Eliprodil

Eliprodil
Clinical data
ATC code
  • None
Identifiers
  • 1-(4-Chlorophenyl)-2-[4-[(4-fluorophenyl)methyl]piperidin-1-yl]ethanol
CAS Number
PubChem CID
ChemSpider
UNII
ChEBI
ChEMBL
CompTox Dashboard (EPA)
ECHA InfoCard100.162.249 Edit this at Wikidata
Chemical and physical data
FormulaC20H23ClFNO
Molar mass347.86 g·mol−1
3D model (JSmol)
  • C1CN(CCC1CC2=CC=C(C=C2)F)CC(C3=CC=C(C=C3)Cl)O
  • 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 checkY
  • Key:GGUSQTSTQSHJAH-UHFFFAOYSA-N checkY
 ☒NcheckY (what is this?)  (verify)

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.[1][2][3]

NMDA receptors are a key component in mediating glutamate-induced excitotoxicity, and it is believed that NMDA antagonists would be neuroprotective after a stroke or other traumatic brain injury.[4] 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.[3]

  1. ^ The Pharma Letter. 2 December 1996 Synthelabo's Eliprodil Fails In Stroke Trials
  2. ^ De Keyser J, Sulter G, Luiten PG (December 1999). "Clinical trials with neuroprotective drugs in acute ischaemic stroke: are we doing the right thing?". Trends in Neurosciences. 22 (12): 535–40. doi:10.1016/s0166-2236(99)01463-0. PMID 10542428. S2CID 16302841.
  3. ^ a b Lee JM, Zipfel GJ, Choi DW (June 1999). "The changing landscape of ischaemic brain injury mechanisms". Nature. 399 (6738 Suppl): A7-14. doi:10.1038/399a007. PMID 10392575. S2CID 10086931.
  4. ^ Ikonomidou C, Turski L (October 2002). "Why did NMDA receptor antagonists fail clinical trials for stroke and traumatic brain injury?". The Lancet. Neurology. 1 (6): 383–6. doi:10.1016/s1474-4422(02)00164-3. PMID 12849400. S2CID 31477519.