Pancuronium dibromideAChR antagonist CAS# 15500-66-0 |
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Quality Control & MSDS
Number of papers citing our products
Chemical structure
3D structure
Cas No. | 15500-66-0 | SDF | Download SDF |
PubChem ID | 27350 | Appearance | Powder |
Formula | C35H60Br2N2O4 | M.Wt | 732.67 |
Type of Compound | N/A | Storage | Desiccate at -20°C |
Solubility | H2O : 100 mg/mL (136.49 mM; Need ultrasonic) DMSO : ≥ 100 mg/mL (136.49 mM) *"≥" means soluble, but saturation unknown. | ||
Chemical Name | [(2S,3S,5S,8R,9S,10S,13S,14S,16S,17R)-17-acetyloxy-10,13-dimethyl-2,16-bis(1-methylpiperidin-1-ium-1-yl)-2,3,4,5,6,7,8,9,11,12,14,15,16,17-tetradecahydro-1H-cyclopenta[a]phenanthren-3-yl] acetate;dibromide | ||
SMILES | CC(=O)OC1CC2CCC3C(C2(CC1[N+]4(CCCCC4)C)C)CCC5(C3CC(C5OC(=O)C)[N+]6(CCCCC6)C)C.[Br-].[Br-] | ||
Standard InChIKey | NPIJXCQZLFKBMV-YTGGZNJNSA-L | ||
Standard InChI | InChI=1S/C35H60N2O4.2BrH/c1-24(38)40-32-21-26-13-14-27-28(35(26,4)23-31(32)37(6)19-11-8-12-20-37)15-16-34(3)29(27)22-30(33(34)41-25(2)39)36(5)17-9-7-10-18-36;;/h26-33H,7-23H2,1-6H3;2*1H/q+2;;/p-2/t26-,27+,28-,29-,30-,31-,32-,33-,34-,35-;;/m0../s1 | ||
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 | Nicotine (neuromuscular) antagonist. Skeletal muscle relaxant. |
Pancuronium dibromide Dilution Calculator
Pancuronium dibromide Molarity Calculator
1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
1 mM | 1.3649 mL | 6.8244 mL | 13.6487 mL | 27.2974 mL | 34.1218 mL |
5 mM | 0.273 mL | 1.3649 mL | 2.7297 mL | 5.4595 mL | 6.8244 mL |
10 mM | 0.1365 mL | 0.6824 mL | 1.3649 mL | 2.7297 mL | 3.4122 mL |
50 mM | 0.0273 mL | 0.1365 mL | 0.273 mL | 0.5459 mL | 0.6824 mL |
100 mM | 0.0136 mL | 0.0682 mL | 0.1365 mL | 0.273 mL | 0.3412 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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Pancuronium dibromide is a competitive AChR antagonist (IC50 = 5.5 nM) and acts as a skeletal muscle relaxant. Pancuronium dibromide interrupts neuromuscular transmission by competing with acetylcholine for receptor sites on the motor end-plate. Pancuroni
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Neurokinin-1 receptors and spinal cord control of blood pressure in spontaneously hypertensive rats.[Pubmed:9974130]
Brain Res. 1999 Jan 2;815(1):116-20.
In this study we examined blood pressure and heart rate responses to intrathecal administration of a synthetic NK1-receptor agonist, H2N-(CH2)4-CO-Phe-Phe-Pro-NmeLeu-Met-NH2 (GR 73,632), in spontaneously hypertensive rats (SHR) and their progenitor strain, the Wistar-Kyoto rat (WKY). Sodium pentobarbitone anaesthetised rats with implanted intrathecal catheters were paralysed (Pancuronium dibromide) and artificially ventilated. Injection of GR 73,632 at the T9 spinal level evoked dose-dependent increases in mean arterial pressure (MAP) in WKY and SHR. SHR had a lower MAP response threshold than WKY but increase in response with increasing dose was less in SHR than WKY. Biphasic blood pressure responses at high doses were observed in both strains. Prior administration of the NK1-receptor antagonist (3 aR,7aR)-7,7-diphenyl-2-[1-imino-2(methoxyphenyl)ethyl] perhydroisoindol-4-one (RP 67,580) significantly reduced the pressor response in WKY but not SHR. The depressor response was not attenuated in either strain.
[Current place of neuroleptics in cardiac surgery under extracorporeal circulation. Cardiovascular effects of different combinations].[Pubmed:14567]
Ann Anesthesiol Fr. 1976;17(10):1155-65.
