Decamethonium BromideCAS# 541-22-0 |
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Chemical structure
3D structure
Cas No. | 541-22-0 | SDF | Download SDF |
PubChem ID | 10921 | Appearance | Powder |
Formula | C16H38Br2N2 | M.Wt | 418.29 |
Type of Compound | N/A | Storage | Desiccate at -20°C |
Solubility | DMSO : 50 mg/mL (119.53 mM; Need ultrasonic) H2O : ≥ 50 mg/mL (119.53 mM) *"≥" means soluble, but saturation unknown. | ||
Chemical Name | trimethyl-[10-(trimethylazaniumyl)decyl]azanium;dibromide | ||
SMILES | C[N+](C)(C)CCCCCCCCCC[N+](C)(C)C.[Br-].[Br-] | ||
Standard InChIKey | HLXQFVXURMXRPU-UHFFFAOYSA-L | ||
Standard InChI | InChI=1S/C16H38N2.2BrH/c1-17(2,3)15-13-11-9-7-8-10-12-14-16-18(4,5)6;;/h7-16H2,1-6H3;2*1H/q+2;;/p-2 | ||
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 | Decamethonium Bromide is a nicotinic AChR partial agonist and neuromuscular blocking agent.
Target: nAChR
Decamethonium (Syncurine) is a depolarizing muscle relaxant or neuromuscular blocking agent, and is used in anesthesia to induce paralysis. Decamethonium, which has a short action time, is similar to acetylcholine and acts as a partial agonist of the nicotinic acetylcholine receptor. In the motor endplate, it causes depolarization, preventing further effects to the normal release of acetylcholine from the presynaptic terminal, and therefore preventing the neural stimulus from affecting the muscle. In the process of binding, decamethonium actually activates (depolarizes) the motor endplate, but since the decamethonium itself is not degraded, the membrane remains depolarized and unresponsive to normal acetylcholine release [1]. References: |
Decamethonium Bromide Dilution Calculator
Decamethonium Bromide Molarity Calculator
1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
1 mM | 2.3907 mL | 11.9534 mL | 23.9069 mL | 47.8137 mL | 59.7671 mL |
5 mM | 0.4781 mL | 2.3907 mL | 4.7814 mL | 9.5627 mL | 11.9534 mL |
10 mM | 0.2391 mL | 1.1953 mL | 2.3907 mL | 4.7814 mL | 5.9767 mL |
50 mM | 0.0478 mL | 0.2391 mL | 0.4781 mL | 0.9563 mL | 1.1953 mL |
100 mM | 0.0239 mL | 0.1195 mL | 0.2391 mL | 0.4781 mL | 0.5977 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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Decamethonium Bromide is a nicotinic AChR partial agonist and neuromuscular blocking agent.
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Decamethonium bromide-mediated inhibition of embryonic muscle development.[Pubmed:14997390]
Anat Embryol (Berl). 2004 Apr;208(1):75-85.
This study determined the effect of Decamethonium Bromide (DMBr), a non-competitive blocker of the neuromuscular junction, on skeletal muscle development during chick embryogenesis. Decamethonium Bromide caused generalized edema and high mortality with treated embryos rarely surviving beyond day 16 of incubation. Muscle degeneration was grossly evident on the muscles of abdomen, pectoral girdle, and leg. Semi-thin sections showed a high infiltration of macrophages in treated embryos and a massive degenerative process. Electron microscopy showed that both fast and slow fibers formed in the control and treated embryos, but those of the treated embryos failed to form myofibrils. Other organ systems, such as the heart and the gut, appeared histologically normal throughout the course of treatment. To investigate possible nerve independent action of DMBr on muscle development we determined the effect of this compound on the growth and differentiation of the C2C12 skeletal muscle cell line. DMBr treatment of C2C12 cell cultures did not affect the growth or survival of the cells, even at a tenfold higher concentration than that used in ovo, but myosin heavy chain expression was dramatically inhibited. We conclude that DMBr has a nerve independent blocking inhibition effect on myosin heavy chain synthesis in the developing avian embryo besides the recognized role as a non-competitive post-synaptic blocker of the neuromuscular junction.