Wikipedia:WikiProject Chemicals/Chembox validation/VerifiedDataSandbox and Eliprodil: Difference between pages

{{Short description|Chemical compound}}

| Watchedfields = changed

| verifiedrevid = 461093042

| IUPAC_name = 1-(4-Chlorophenyl)-2-[4-[(4-fluorophenyl)methyl]piperidin-1-yl]ethanol

| image = Eliprodil.svg

| width = 250px

| pregnancy_US = <!-- A / B / C / D / X -->

| legal_US =

| legal_status =

| bioavailability =

| protein_bound =

| metabolism =

| excretion =

| CAS_number_Ref = {{cascite|changed|??}}

| CAS_number = 119431-25-3

| ATC_prefix = None

| ATC_suffix =

| DrugBank =

| ChEBI = 91784

| UNII_Ref = {{fdacite|correct|FDA}}

| synonyms =

'''Eliprodil''' (codenamed '''SL-82.0715''') is an [[NMDA antagonist]] drug candidate which selectively inhibits the NR2B (GLUN2B) subtype NMDA receptor at submicromolar concentrations. Eliprodil failed a Phase III clinical trial for the treatment of acute [[ischemic stroke]] in 1996, sponsored by Synthélabo Recherche.<ref>The Pharma Letter. 2 December 1996 [http://www.thepharmaletter.com/article/synthelabo-s-eliprodil-fails-in-stroke-trials Synthelabo's Eliprodil Fails In Stroke Trials]</ref><ref name=DeKeyser>{{cite journal | vauthors = De Keyser J, Sulter G, Luiten PG | title = Clinical trials with neuroprotective drugs in acute ischaemic stroke: are we doing the right thing? | journal = Trends in Neurosciences | volume = 22 | issue = 12 | pages = 535–40 | date = December 1999 | pmid = 10542428 | doi = 10.1016/s0166-2236(99)01463-0 | s2cid = 16302841 | url = https://www.rug.nl/research/portal/en/publications/clinical-trials-with-neuroprotective-drugs-in-acute-ischaemic-stroke(7deb2c8f-aa7e-4685-8dc2-2d41a70da739).html }}</ref><ref name=Lee>{{cite journal | vauthors = Lee JM, Zipfel GJ, Choi DW | title = The changing landscape of ischaemic brain injury mechanisms | journal = Nature | volume = 399 | issue = 6738 Suppl | pages = A7-14 | date = June 1999 | pmid = 10392575 | doi = 10.1038/399a007 | s2cid = 10086931 }}</ref>

[[NMDA receptors]] are a key component in mediating glutamate-induced [[excitotoxicity]], and it is believed that [[NMDA antagonists]] would be [[Neuroprotection|neuroprotective]] after a stroke or other [[traumatic brain injury]].<ref name=Ikonomidou>{{cite journal | vauthors = Ikonomidou C, Turski L | title = Why did NMDA receptor antagonists fail clinical trials for stroke and traumatic brain injury? | journal = The Lancet. Neurology | volume = 1 | issue = 6 | pages = 383–6 | date = October 2002 | pmid = 12849400 | doi = 10.1016/s1474-4422(02)00164-3 | s2cid = 31477519 }}</ref> After a traumatic brain injury, neurons become deprived of glucose and oxygen. These neurons quickly lose ATP and become depolarized, which releases glutamate. The extracellular buildup of glutamate triggers the overstimulation of [[AMPA]] and NMDA receptors. This, in turn, causes an influx of Na⁺ and Ca²⁺. Therefore, when NMDA receptors are activated, there is an increase in intracellular Ca²⁺ concentration. High Ca²⁺ causes fatal metabolic consequences, including neuronal cell death.<ref name=Lee/>

== References ==

{{Reflist}}

{{Ionotropic glutamate receptor modulators}}

{{Sigma receptor modulators}}

[[Category:Abandoned drugs]]

[[Category:Chloroarenes]]

[[Category:NMDA receptor antagonists]]

[[Category:Fluoroarenes]]

[[Category:Phenylethanolamines]]

[[Category:Piperidines]]

{{nervous-system-drug-stub}}