Decamethonium

Substantial

7.04e-06 g/L

268-270 °C

MP: 188-189 °C /Bromide/

268 - 270 °C

Manufacturers, packers, and distributors of drug and drug products for human use are responsible for complying with the labeling, certification, and usage requirements as prescribed by the Federal Food, Drug, and Cosmetic Act, as amended (secs 201-902, 52 Stat. 1040 et seq., as amended; 21 U.S.C. 321-392).

SRP: At the time of review, criteria for land treatment or burial (sanitary landfill) disposal practices are subject to significant revision. Prior to implementing land disposal of waste residue (including waste sludge), consult with environmental regulatory agencies for guidance on acceptable disposal practices.

... IN MAN ... DECAMETHONIUM ... PRODUCE & MAINTAIN NEUROMUSCULAR BLOCKADE THAT HAS ALL CHARACTERISTICS OF DEPOLARIZING BLOCKADE ... THIS APPLIES IN PARTICULAR TO ITS INTENSIFICATION BY EDROPHONIUM, NEOSTIGMINE, & OTHER ANTI-CHOLINESTERASE AGENTS THAT ANTAGONIZE COMPETITIVE BLOCK.

DEPOLARIZING MUSCLE RELAXANTS DECAMETHONIUM...HAVE BEEN SHOWN TO INTERACT WITH PROPRANOLOL...

IN PRESENCE OF DIGITALIS, ESP...IF K LOSS, CARDIAC ARRHYTHMIAS, & EVEN CARDIAC ARREST, MAY OCCUR.

DEPOLARIZING MUSCLE RELAXANTS DECAMETHONIUM...HAVE BEEN SHOWN TO INTERACT WITH QUINIDINE IN ANIMALS.

For more Interactions (Complete) data for DECAMETHONIUM (8 total), please visit the HSDB record page.

Manufacturers, packers, and distributors of drug and drug products for human use are responsible for complying with the labeling, certification, and usage requirements as prescribed by the Federal Food, Drug, and Cosmetic Act, as amended (secs 201-902, 52 Stat. 1040 et seq., as amended; 21 U.S.C. 321-392).

Decamethonium acts as a depolarizing muscle relaxant or neuromuscular blocking agent. It acts as an agonist of nicotinic acetycholine receptors in the motor endplate and causes depolarization. This class of drugs has its effect at the neuromuscular junction by preventing the effects of acetylcholine. Normally, when a nerve stimulus acts to contract a muscle, it releases acetylcholine. The binding of this acetylcholine to receptors causes the muscle to contract. Muscle relaxants play an important role in anesthesia even though they don't provide any pain relief or produce unconsciousness.

Binds to the nicotinic acetycholine receptors (by virtue of its similarity to acetylcholine) in the motor endplate and blocks access to the receptors. In the process of binding, the receptor is actually activated - causing a process known as depolarization. Since it is not degraded in the neuromuscular junction, the depolarized membrance remains depolarized and unresponsive to any other impulse, causing muscle paralysis.

... DECAMETHONIUM ... COMBINES CERTAIN FEATURES OF BOTH THE DEPOLARIZING & THE COMPETITIVE AGENTS ... TERMED "DUAL" MECHANISM ...

/IN CASES OF DUAL MECHANISM/ ... DEPOLARIZING AGENTS PRODUCE INITIALLY THE CHARACTERISTIC FASCICULATIONS & POTENTIATION OF THE MAXIMAL TWITCH, FOLLOWED BY THE RAPID ONSET OF NEUROMUSCULAR BLOCK ... THERE IS A POORLY SUSTAINED RESPONSE TO TETANIC STIMULATION OF THE MOTOR NERVE, INTENSIFICATION OF THE BLOCK BY TUBOCURARINE, & USUAL REVERSAL BY ANTI-CHOLINESTERASE AGENTS.

