Flupirtine - CAS 56995-20-1
Catalog number:
Not Intended for Therapeutic Use. For research use only.
Molecular Formula:
Molecular Weight:
Potassium Channel
Flupirtine is a selective neuronal potassium channel opener act as an Analgesic, having substituted pyridine with central analgesic properties.
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Off-White Solid
D 9998; Katadolon; ethyl N-[2-amino-6-[(4-fluorophenyl)methylamino]pyridin-3-yl]carbamate;
Soluble in DMSO
Store at -20 °C
An Analgesic, having substituted pyridine with central analgesic properties.
Quality Standard:
Enterprise Standard
Shelf Life:
As supplied, 2 years from the QC date provided on the Certificate of Analysis, when stored properly
Melting Point:
114-116 °C
Canonical SMILES:
Current Developer:
Meda; NNRI; Synthetic Biologics
1.Inhibition of KV7 Channels Protects the Rat Heart against Myocardial Ischemia and Reperfusion Injury.
Hedegaard ER1, Johnsen J2, Povlsen JA2, Jespersen NR2, Shanmuganathan JA2, Laursen MR2, Kristiansen SB2, Simonsen U2, Bøtker HE2. J Pharmacol Exp Ther. 2016 Apr;357(1):94-102. doi: 10.1124/jpet.115.230409. Epub 2016 Feb 11.
The voltage-gated KV7 (KCNQ) potassium channels are activated by ischemia and involved in hypoxic vasodilatation. We investigated the effect of KV7 channel modulation on cardiac ischemia and reperfusion injury and its interaction with cardioprotection by ischemic preconditioning (IPC). Reverse-transcription polymerase chain reaction revealed expression of KV7.1, KV7.4, and KV7.5 in the left anterior descending rat coronary artery and all KV7 subtypes (KV7.1-KV7.5) in the left and right ventricles of the heart. Isolated hearts were subjected to no-flow global ischemia and reperfusion with and without IPC. Infarct size was quantified by 2,3,5-triphenyltetrazolium chloride staining. Two blockers of KV7 channels, XE991 [10,10-bis(4-pyridinylmethyl)-9(10H)-anthracenone] (10 µM) and linopirdine (10 µM), reduced infarct size and exerted additive infarct reduction to IPC. An opener of KV7 channels, flupirtine (10 µM) abolished infarct size reduction by IPC.
2.Expression and function of Kv7.4 channels in rat cardiac mitochondria: possible targets for cardioprotection.
Testai L1, Barrese V2, Soldovieri MV3, Ambrosino P3, Martelli A1, Vinciguerra I3, Miceli F4, Greenwood IA5, Curtis MJ6, Breschi MC1, Sisalli MJ4, Scorziello A4, Canduela MJ7, Grandes P7, Calderone V1, Taglialatela M8. Cardiovasc Res. 2016 May 1;110(1):40-50. doi: 10.1093/cvr/cvv281. Epub 2015 Dec 29.
AIMS: Plasmalemmal Kv7.1 (KCNQ1) channels are critical players in cardiac excitability; however, little is known on the functional role of additional Kv7 family members (Kv7.2-5) in cardiac cells. In this work, the expression, function, cellular and subcellular localization, and potential cardioprotective role against anoxic-ischaemic cardiac injury of Kv7.4 channels have been investigated.
3.Pharmacokinetics and disposition of flupirtine in the horse.
Giorgi M1, De Vito V2, Poapolathep A3, Rychshanova R4, Sgorbini M2, Owen H5. Vet J. 2016 Feb;208:76-80. doi: 10.1016/j.tvjl.2015.08.019. Epub 2015 Aug 20.
Flupirtine (FLU) is a non-opioid analgesic drug, with no antipyretic or anti-inflammatory effects, used in the treatment of a wide range of pain states in human beings. It does not induce the side effects associated with the classical drugs used as pain relievers. The aim of this study was to evaluate the pharmacokinetic profiles of FLU after IV and PO administration in healthy horses. Six mixed breed adult mares were randomly assigned to two treatment groups using an open, single-dose, two-treatment, two-phase, paired, cross-over design (2 × 2 Latin-square). Group 1 (n = 3) received a single dose of 1 mg/kg of FLU injected IV into the jugular vein. Group 2 (n = 3) received FLU (5 mg/kg) via nasogastric tube. The animals then swapped groups after a 1-week wash-out period and the doses were repeated. Blood samples (5 mL) were collected at 0.25, 0.5, 0.75, 1, 1.5, 2, 4, 6, 8, 10, 24, 36 and 48 h and plasma was then analysed by a validated HPLC method.
4.KV7 channels contribute to paracrine, but not metabolic or ischemic, regulation of coronary vascular reactivity in swine.
Goodwill AG1, Fu L2, Noblet JN1, Casalini ED1, Sassoon D1, Berwick ZC2, Kassab GS2, Tune JD1, Dick GM3. Am J Physiol Heart Circ Physiol. 2016 Mar 15;310(6):H693-704. doi: 10.1152/ajpheart.00688.2015. Epub 2016 Jan 29.
Hydrogen peroxide (H2O2) and voltage-dependent K(+) (KV) channels play key roles in regulating coronary blood flow in response to metabolic, ischemic, and paracrine stimuli. The KV channels responsible have not been identified, but KV7 channels are possible candidates. Existing data regarding KV7 channel function in the coronary circulation (limited to ex vivo assessments) are mixed. Thus we examined the hypothesis that KV7 channels are present in cells of the coronary vascular wall and regulate vasodilation in swine. We performed a variety of molecular, biochemical, and functional (in vivo and ex vivo) studies. Coronary arteries expressed KCNQ genes (quantitative PCR) and KV7.4 protein (Western blot). Immunostaining demonstrated KV7.4 expression in conduit and resistance vessels, perhaps most prominently in the endothelial and adventitial layers. Flupirtine, a KV7 opener, relaxed coronary artery rings, and this was attenuated by linopirdine, a KV7 blocker.
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CAS 56995-20-1 Flupirtine

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