Gallamine Triethiodide targets muscarinic acetylcholine receptors, specifically the mAChR M2 subtype. It is a cholinergic receptor blocker with an IC50 of 68.0 ± 8.4 µM. By blocking nicotinic receptors at the neuromuscular junction, it causes skeletal muscle relaxation. Its cardioselective M2 antagonism contributes to its cardiovascular effects, including sinus tachycardia.

In vitro, Gallamine Triethiodide is a cholinergic receptor blocker with an IC50 of 68.0 ± 8.4 µM. It is a cardioselective mAChR M2 antagonist. Its activity has been characterized in various binding and functional assays using cells expressing muscarinic receptors. These in vitro studies confirm its mechanism as a cholinergic receptor blocker.

In vivo, Gallamine Triethiodide is used as a nondepolarizing nerve blocker in addition to anesthesia to cause skeletal muscle relaxation. Its actions are similar to those of tubocurarine, but it blocks the cardiac vagus and may cause sinus tachycardia and, occasionally, hypertension and increased cardiac output. Its use in clinical anesthesia has been established.

Non-cellular binding assays for Gallamine Triethiodide typically involve measuring its affinity for muscarinic receptors, particularly the M2 subtype. These assays use membrane preparations from tissues or cells expressing the receptors and measure the displacement of a labeled ligand, such as [3H]N-methylscopolamine. The compound's ability to inhibit receptor binding is assessed by determining the IC50. Such assays are essential for characterizing its potency as a cholinergic receptor blocker.

In vitro cell-based assays for Gallamine Triethiodide are conducted using cells expressing muscarinic or nicotinic receptors to assess its effects on receptor signaling. Cells are treated with the compound, and changes in intracellular calcium levels or other downstream signaling pathways are measured. These experiments are crucial for confirming its mechanism of action.

In vivo animal studies for Gallamine Triethiodide are typically conducted in animal models to evaluate its neuromuscular blocking effects. The compound is administered intravenously, and its effects on muscle relaxation and cardiovascular function are assessed. These studies are essential for validating its in vivo efficacy.

Absorption, Distribution and Excretion
Studies have shown that galamine is excreted from canine urine more rapidly than other muscle relaxants. ... It does not cross the blood-brain barrier. Other studies... Within 1 hour of intravenous injection, galamine concentrations in cerebrospinal fluid were detected to be close to plasma concentrations. /galamine/
Galamin is primarily excreted via the kidneys...
...Galamin can cross the placental barrier...
Trace amounts of galamine were detectable in the fetus 3 minutes after administration. /galamine, data from table/
For more complete data on the absorption, distribution, and excretion of galamine triiodides (6 metabolites), please visit the HSDB record page.

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Metabolism/Metabolites
... /galamine/ is not metabolized. /galamine/

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Biological Half-Life
135 minutes/Data from table/
Gallamine Triethiodide has a molecular weight of 891.53 g/mol. It is administered intravenously. It is a synthetic nondepolarizing neuromuscular blocking drug. Its pharmacokinetic properties have been studied in clinical settings. It is a prescription drug for use in anesthesia.

Interactions
In anesthetized patients, intravenous diazepam may enhance and prolong the neuromuscular blockade induced by galamine triiodide. Clinical reports…are contradictory…/and/there is currently insufficient data to explain the possible mechanisms of interaction between galamine triiodide and diazepam. In two patients with thyrotoxicosis treated with high doses (120 mg/day for 14 days) of propranolol, the neuromuscular blockade induced by tubocurarine was prolonged. Although not documented, the non-depolarizing muscle relaxant gallium triiodide…may also interact with propranolol. Neomycin and related antibiotics can cause neuromuscular transmission disorders, which may lead to persistent respiratory depression or apnea in surgical patients receiving concurrent treatment with tubocurarine and neuromuscular inhibitors. ...galamine triiodide can cause neuromuscular inhibition.../It has been reported to occur with galamine triiodide/.
Quinidine, when administered parenterally shortly after or concurrently with tubocurarine, may enhance or cause a relapse of the neuromuscular inhibitory effects of tubocurarine, leading to prolonged or exacerbated respiratory depression and apnea. ...Gallium triiodide... has been shown to interact with quinidine in animals.
For more complete data on interactions of gallium triiodide (out of 25), please visit the HSDB record page.

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Non-human toxicity values
Rat intraperitoneal LD50: 23,200 μg/kg
Rat subcutaneous LD50: 28,500 μg/kg
Rat intravenous LD50: 5,100 μg/kg
Rat duodenal LD50: 380 mg/kg
For more complete data on non-human toxicity values of gallium triiodide (out of 13), please visit the HSDB record page.
Gallamine Triethiodide has an established safety profile from its clinical use. Common side effects include sinus tachycardia, hypertension, and increased cardiac output. As with all neuromuscular blocking agents, it can cause respiratory depression. Comprehensive toxicological data are available from its clinical use. Gallamine Triethiodide is an approved drug.

