갈라민 트리에티오다이드

WHITE AMORPHOUS POWDER

White crystals from acetone/water

Soluble

Freely sol in water, alcohol, dil acetone; sparingly sol in anhyd acetone, ether, benzene, chloroform

Very soluble in water and ethanol; slightly soluble in ethyl ether and acetone.

FDA approved drugs -> Active ingredient

FDA approved drugs -> Active ingredient

152-153

147.5 °C

Warning

H302 (100%): Harmful if swallowed [Warning Acute toxicity, oral]

P261, P264, P264+P265, P270, P271, P280, P301+P317, P302+P352, P304+P340, P305+P351+P338, P319, P321, P330, P332+P317, P337+P317, P362+P364, P403+P233, P405, and P501 (click each P-code to see the statement)

Aggregated GHS information provided per 39 reports by companies from 2 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

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 ANESTHETIZED PT, IV ADMIN OF DIAZEPAM MAY INCR INTENSITY & PROLONG DURATION OF NEUROMUSCULAR BLOCKADE PRODUCED BY GALLAMINE TRIETHIODIDE. CLINICAL REPORTS...ARE CONFLICTING.../&/ THERE ARE INSUFFICIENT DATA TO EXPLAIN POSSIBLE MECHANISM FOR GALLAMINE TRIETHIODIDE-DIAZEPAM INTERACTION.

NEUROMUSCULAR BLOCKADE PRODUCED BY TUBOCURARINE WAS PROLONGED IN TWO THYROTOXIC PT RECEIVING HIGH DOSES (120 MG/DAY FOR 14 DAYS) OF PROPRANOLOL. ... ALTHOUGH THERE IS NO DOCUMENTATION, THE NONDEPOLARIZING MUSCLE RELAXANT GALLAMINE TRIETHIODIDE...ALSO SHOULD INTERACT WITH PROPRANOLOL.

NEOMYCIN &...RELATED ANTIBIOTICS PRODUCE NEUROMUSCULAR TRANSMISSION FAILURE WHICH MAY CAUSE PROLONGED RESP DEPRESSION OR APNEA IN SURGICAL PT TREATED CONCURRENTLY WITH TUBOCURARINE &...NEUROMUSCULAR DEPRESSANTS. ...ADDITIVE NEUROMUSCULAR DEPRESSION.../REPORTED TO OCCUR WITH GALLAMINE TRIETHIODIDE/.

QUINIDINE, ADMIN PARENTERALLY SHORTLY AFTER OR SIMULTANEOUSLY WITH TUBOCURARINE, MAY ENHANCE OR CAUSE RECURRENT NEUROMUSCULAR EFFECTS OF TUBOCURARINE, RESULTING IN PROLONGATION OR INTENSIFICATION OF RESP DEPRESSION & APNEA. ... GALLAMINE TRIETHIODIDE...HAS BEEN SHOWN TO INTERACT WITH QUINIDINE IN ANIMALS.

For more Interactions (Complete) data for GALLAMINE TRIETHIODIDE (25 total), please visit the HSDB record page.

POISONING ... IS ALMOST ALWAYS RESULT OF CLINICAL OVERDOSAGE ... DIRECTLY RELATED FACTORS MAY ... INCL ALTERATIONS IN BODY TEMP ... ELECTROLYTE IMBALANCE, PARTICULARLY OF POTASSIUM ... /NEUROMUSCULAR BLOCKING AGENTS/

THREE CASES OF SEVERE ANAPHYLAXIS TO GALLAMINE TRIETHIODIDE ARE DESCRIBED. ALL REPORTED CASES HAVE OCCURRED IN WOMEN, & ALL CONFIRMED CASES IN AUSTRALASIA. THERE IS EVIDENCE THAT WOMEN MAY BE EXPOSED TO SOME SUBSTANCE WHICH LEAVES THEM SENSITIVE TO GALLAMINE TRIETHIODIDE.