We have been using narconeuroleptanalgesia for anesthesia in cardiac surgery under extra-corporeal circulation since 1969, and we have carried out about 3,500 anesthetics of this type on the 1st of October 1975. For all these anesthetics, the neuroleptic used was droperidol. The other components were: - in the case of the narcotic, penthiobarbital, then more recently Alfatesine; - in the case of the analgesic, either dextromoramide or phenoperidine or Fentanyl; in the case of the curare derivative, D, tubocurarine, and above all, Pancuronium dibromide. The advantages of neuroleptanalgesia for such surgery seemed to us mainly: - greater cardio-vascular stability in patients with a heart lesion; - the possibility of better control of cardiac output, i.e. by fillingor by inotropic drugs, thanks to the relative vasoplegia produced by the neuroleptic. Finally, in a recent study, we attempted to determine the hemodynamic effect of droperidol and its association on various analgesic drugs measuring in a few patients the cardiac output, the peripheral resistances the the circulating blood volume. We will report the preliminary results of this study.
Open channel and competitive block of nicotinic receptors by pancuronium and atracurium.[Pubmed:11173060]
Eur J Pharmacol. 2001 Feb 9;413(1):31-5.
Mouse myotubes were used to investigate effects of the nondepolarizing neuromuscular blocking drugs pancuronium and atracurium on embryonic-type nicotinic acetylcholine receptor channels. Experiments were performed using patch-clamp techniques in combination with devices for ultra-fast solution exchange at outside--out patches. Application of 0.1 mM acetylcholine resulted in a fast current transient. When the peak amplitude was achieved, the current decayed monoexponentially due to desensitization. After application of drugs (pancuronium or atracurium), two different mechanisms of block were observed: (1) open channel block of embryonic-type nicotinic acetylcholine receptor channels after coapplication of blocker and acetylcholine, characterized by decrease of the time constant of current decay; (2) competitive block of embryonic-type nicotinic acetylcholine receptor channels by pancuronium or atracurium after preincubation of outside-out patches with the respective blocker. Different affinities of pancuronium (K(B) approximately 0.01 microM) and atracurium (K(B) approximately 1 microM) to embryonic-type nicotinic acetylcholine receptor channels were observed.
Extracellular pancuronium affects sodium current in chick embryo sensory neurones.[Pubmed:8012707]
Br J Pharmacol. 1994 Jan;111(1):283-7.
1. The action of pancuronium on transmembrane sodium conductance was investigated in dorsal root ganglion neurones of chick embryos. The Na+ current was measured by use of the patch-clamp technique in whole-cell configuration. 2. Externally perfused pancuronium (50 microM to 1 mM) reversibly inhibited the current by a fast mechanism of action. Inhibition was concentration-dependent (with a half-effective dose of 170 microM) but not voltage-dependent. 3. The activation and inactivation kinetics of the Na+ current were estimated in pancuronium and in control solution by fitting experimental data with a Hodgkin-Huxley theoretical model. 4. The activation time constant tau m, at negative membrane voltages, was larger in the presence of pancuronium than in the control. In contrast, the inactivation time constant tau h was smaller during drug perfusion at membrane voltages < -10 mV. The steady-state inactivation h infinity was not affected by pancuronium. 5. These results suggest that pancuronium may reduce the sodium current by interacting with the sodium channels in both the resting and open states.
Pancuronium and gallamine are antagonists for pre- and post-junctional muscarinic receptors in the guinea-pig lung.[Pubmed:3600815]
Naunyn Schmiedebergs Arch Pharmacol. 1987 Apr;335(4):367-71.
The effects of atropine, pancuronium and gallamine were tested on pre- and post-junctional muscarinic receptors in the lung. Inhibition of bronchoconstriction induced by intravenous injection of acetylcholine (ACh) was used as a measure of post-junctional receptor blockade. All three antagonists reduced ACh-induced bronchoconstriction. The effects were dose-related for atropine and pancuronium and complete inhibition was obtained with 0.01 mg/kg and 10 mg/kg respectively. Gallamine was much less potent than the other two drugs; the inhibitory effect was not dose-related and never exceeded 50% even at a dose of 10 mg/kg. In contrast, blockade of pre-junctional inhibitory muscarinic receptors in pulmonary parasympathetic nerves by these three antagonists, produced potentiation of bronchoconstriction induced by vagal-nerve stimulation. Consequently, the effect of the three antagonists on vagally-induced bronchoconstriction is dependent on the balance between their pre- and post-junctional blocking activity. Gallamine was the most effective and atropine the least effective antagonist for potentiating nerve-induced bronchoconstriction. At doses which produce 100% neuromuscular blockade, both pancuronium (0.04 mg/kg) and gallamine (4 mg/kg) potentiated vagally-induced bronchoconstriction. At these doses, pancuronium doubled and gallamine caused a four-fold increase in vagally-induced bronchoconstriction, despite partial concurrent blockade of muscarinic receptors in the smooth muscle of the airways.