Gallamine Triethiodide - CAS 65-29-2
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Not Intended for Therapeutic Use. For research use only.
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Gallamine Triethiodide is a cholinergic receptor blocker with an IC50 of 68.0 ± 8.4 μM. It is is a non-depolarising muscle relaxant.
Publictions citing BOC Sciences Products
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1.Carbachol dimers as homobivalent modulators of muscarinic receptors.
Matucci R1, Nesi M2, Martino MV3, Bellucci C3, Manetti D3, Ciuti E2, Mazzolari A4, Dei S3, Guandalini L3, Teodori E3, Vistoli G4, Romanelli MN3. Biochem Pharmacol. 2016 Mar 17. pii: S0006-2952(16)00179-9. doi: 10.1016/j.bcp.2016.03.012. [Epub ahead of print]
A series of homodimers of the well-known cholinergic agonist carbachol have been synthesized, showing the two agonist units symmetrically connected through a methylene chain of variable length. The new compounds have been tested on the five cloned muscarinic receptors (hM1-5) expressed in CHO cells by means of equilibrium binding studies, showing an increase in affinity by rising the number of methylene units up to 7 and 9. Functional experiments on guinea-pig ileum and assessment of ERK1/2 phosphorylation on hM1, hM2 and hM3 on CHO cells have shown that the new compounds are endowed with muscarinic antagonistic properties. Kinetic binding studies have revealed that some of the tested compounds are able to slow the rate of dissociation of NMS, suggesting a bitopic behavior. Docking simulations, performed on the hM1 and hM2 receptors, give a sound rationalization of the experimental data revealing how these compounds are able to interact with both orthosteric and allosteric binding sites depending on the length of their connecting chain.
2.Episcleral venous pressure and IOP responses to central electrical stimulation in the rat.
Strohmaier CA1, Reitsamer HA, Kiel JW. Invest Ophthalmol Vis Sci. 2013 Oct 21;54(10):6860-6. doi: 10.1167/iovs.13-12781.
PURPOSE: Histological evidence suggests a role for the central nervous system in controlling episcleral venous pressure (EVP). Based on prior studies that identified candidate regions in the brain stem, the present study assessed the effect of electrical stimulation at the location of the superior salivatory nucleus (SSN) on EVP in rats.
3.Further evidence for the role of histamine H3, but not H1, H2 or H4, receptors in immepip-induced inhibition of the rat cardioaccelerator sympathetic outflow.
Pinacho-García M1, Marichal-Cancino BA2, Villalón CM3. Eur J Pharmacol. 2016 Feb 15;773:85-92. doi: 10.1016/j.ejphar.2016.01.014. Epub 2016 Jan 27.
Since histamine H3 and H4 receptors are coupled to heterotrimeric Gi/o proteins, a signal transduction pathway associated with inhibition of neurotransmitter release, the present study has investigated the inhibition of the rat cardioaccelerator sympathetic outflow induced by the H3/H4 receptor agonist immepip by using antagonists for histamine H1 (ketotifen), H2 (ranitidine), H3 (thioperamide) and H4 (JNJ7777120) receptors. For this purpose, 102 male Wistar rats were pithed, artificially ventilated and prepared for either preganglionic spinal (C7-T1) stimulation of the cardioaccelerator sympathetic outflow (n=90) or i.v. bolus injections of noradrenaline (n=12). This approach resulted in frequency-dependent and dose-dependent tachycardic responses, respectively. I.v. continuous infusions of immepip (3 and 10μg/kgmin), but not of saline (0.02ml/min), dose-dependently inhibited the sympathetically-induced tachycardic responses. Moreover, the cardiac sympatho-inhibition induced by 10μg/kgmin immepip (which failed to affect the tachycardic responses to i.
4.Pharmacological evidence that histamine H3 receptors inhibit the vasodepressor responses by selective stimulation of the rat perivascular sensory CGRPergic outflow.
Manrique-Maldonado G1, Altamirano-Espinoza AH2, Marichal-Cancino BA3, Rivera-Mancilla E4, Avilés-Rosas V5, Villalón CM6. Eur J Pharmacol. 2015 May 5;754:25-31. doi: 10.1016/j.ejphar.2015.02.017. Epub 2015 Feb 19.
This study has investigated whether pharmacological activation of Gi/o coupled histamine H3/H4 receptors inhibits the rat vasodepressor sensory outflow. For this purpose, 100 male Wistar rats were pithed, artificially ventilated and pretreated (i.v.) with: 25mg/kg gallamine, 2mg/kg/min hexamethonium and 20μg/kg/min methoxamine, followed by i.v. continuous infusions of physiological saline (0.02ml/min) or immepip (3.1, 10 or 31μg/kg/min; a histamine H3/H4 receptor agonist). Under these conditions, electrical stimulation (0.56-5.6Hz; 50V and 2ms) of the spinal cord (T9-T12) resulted in frequency-dependent vasodepressor responses, which were: (i) unchanged during the infusions of saline or immepip (3.1μg/kg/min); and (ii) significantly but, surprisingly, not dose-dependently inhibited by 10 and 31μg/kg/min immepip. Moreover, the sensory-inhibition by 10μg/kg/min immepip (which failed to inhibit the vasodepressor responses by i.v. bolus injections of α-CGRP; 0.
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CAS 65-29-2 Gallamine Triethiodide

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