chlorophenyl)-4-[(4-fluorophenyl)methyl]-1-piperidineethanol | [Molecular Formula]
C20H23ClFNO | [MDL Number]
MFCD00866651 | [MOL File]
119431-25-3.mol | [Molecular Weight]
347.85 |
| Chemical Properties | Back Directory | [Boiling point ]
474.1±35.0 °C(Predicted) | [density ]
1.205±0.06 g/cm3(Predicted) | [storage temp. ]
2-8°C
| [solubility ]
DMSO: ~17 mg/mL
| [form ]
solid
| [pka]
13.99±0.20(Predicted) | [color ]
white
| [InChI]
1S/C20H23ClFNO/c21-18-5-3-17(4-6-18)20(24)14-23-11-9-16(10-12-23)13-15-1-7-19(22)8-2-15/h1-8,16,20,24H,9-14H2 | [InChIKey]
GGUSQTSTQSHJAH-UHFFFAOYSA-N | [SMILES]
OC(CN1CCC(CC1)Cc2ccc(F)cc2)c3ccc(Cl)cc3 |
| Hazard Information | Back Directory | [Description]
N-Methyl-D-aspartate (NMDA) receptors are calcium permeable ligand-gated channels of the central nervous system that are activated after binding of the co-agonists glutamate and glycine. Eliprodil is a non-competitive NMDA receptor antagonist that inhibits neuronal calcium channel currents. It is selective for NR2B subunit-containing receptors (IC50 = 1 μM), displaying greater than 100-fold selectivity for NR2B over NR2A and NR2C subunits. Eliprodil also avidly binds σ1 and σ2 sites (Kis = 0.013 and 0.63 μM, respectively). It is effective in vivo, blocking ischemia-induced neurodegeneration in the CA1 region of the hippocampus of gerbils subjected to bilateral carotid artery occlusion. Eliprodil can also have proarrhythmic actions in hearts under normal conditions. | [Uses]
Eliprodil is a noncardiac drug with neuroprotective properties. It is also a N-Methyl-D-aspartate receptor (NMDAR) antagonist. | [Definition]
ChEBI: Eliprodil is a racemate comprising equimolar amounts of (R)- and (S)-eliprodil. It is a non-competitive N-methyl-D-aspartate (NMDA) receptor antagonist and an anti-ischaemic agent that exhibits neuroprotective properties. It has a role as a geroprotector, a NMDA receptor antagonist, a neuroprotective agent and a calcium channel blocker. It contains a (R)-eliprodil and a (S)-eliprodil. | [Biological Activity]
Non-competitive NMDA receptor antagonist that acts at the polyamine modulatory site. Selective for NR2B- over NR2A- and NR2C-containing receptors (IC 50 values are 1, > 100 and > 100 μ M respectively). Also σ 1 ligand (K i = 0.013 μ M). Antagonizes neuronal voltage-gated Ca 2+ channels and selectively inhibits the rapid component of the delayed rectifier K + current (I Kr ). Neuroprotective. | [storage]
+4°C (desiccate) | [References]
[1] CATHERINE P. BATH. The effects of ifenprodil and eliprodil on voltage-dependent Ca2+ channels and in gerbil global cerebral ischaemia[J]. European journal of pharmacology, 1996, 299 1: Pages 103-112. DOI: 10.1016/0014-2999(95)00846-2
[2] E R WHITTEMORE R M W V I Ilyin. Antagonism of N-methyl-D-aspartate receptors by sigma site ligands: potency, subtype-selectivity and mechanisms of inhibition.[J]. Journal of Pharmacology and Experimental Therapeutics, 1997, 282 1: 326-338.
[3] SARAH GRIMWOOD. Characterisation of N-Methyl-D-Aspartate Receptor-Specific [3H]Ifenprodil Binding to Recombinant Human NR1a/NR2B Receptors Compared with Native Receptors in Rodent Brain Membranes[J]. Journal of Neurochemistry, 2008, 75 6: 2455-2463. DOI: 10.1046/j.1471-4159.2000.0752455.x
[4] CSABA LENGYEL. Effect of a neuroprotective drug, eliprodil on cardiac repolarisation: importance of the decreased repolarisation reserve in the development of proarrhythmic risk[J]. British Journal of Pharmacology, 2009, 143 1: 152-158. DOI: 10.1038/sj.bjp.0705901 |
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