Accidental subarachnoid injection of gallamine in an adult is followed by muscle spasms of the lower limbs and anxiety; by 3 hr the arterial pressure and pulse rate increases followed by hyperthermia, profuse sweating, intense hyperesthesia, loss of consciousness, and pinpoint pupils. Within 24 hr the muscle spasms lessen.

Drug-Induced Liver Injury Severity and Toxicity (DILIst)

gallamine triethiodide

DILI Negative

Intravenous

DOI:10.1016/j.drudis.2019.09.022

LD50 VALUES OF GALLAMINE TRIETHIODIDE AFTER IV, IP, & SC INJECTIONS WERE 3.0-3.3, 15.3-15.8, & 16.4-17.1 MG/KG IN MICE. VALUES AFTER ORAL ADMIN WERE GREATER THAN 1000 MG/KG. RESP DISORDER WAS MAJOR CAUSE OF DEATH.

LD50 VALUES OF GALLAMINE TRIETHIODIDE AFTER IV, IP, & SC INJECTIONS WERE 5.1-5.4, 23.2-26.7 & 28.5-34.3 MG/KG IN RATS. VALUES AFTER ORAL ADMIN WERE GREATER THAN 1000 MG/KG. IV LD50 IN RABBITS WAS 0.46 MG/KG. RESP DISORDER WAS MAJOR CAUSE OF DEATH IN THESE ANIMALS.

COMPARED TO CONTROL ANIMALS, ONSET OF ACTION OF GALLAMINE TRIETHIODIDE WAS SIGNIFICANTLY DELAYED IN HEMORRHAGIC (HYPOTENSIVE) DOGS. RECOVERY FROM GALLAMINE TRIETHIODIDE INDUCED PARALYSIS OCCURRED IN CONTROL DOGS, BUT NO SIGNS OF RECOVERY IN HEMORRHAGIC ANIMALS.

BLOOD & TISSUE SAMPLES WERE TAKEN FROM MALE RATS PREVIOUSLY TREATED IV WITH NEUROMUSCULAR BLOCKING AGENTS. GALLAMINE TRIETHIODIDE (40 MG/KG) WAS MODERATE HISTAMINE LIBERATOR. PANCURONIUM BROMIDE (2 MG/KG) RELEASED NO HISTAMINE. SOURCES OF INCR BLOOD HISTAMINE CONCN ARE TONGUE & SKIN WITH HIGH HISTAMINE CONTENT. NO RELEASE OF HISTAMINE FROM LUNG WAS OBSERVED.

For more Non-Human Toxicity Excerpts (Complete) data for GALLAMINE TRIETHIODIDE (7 total), please visit the HSDB record page.

LD50 Rat ip 23,200 ug/kg

LD50 Rat sc 28,500 ug/kg

LD50 Rat iv 5100 ug/kg

LD50 Rat intraduodenal 380 mg/kg

For more Non-Human Toxicity Values (Complete) data for GALLAMINE TRIETHIODIDE (13 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).

Gallamine Triethiodide is a nondepolarizing neuromuscular blocking drug (NDMRD) used as an adjunct to anesthesia to induce skeletal muscle relaxation. The actions of gallamine triethiodide are similar to those of tubocurarine, but this agent blocks the cardiac vagus and may cause sinus tachycardia and, occasionally, hypertension and increased cardiac output. Muscle groups differ in their sensitivity to these types of relaxants with ocular muscles (controlling eyelids) being most sensitive, followed by the muscles of the neck, jaw, limbs and then abdomen. The diaphragm is the least sensitive muscle to NDMRDs. Although the nondepolarizing neuromuscular blocking drugs do not have the same adverse effects as succinylcholine, their onset of action is slower. They also have a longer duration of action, making them more suitable for maintaining neuromuscular relaxation during major surgical procedures.

It competes with acetylcholine (ACh) molecules and binds to muscarinic acetylcholine receptors on the post-synaptic membrane of the motor endplate. It acts by combining with the cholinergic receptor sites in muscle and competitively blocking the transmitter action of acetylcholine. It blocks the action of ACh and prevents activation of the muscle contraction process. It can also act on nicotinic presynaptic acetylcholine receptors which inhibits the release of ACh.