J Pharmacol Exp Ther.1986 Jan;236(1):219-23.

synthetic non-depolarizing blocker. Gallium triiodide has similar effects to tubocurarine, but it blocks the vagus nerve in the heart, potentially causing sinus tachycardia, and occasionally hypertension and increased cardiac output. It should be used with caution in patients at risk of tachycardia, but may be more suitable for patients with bradycardia. (From JAMA Drug Evaluation Yearbook, 1992, p. 198)

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Drug Indications
Used as an adjunct to anesthesia to induce skeletal muscle relaxation and to assist in the management of mechanically ventilated patients.

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Mechanism of Action
It competes with acetylcholine (ACh) molecules and binds to muscarinic acetylcholine receptors on the postsynaptic membrane of the motor endplate. It exerts its effect by competitively blocking the neurotransmitter action of acetylcholine through binding to cholinergic receptors in muscle. It blocks the action of ACh, thereby preventing the activation of muscle contraction. It can also act on presynaptic acetylcholine receptors of nicotine, inhibiting the release of acetylcholine. Gallium triiodide… produces skeletal muscle relaxation by binding to receptors at the neuromuscular junction and blocking the action of the neurotransmitter acetylcholine. In the rat phrenic nerve-diaphragm, gallium amine had no significant effect on the electrogenic properties of the excitable membranes of motor nerve endings and muscle fibers; it inhibited the postsynaptic receptor response to acetylcholine. At the neuromuscular junction in mice and frogs, after a step change in membrane potential from -70 MV to -130 MV, galamine (5 UMOL) caused an initial rapid decrease in current in the presence of acetylcholine (3 UMOL), followed by a slower channel opening rate than with acetylcholine alone. When the internal potential decreased to -70 MV, the current initially rose rapidly, followed by the usual decrease, but at a slower rate than normal. Therefore, galamine may produce a potential-dependent blocking effect on opening ion channels.

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Therapeutic Use
Non-depolarizing neuromuscular blockade; nicotine antagonist
A neuromuscular blockade agent with effects and uses similar to tubocurarine chloride. …Generally, it has little effect on autonomic ganglia, but usually blocks the cardiac vagus nerve…It does not release histamine at low doses.
…In cesarean section and vaginal delivery, regular doses have no significant effect on the newborn, nor do they affect uterine tone.
…It has been reported to slightly lower intraocular pressure in patients.
For more complete data on the therapeutic uses of galamine triiodides (9 in total), please visit the HSDB record page.

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Drug Warnings
Neuromuscular blockade agents are potentially…dangerous drugs…These drugs should only be used on patients by well-trained anesthesiologists and other clinicians in facilities equipped with respiratory and cardiovascular resuscitation facilities. /Neuromuscular Blockade Agents/
Caution should be exercised if the patient has tachycardia. Because this product is mainly excreted by the kidneys, its duration of action may be prolonged in patients with renal insufficiency.
Contraindicated in patients with kidney disease.
Cross-sensitivity exists between acuronium and D-tubocurarine, and a similar situation may exist between succinylcholine and galamine.
For more complete data on drug warnings for galamine triiodide (6 in total), please visit the HSDB record page.

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Pharmacodynamics
Galaminide triiodide is a non-depolarizing neuromuscular blocker (NDMRD) used as an adjunct to anesthesia to induce skeletal muscle relaxation. Gallium triiodide has similar effects to tubocurarine, but it blocks the vagus nerve of the heart, which may cause sinus tachycardia and occasionally hypertension and increased cardiac output. Different muscle groups have varying sensitivities to these muscle relaxants, with the ocular muscles (controlling the eyelids) being the most sensitive, followed by the neck, jaw, and limb muscles, and finally the abdominal muscles. The diaphragm has the lowest sensitivity to NDMRDs. Although NDMRDs do not have the adverse reactions of succinylcholine, they have a slower onset of action. In addition, they have a longer duration of action, making them more suitable for maintaining neuromuscular relaxation during major surgeries.
Gallamine Triethiodide is a synthetic nondepolarizing neuromuscular blocking drug. It is a cholinergic receptor blocker with an IC50 of 68.0 ± 8.4 µM. It is used as an adjunct to anesthesia to cause skeletal muscle relaxation. Gallamine Triethiodide is an approved drug.

C30H60I3N3O3

891.53

891.176

65-29-2

6172

White to yellow solid powder

0.983g/cm3

502.6ºC at 760 mmHg

235ºC (dec.)

125.9ºC

1.501

0

6

21

39

489

0

REEUVFCVXKWOFE-UHFFFAOYSA-K

InChI=1S/C30H60N3O3.3HI/c1-10-31(11-2,12-3)22-25-34-28-20-19-21-29(35-26-23-32(13-4,14-5)15-6)30(28)36-27-24-33(16-7,17-8)18-9;;;/h19-21H,10-18,22-27H2,1-9H3;3*1H/q+3;;;/p-3

2-[2,3-bis[2-(triethylazaniumyl)ethoxy]phenoxy]ethyl-triethylazanium triiodide

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Note: Please store this product in a sealed and protected environment (e.g. under nitrogen), avoid exposure to moisture and light.

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

Solubility in Formulation 1: 50 mg/mL (56.08 mM) in PBS (add these co-solvents sequentially from left to right, and one by one), clear solution; with sonication.

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 (Please use freshly prepared in vivo formulations for optimal results.)