FlupirtineAnalgesic agent CAS# 56995-20-1 |
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Quality Control & MSDS
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| Cas No. | 56995-20-1 | SDF | Download SDF |
| PubChem ID | 53276 | Appearance | Powder |
| Formula | C15H17FN4O2 | M.Wt | 304.32 |
| Type of Compound | N/A | Storage | Desiccate at -20°C |
| Synonyms | D 9998 | ||
| Solubility | Soluble in DMSO | ||
| Chemical Name | ethyl N-[2-amino-6-[(4-fluorophenyl)methylamino]pyridin-3-yl]carbamate | ||
| SMILES | CCOC(=O)NC1=C(N=C(C=C1)NCC2=CC=C(C=C2)F)N | ||
| Standard InChIKey | JUUFBMODXQKSTD-UHFFFAOYSA-N | ||
| Standard InChI | InChI=1S/C15H17FN4O2/c1-2-22-15(21)19-12-7-8-13(20-14(12)17)18-9-10-3-5-11(16)6-4-10/h3-8H,2,9H2,1H3,(H,19,21)(H3,17,18,20) | ||
| General tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months. We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months. Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it. |
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| About Packaging | 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial. 2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial. 3. Try to avoid loss or contamination during the experiment. |
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| Shipping Condition | Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request. | ||
| Description | Flupirtine(D 9998) is a selective neuronal potassium channel opener that also has NMDA receptor antagonist properties.
IC50 Value:
Target: Potassium channel; NMDA receptor
in vitro: High concentrations of flupirtine antagonized inward currents to NMDA(200 microM) at -70 mV with an lC50 against steady-state responses of 182.1+/-12.1 microM. The effects of flupirtine were voltage-independent and not associated with receptor desensitization making actions within the NMDA receptor channel or at the glycine modulatory site unlikely. NMDA receptor antagonism probably has little relevance for the clinical efficacy of flupirtine as the concentrations needed were far higher than those achieved in clinical practice. However, the activation of a G-protein-regulated inwardly rectifying K+ channel was identified as an interesting molecular target site of flupirtine. In the next stage, the central nervous spectrum of action of experimental K+ channel openers (PCO) was considered. As far as they have been studied, experimental K+ channel openers display a spectrum of action comparable to that of flupirtine [1]. Therapeutic flupirtine concentrations (≤10 ?M) did not affect voltage-gated Na(+) or Ca(2+) channels, inward rectifier K(+) channels, nicotinic acetylcholine receptors, glycine or ionotropic glutamate receptors. Flupirtine shifted the gating of K(V)7 K(+) channels to more negative potentials and the gating of GABA(A) receptors to lower GABA concentrations [2]. Cell exposure to flupirtine decreased the amplitude of delayed rectifier K(+) current (I(K(DR))) with a concomitant raise in current inactivation in NSC-34 neuronal cells [4].
in vivo: Rats were trained to discriminate the novel analgesic flupirtine (10.0 mg/kg i.p., 10 min) from no drug under a two-choice fixed-ratio 5 shock-termination schedule. Flupirtine yielded a dose-response curve with an ED50 of 3.87 mg/kg. The opioid analgesics pentazocine, codeine and tramadol failed to produce flupirtine appropriate responding. The opioid antagonist naltrexone did not antagonize the discriminative effects of flupirtine [3]. Both morphine (ED?? =?0.74?mg/kg) and flupirtine (ED???=?3.32?mg/kg) caused dose-related anti-hyperalgesia at doses that did not cause sedation [5].
Toxicity: Based on study-end data, hepatotoxicity was detected in 31% of patients receiving flupirtine for ≥ 6 weeks [6]. References: | |||||
Flupirtine Dilution Calculator
Flupirtine Molarity Calculator
| 1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
| 1 mM | 3.286 mL | 16.4301 mL | 32.8601 mL | 65.7203 mL | 82.1504 mL |
| 5 mM | 0.6572 mL | 3.286 mL | 6.572 mL | 13.1441 mL | 16.4301 mL |
| 10 mM | 0.3286 mL | 1.643 mL | 3.286 mL | 6.572 mL | 8.215 mL |
| 50 mM | 0.0657 mL | 0.3286 mL | 0.6572 mL | 1.3144 mL | 1.643 mL |
| 100 mM | 0.0329 mL | 0.1643 mL | 0.3286 mL | 0.6572 mL | 0.8215 mL |
| * Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations. | |||||
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Flupirtine is a non-opioid analgesic reagent [1].
Flupirtine is a unique analgesic agent with a variety of pharmacological activities. Flupirtine is firstly found to activate the inwardly rectifying potassium current in rat cultured hippocampal neurons. Then it is proved that flupirtine is a positive modulator of KCNQ channels. It can active recombinant KV7.2 channels at concentration ranging from 2-6μM. Flupirtine is also found to have NMDA receptor-antagonistic properties both in vitro and in vivo although it has no relevant affinity to all the known binding site of NMDA receptor [1, 2].
Flupirtine plays its analgesic role through the muscle relaxing activity. It attenuates the reserpine-induced muscle rigidity with ED50 of 5.6 mg/kg in conscious rats. Besides that, it also exerts neuroprotective activities. Flupirtine can protect neurons from the glutamate-induced cell damage. In animal models, flupirtine relieves both global cerebral ischemia and retinal ischemic dysfunction [1, 2].
References:
[1] Schuster G, Schwarz M, Block F, et al. Flupirtine: a review of its neuroprotective and behavioral properties. CNS Drug Reviews, 1998, 4(2): 149-164.