THEIR INITIAL EFFECT IS TO DEPOLARIZE THE MEMBRANE BY OPENING CHANNELS IN THE SAME MANNER AS ACETYLCHOLINE. HOWEVER, SINCE THEY PERSIST FOR LONGER DURATIONS AT THE NEUROMUSCULAR JUNCTION, PRIMARILY BECAUSE OF THEIR RESISTANCE TO ACETYLCHOLINESTERASE, THE DEPOLARIZATION IS LONGER LASTING, RESULTING IN A BRIEF PERIOD OF REPETITIVE EXCITATION THAT MAY ELICIT TRANSIENT MUSCLE FASCICULATIONS. THE INITIAL PHASE IS FOLLOWED BY BLOCK OF NEUROMUSCULAR TRANSMISSION AND FLACCID PARALYSIS. /DEPOLARIZING AGENTS/

DURING DEPOLARIZED STATE, K IS RAPIDLY LOST FROM MUSCLE... DESPITE CONTINUING PRESENCE OF DECAMETHONIUM, SOME MOTOR END-PLATE MEMBRANES...REPOLARIZE, BUT... ARE INCAPABLE OF...NERVE STIMULATION; IN THIS STAGE, BLOCK CAN BE ANTAGONIZED BY ANTICHOLINESTERASES & AUGMENTED BY STABILIZING BLOCKING DRUGS & OTHER DRUGS...

... IS NOT HYDROLYZED BY PLASMA CHOLINESTERASE BUT IS EXCRETED UNCHANGED BY KIDNEYS.

NO EVIDENCE WAS FOUND FOR DECAMETHONIUM BIOTRANSFORMATION IN SMALL ANIMALS. ...

Rapidly absorbed.

QUATERNARY AMMONIUM NEUROMUSCULAR BLOCKING AGENTS ARE VERY POORLY & IRREGULARLY ABSORBED FROM THE GI TRACT. /NEUROMUSCULAR BLOCKING AGENTS/

ONSET OF PARALYSIS IS ABOUT 2 MIN, & DURATION OF ACTION IS USUALLY ABOUT 15 MIN; PLASMA T/2 IS APPROX 0.5-1 HR. ELIMINATION IS MAINLY BY COMBINATION OF GLOMERULAR FILTRATION & TUBULAR SECRETION...

DISTRIBUTION OF (14)C AFTER IP ADMIN OF [(14)C]DECAMETHONIUM...IN MICE WERE COMPARED BY WHOLE BODY AUTORADIOGRAM. RATE & EXTENT OF HEPATIC UPTAKE OF (14)C WERE INVERSELY PROPORTIONAL TO RATE OF URINARY EXCRETION. ...(14)C WAS RAPIDLY ACCUM IN CARTILAGE...ALSO TAKEN UP IN MUSCULAR TISSUES AFTER DOSING...

NO EVIDENCE WAS FOUND FOR DECAMETHONIUM BIOTRANSFORMATION IN SMALL ANIMALS. IN RABBITS, 80% OF IV INJECTION WAS EXCRETED RAPIDLY IN 24 HR URINE AS UNCHANGED DRUG, & BILIARY & PULMONARY ELIMINATIVE ROUTES WERE NOT UTILIZED. BLOOD-BRAIN BARRIER & PLACENTA PROTECT AGAINST TRANSFER...INTO BRAIN & FETUS.

Neuromuscular blocking agent

Therap cat: Muscle relaxant (skeletal) /Bromide/

MEDICATION (VET)

Blomquist et al; J Am Chem Soc 81: 678 (1959). /Decamethonium bromide/

Prepared by reaction of 1,10-dibromodecane with trimethylamine in a sealed tube. /Bromide/

INCOMPATIBILITIES: SOLN ARE COMPATIBLE WITH PROCAINE HYDROCHLORIDE & THIOPENT. /DECAMETHONIUM BROMIDE/

Decamethonium is no longer manufactured in the United States.

Decamethonium bromide is no longer marketed in the United States.