GALLAMINE TRIETHIODIDE...PRODUCES SKELETAL MUSCLE RELAXATION BY COMBINING WITH RECEPTOR SITE AT NEUROMUSCULAR JUNCTION & BLOCKING ACTION OF NEUROTRANSMITTER ACETYLCHOLINE.

IN RAT PHRENIC NERVE-DIAPHRAGM GALLAMINE HAD NO SIGNIFICANT EFFECTS ON ELECTROGENIC PROPERTIES OF EXCITABLE MEMBRANES OF MOTOR NERVE TERMINALS & MUSCLE FIBERS; IT DEPRESSED RESPONSE OF POSTSYNAPTIC RECEPTORS TO ACTION OF ACETYLCHOLINE.

AT NEUROMUSCULAR JUNCTIONS IN MICE AND FROGS, FOLLOWING STEP CHANGES OF MEMBRANE POTENTIAL FROM -70 TO -130 MV, GALLAMINE (5 UMOL) IN THE PRESENCE OF ACETYLCHOLINE (3 UMOL) CAUSED AN INITIAL RAPID DECR IN CURRENT FOLLOWED BY OPENING OF CHANNELS AT A SLOWER RATE THAN WITH ACETYLCHOLINE ALONE. WHEN THE INTERNAL POTENTIAL WAS REDUCED TO -70 MV, THERE WAS A RAPID INCR IN CURRENT AT FIRST, FOLLOWED BY THE USUAL DECR WHICH WAS AGAIN SLOWER THAN NORMAL. THUS, GALLAMINE MAY PRODUCE A POTENTIAL-DEPENDENT BLOCK OF OPEN ION CHANNELS.

Drugs that interrupt transmission at the skeletal neuromuscular junction without causing depolarization of the motor end plate. They prevent acetylcholine from triggering muscle contraction and are used as muscle relaxants during electroshock treatments, in convulsive states, and as anesthesia adjuvants.

Drugs that bind to nicotinic cholinergic receptors (RECEPTORS, NICOTINIC) and block the actions of acetylcholine or cholinergic agonists. Nicotinic antagonists block synaptic transmission at autonomic ganglia, the skeletal neuromuscular junction, and at central nervous system nicotinic synapses.

STUDIES HAVE DEMONSTRATED THAT GALLAMINE IS EXCRETED IN DOG URINE AT RATE FASTER THAN OTHER MUSCLE RELAXANTS. .../IT/ DID NOT CROSS BLOOD-CEREBROSPINAL FLUID BARRIER. OTHER STUDIES...HAVE DETECTED GALLAMINE IN CEREBROSPINAL FLUID IN CONCN APPROACHING THOSE IN PLASMA DURING 1ST HR AFTER IV INJECTION. /GALLAMINE/

GALLAMINE IS ELIMINATED MAINLY BY RENAL EXCRETION...

... GALLAMINE CROSSES PLACENTAL BARRIER ...

TRACE AMT OF GALLAMINE APPEARS IN FETUS 3 MIN AFTER ADMIN. /GALLAMINE, FROM TABLE/

For more Absorption, Distribution and Excretion (Complete) data for GALLAMINE TRIETHIODIDE (6 total), please visit the HSDB record page.

PYROGALLOL IS CONDENSED WITH 2-CHLOROTRIETHYLAMINE & RESULTING TRIAMINE [2,2''',2''''''-(V-PHENENYLTRIOXY)TRIS(TRIETHYLAMINE)] IS QUATERNIZED WITH ETHYL IODIDE IN BOILING ACETONE. CRUDE PRODUCT WHICH PPT IS PURIFIED BY REPEATED CRYSTALLIZATION FROM HOT ETHANOL.

Prepared by reaction of pyrogallol with diethylaminoethyl chloride and subsequent alkylation with ethyl iodide.