[2] Szelenyi I. Flupirtine, a re-discovered drug, revisited. Inflammation Research, 2013, 62(3): 251-258.
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KCNQ2/3 channel agonist flupirtine reduces cocaine place preference in rats.[Pubmed:28125509]
Behav Pharmacol. 2017 Aug;28(5):405-407.
The efficacy of KCNQ2/3 channel agonists against drug reward has not been defined despite their ability to reduce locomotor-stimulant and dopamine-activating effects of psychostimulants. We tested the hypothesis that Flupirtine (FLU) (2.5, 10, 20 mg/kg), a KCNQ2/3 agonist, reduces cocaine (15 mg/kg) conditioned place preference. FLU (20 mg/kg), injected concurrently with cocaine during conditioning, reduced the development of cocaine conditioned place preference. FLU (20 mg/kg) also reduced cocaine locomotor activation without affecting baseline activity. The disruption of cocaine place preference by FLU suggests that KCNQ2/3 channels influence cocaine's rewarding effects.
Pharmacokinetics and disposition of flupirtine in the horse.[Pubmed:26681139]
Vet J. 2016 Feb;208:76-80.
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 x 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. Some mild and transient adverse effects (that spontaneously resolved within 5 min) were observed in 2/6 animals after IV administration. No adverse effects were noticed in the PO administration group. After IV and PO administrations, FLU was detectable in plasma for up to 36 h. The mean elimination half-life was longer after PO (10.27 h) than after IV (3.02 h) administration. The oral bioavailability was 71.4 +/- 33.1%. After compartmental simulation/modelling, an oral dose of 2.6 mg/kg was calculated to give Cmax and AUC values in horses similar to those reported in humans after a clinical dose administration with a theoretical FLU effective plasma concentration of 187 ng/mL. These findings may form the basis for further studies concerning this active ingredient in equine medicine.
HLA-DRB1*16: 01-DQB1*05: 02 is a novel genetic risk factor for flupirtine-induced liver injury.[Pubmed:26959717]
Pharmacogenet Genomics. 2016 May;26(5):218-24.
OBJECTIVE: Flupirtine is a nonopioid analgesic with regulatory approval in a number of European countries. Because of the risk of serious liver injury, its use is now limited to short-term pain management. We aimed to identify genetic risk factors for Flupirtine-related drug-induced liver injury (DILI) as these are unknown. MATERIALS AND METHODS: Six Flupirtine-related DILI patients from Germany were included in a genome-wide association study (GWAS) involving a further 614 European cases of DILI because of other drugs and 10,588 population controls. DILI was diagnosed by causality assessment and expert review. Human leucocyte antigen (HLA) and single nucleotide polymorphism genotypes were imputed from the GWAS data, with direct HLA typing performed on selected cases to validate HLA predictions. Four replication cases that were unavailable for the GWAS were genotyped by direct HLA typing, yielding an overall total of 10 Flupirtine DILI cases. RESULTS: In the six Flupirtine DILI cases included in the GWAS, we found a significant enrichment of the DRB1*16:01-DQB1*05:02 haplotype compared with the controls (minor allele frequency cases 0.25 and minor allele frequency controls 0.013; P=1.4 x 10(-5)). We estimated an odds ratio for haplotype carriers of 18.7 (95% confidence interval 2.5-140.5, P=0.002) using population-specific HLA control data. The result was replicated in four additional cases, also with a haplotype frequency of 0.25. In the combined cohort (six GWAS plus four replication cases), the haplotype was also significant (odds ratio 18.7, 95% confidence interval 4.31-81.42, P=6.7 x 10(-5)). CONCLUSION: We identified a novel HLA class II association for DILI, confirming the important contribution of HLA genotype towards the risk of DILI generally.
Effect of preoperative flupirtine on postoperative morphine sparing in patients undergoing total abdominal hysterectomy.[Pubmed:26955312]
Saudi J Anaesth. 2016 Jan-Mar;10(1):58-63.
BACKGROUND: Flupirtine is a unique non-opioid, centrally acting analgesic with muscle relaxant properties. So far no study has evaluated, use of preoperative Flupirtine on postoperative morphine sparing effect in patients undergoing total abdominal hysterectomy (TAH). MATERIALS AND METHODS: We performed a prospective, controlled, and randomized study in 50 female patients of American Society of Anesthesiologists physical status I-II, aged between 30 and 60 years scheduled for TAH under general anesthesia (GA). Patients were randomized to receive either single dose Flupirtine 100 mg or placebo 1 h prior to surgery. A standard anesthetic and analgesic protocol was followed in both the groups. Postoperatively, a titrated loading dose of intravenous morphine 0.1 mg/kg was followed with patient-controlled analgesia with morphine (bolus of 0.01 mg/kg with a lockout time of 7 min). The primary outcome was cumulative morphine consumption at 48 h postoperatively. Secondary outcomes included hemodynamics, visual analog scale (VAS) at rest, VAS on cough, and any adverse effects. RESULTS: All enrolled 50 patients completed the follow-up. The cumulative mean morphine consumption (standard deviation [SD]) at 48 h (40.4 [6.0] vs. 47 [6.6] mg, P = 0.001) was reduced in-group Flupirtine as compared with placebo. The cumulative mean VAS at rest (SD) (3 [0.7] vs. 3.7 [0.7], P = 0.001) and on cough (3 [0.9] vs. 3.8 [0.5], P = 0.002) were reduced in-group Flupirtine as compared with placebo at 48 h postoperatively. CONCLUSION: Preoperative use of Flupirtine exhibited morphine sparing effect in patients following TAH under GA at 48 h.
