. . . . . . . "150812-12-7"@en . "Approximately 80% protein bound. "@en . "Humans and other mammals"@en . "RTG"@en . . . . "Lethal Dose, acute, oral, rat = 100 mg/kg; Lethal Dose, chronic, oral, rat = 5.1 mg/kg/day, 90-day; Most common adverse effects that lead to discontinuation of therapy include dizziness and somnolence. "@en . "Potiga"@en . . . "8.7 L/kg "@en . "N-(2-Amino-4-(4-fluorobenzylamino)-phenyl) carbamic acid ethyl ester"@en . . "0.58 - 0.76 L/h\u00B7kg. Clearance may differ between ethnic groups with Black Americans having 20% lower clearance than Caucasian Americans. "@en . "Ezogabine has a novel mechanism of action that involves opening of neuronal Kv7.2-7.5 (formerly KCNQ2-5) voltage activated potassium channels. These channels (primarily Kv7.2/7.3) enable generation of the M-current, a sub-threshold potassium current that serves to stabilize the membrane potential and control neuronal excitability. In addition to acting on potassium ion channels, retigabine also affects GABA neurotransmission in the GABA-A receptor, which is a key inhibitory receptor in the central nervous system and is implicated in epilepsy. Malfunctioning of the GABA-A receptor leads to hyperexcitability in the brain, which causes seizures, making this receptor an important target for antiepileptic therapeutics. Apart from increasing the concentration of GABA in the brain (by either enhancing GABA synthesis or blocking GABA metabolism), retigabine allosterically potentiates GABA-induced current in rat cortical neurons in a concentration-dependent manner. Numerous studies have demonstrated that retigabine is effective in a broad spectrum of in vivo epilepsy and seizure models."@en . "N-(2-Amino-4-(4-fluorobenzylamino)phenyl)carbamic acid ethyl ester"@en . . . . . . . . . "D-23129"@en . "With a high-fat meal, Cmax is moderately increased. "@en . "Retigabine"@en . "Urine (85%, 36% of total dose as unchanged drug, 18% of total dose as NAMR) and feces (14%, 3% of total dose as unchanged drug) "@en . . . "# Porter RJ, Nohria V, Rundfeldt C: Retigabine. Neurotherapeutics. 2007 Jan;4(1):149-54. \"Pubmed\":http://www.ncbi.nlm.nih.gov/pubmed/17199031 # Hermann R, Ferron GM, Erb K, Knebel N, Ruus P, Paul J, Richards L, Cnota HP, Troy S: Effects of age and sex on the disposition of retigabine. Clin Pharmacol Ther. 2003 Jan;73(1):61-70. \"Pubmed\":http://www.ncbi.nlm.nih.gov/pubmed/12545144 # Hermann R, Knebel NG, Niebch G, Richards L, Borlak J, Locher M: Pharmacokinetic interaction between retigabine and lamotrigine in healthy subjects. Eur J Clin Pharmacol. 2003 Apr;58(12):795-802. Epub 2003 Feb 28. \"Pubmed\":http://www.ncbi.nlm.nih.gov/pubmed/12698305 # Dost R, Rostock A, Rundfeldt C: The anti-hyperalgesic activity of retigabine is mediated by KCNQ potassium channel activation. Naunyn Schmiedebergs Arch Pharmacol. 2004 Apr;369(4):382-90. Epub 2004 Mar 9. \"Pubmed\":http://www.ncbi.nlm.nih.gov/pubmed/15007538 # Mikkelsen JD: The KCNQ channel activator retigabine blocks haloperidol-induced c-Fos expression in the striatum of the rat. Neurosci Lett. 2004 May 27;362(3):240-3. \"Pubmed\":http://www.ncbi.nlm.nih.gov/pubmed/15158023 # Punke MA, Friederich P: Retigabine stimulates human KCNQ2/Q3 channels in the presence of bupivacaine. Anesthesiology. 2004 Aug;101(2):430-8. \"Pubmed\":http://www.ncbi.nlm.nih.gov/pubmed/15277926 # Wuttke TV, Seebohm G, Bail S, Maljevic S, Lerche H: The new anticonvulsant retigabine favors voltage-dependent opening of the Kv7.2 (KCNQ2) channel by binding to its activation gate. Mol Pharmacol. 2005 Apr;67(4):1009-17. Epub 2005 Jan 20. \"Pubmed\":http://www.ncbi.nlm.nih.gov/pubmed/15662042 # Fatope MO: Retigabine (ASTA Medica). IDrugs. 2001 Jan;4(1):93-8. \"Pubmed\":http://www.ncbi.nlm.nih.gov/pubmed/16034707 # Orhan G, Wuttke TV, Nies AT, Schwab M, Lerche H: Retigabine/Ezogabine, a KCNQ/K(V)7 channel opener: pharmacological and clinical data. Expert Opin Pharmacother. 2012 Aug;13(12):1807-16. doi: 10.1517/14656566.2012.706278. Epub 2012 Jul 12. \"Pubmed\":http://www.ncbi.nlm.nih.gov/pubmed/22783830 # Amabile CM, Vasudevan A: Ezogabine: a novel antiepileptic for adjunctive treatment of partial-onset seizures. Pharmacotherapy. 2013 Feb;33(2):187-94. doi: 10.1002/phar.1185. \"Pubmed\":http://www.ncbi.nlm.nih.gov/pubmed/23386597 "@en . . . "Adjuvant treatment of partial-onset seizures. "@en . . "Rapidly absorbed and distributed, with an absolute oral bioavailability of 60%. Pharmacokinetics of ezogabine suggest first-order kinetics. Tmax, single oral dose = 30-120 minutes; Time to steady state = 3 days "@en . . . "Ezogabine"@en . "Terminal half-life = 7.5 hours "@en . "Ethyl 2-amino-4-((P-fluorobenzyl)amino)carbanilate"@en . . . . . . "approved"@en . . . " "@en . . . . "EZG"@en . . . . . . . . "Ethyl {2-amino-4-[(4-fluorobenzyl)amino]phenyl}carbamate"@en . . . . "Ezogabine (D23129) is a close structural analog of the centrally acting analgesic flupitrine. It is a neuronal potassium channel opener being developed as a first-in-class antiepileptic drug (AED) and is currently being studied in Phase 3 trials as an adjunctive treatment for partial-onset seizures in adult patients with refractory epilepsy. FDA approved in June 10, 2011 under the name of ezogabine. "@en .