Hexafluorenium bromide - CAS 317-52-2
Catalog number: 317-52-2
Category: Inhibitor
Not Intended for Therapeutic Use. For research use only.
Molecular Formula:
C36H42N2.2Br
Molecular Weight:
662.54008
COA:
Inquire
Targets:
Others
Description:
Hexafluronium bromide is .a cholinesterase inhibitor used in anesthesiology to prolong and potentiate the skeletal muscle relaxing action of suxamethonium during surgery
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Purity:
≥98%
Appearance:
Solid powder
Synonyms:
Mylaxen; 9H-fluoren-9-yl-[6-[9H-fluoren-9-yl(dimethyl)azaniumyl]hexyl]-dimethylazanium;dibromide;
Solubility:
Soluble in DMSO
Storage:
Store at -20 °C
MSDS:
Inquire
Application:
Acetylcholine Receptor
Quality Standard:
Enterprise standard
Shelf Life:
As supplied, 2 years from the QC date provided on the Certificate of Analysis, when stored properly.
Quantity:
Milligrams-Grams
InChIKey:
WDEFPRUEZRUYNW-UHFFFAOYSA-L
InChI:
1S/C36H42N2.2BrH/c1-37(2,35-31-21-11-7-17-27(31)28-18-8-12-22-32(28)35)25-15-5-6-16-26-38(3,4)36-33-23-13-9-19-29(33)30-20-10-14-24-34(30)36;;/h7-14,17-24,35-36H,5-6,15-16,25-26H2,1-4H3;2*1H/q+2;;/p-2
Canonical SMILES:
C[N+](C)(CCCCCC[N+](C)(C)C1C2=CC=CC=C2C3=CC=CC=C13)C4C5=CC=CC=C5C6=CC=CC=C46.[Br-].[Br-]
1.Synergistic effect of acidosis and succinylcholine-induced hyperkalemia in spinal cord transected rats.
Koller ME, Breivik H, Greider P, Jones DJ, Smith RB. Acta Anaesthesiol Scand. 1984 Feb;28(1):87-90.
The effects of spinal cord transection and acidosis on succinylcholine (SCC)-induced hyperkalemia were studied in Sprague-Dawley rats. The effectiveness of pretreatment with subparalyzing doses ("self-taming") of SCC or with the cholinesterase inhibitor hexafluorenium bromide in preventing hyperkalemia was also studied. The increase in plasma potassium after administration of SCC (1 mg/kg) was found to be significantly increased 10 days after spinal cord transection. This potassium increase could not be prevented by pretreatment with either hexafluorenium (0.3 mg/kg) or subparalyzing doses (0.15 mg/kg) of SCC. Respiratory acidosis caused an increase in plasma K+ in both normal and in spinal cord transected rats. Acidosis had a synergistic effect on succinylcholine-induced hyperkalemia. These findings support the clinical practice of not using succinylcholine in patients at risk of having a pathological sensitivity to SCC. Furthermore, SCC may be especially dangerous when administered to patients who are acidotic.
2.In vivo reversal of depolarizing neuromuscular blockade.
Riker WF Jr1, Okamoto M, Artusio JF Jr. Arch Int Pharmacodyn Ther. 1995 Jul-Aug;330(1):90-101.
The antagonism of depolarizing blockers, principally succinylcholine and decamethonium, by tetraethyl- and tetrabutylammonium ions in an in vivo neuromuscular preparation in anesthetized cats is described; possible mechanisms for these effects are discussed. Tetraethyl- (50-100 mg/kg, i.v.) and tetrabutylammonium (1-5 mg/kg, i.v.) produced sharp reversals of 95-99% succinylcholine and decamethonium blocks. These reversals were effective and sustained at any point during the course of the blockades. Tetraethyl- or tetrabutylammonium, administered 2-3 min before succinylcholine or decamethonium, prevented blockade, an effect compatible with an earlier reported in vitro investigation. The studies of others disclose the interaction of depolarizing blockers with acetylcholine receptors, leading to channel opening, channel entry and binding therein of these blockers. The present studies support this in showing the prevention of succinylcholine and decamethonium block by the prior administration of tetraethylammonium, which also interacts with acetylcholine receptors.
3.Characterization of end-plate conductance in transected frog muscle: modification by drugs.
Lambert JJ, Durant NN, Reynolds LS, Volle RL, Henderson EG. J Pharmacol Exp Ther. 1981 Jan;216(1):62-9.
Cutaneous pectoris muscles of Rana pipiens were transected distal to the innervated region. Within 10 min, membrane potentials (Em's) of -33 +/- 2.5 mV and end-plate potentials (3-15 mV) were recorded unaccompanied by muscle action potentials or twitch. The fall in Em was associated with a net loss of [K+]i and a net gain of [Na+]i. Although input resistance fell by 50% and the space constant was slightly reduced in the transected muscle fibers, end-plates could be adequately voltage-clamped with two microelectrodes. End-plate currents (e.p.c.s) with rise times of 350 to 700 musec were recorded as a function of holding potential (Vm). The current-voltage relationship of peak e.p.c.s over the range of -70 to +20 mV was linear and the reversal potential (-6.6 +/- 2.2 mV) was the same as that found for intact muscle fibers. The decay phase of e.p.c.s could be described as a single exponential at all Vm's and had a voltage and temperature dependence similar to that described for e.
4.Bile salts and neuromuscular blocking agents.
Westra P, Houwertjes MC, Wesseling H, Meijer DK. Br J Anaesth. 1981 Apr;53(4):407-15.
The influence of the primary bile salts taurocholate and chenodeoxycholate on the neuromuscular blockade of the non-depolarizing drugs Org 6368, pancuronium, Org NC 45 and hexafluorenium was studied in cats. An increase in the effects of these agents, all possessing widely varying molecular structures, was found following administration of the bile salts. The bile salt concentrations in plasma were similar to those obtained after 9-10 days of extrahepatic cholestasis in cats. The effect of Org NC 45, a new monoquaternary analogue of pancuronium, was increased more than that of pancuronium. This increase in effect is probably a result of inhibition of the hepatic uptake of the neuromuscular blocking drugs. The neuromuscular blocking effect of gallamine was not influenced significantly by the administration of bile salts.
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Chemical Structure

CAS 317-52-2 Hexafluorenium bromide

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