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An exceptionally long lasting nicotinic antagonist (IC50 ~ 1.6 mM); blockade of central nicotinic responses induced by chlorisondamine can persist for several weeks.
|Storage||Desiccate at +4°C|
The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis.
Tocris products are intended for laboratory research use only, unless stated otherwise.
|Solvent||Max Conc. mg/mL||Max Conc. mM|
Preparing Stock Solutions
The following data is based on the product molecular weight 611.95. Batch specific molecular weights may vary from batch to batch due to the degree of hydration, which will affect the solvent volumes required to prepare stock solutions.
|Concentration / Solvent Volume / Mass||1 mg||5 mg||10 mg|
|0.1 mM||16.34 mL||81.71 mL||163.41 mL|
|0.5 mM||3.27 mL||16.34 mL||32.68 mL|
|1 mM||1.63 mL||8.17 mL||16.34 mL|
|5 mM||0.33 mL||1.63 mL||3.27 mL|
References are publications that support the biological activity of the product.
Clarke et al (1994) The pharmacology of the nicotinic antagonist, chlorisondamine investigated in rat brain and autonomic ganglion. Br.J.Pharmacol. 111 397 PMID: 7911713
El-Bizri and Clarke (1994) Blockade of nicotinic receptor-mediated release of DA from striatal synaptosomes by chlorisondamine and other nicotinic antagonists administered in vitro. Br.J.Pharmacol. 111 406 PMID: 8004384
El-Bizri and Clarke (1994) Regulation of nicotinic receptors in rat brain following quasi-irreversible nicotinic blockade by chlorisondamine and chronic treatment with nicotine. Br.J.Pharmacol. 113 917 PMID: 7858886
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Keywords: Chlorisondamine diiodide, Chlorisondamine diiodide supplier, Nicotinic, antagonists, slow, offset, Acetylcholine, Receptors, Non-Selective, nAChR, 3-[[4-(Chlorophenyl)piperazin-1-yl]methyl-1H-pyrrolo[2,3-b]pyridine, diiodide, (Non-selective), 1001, Tocris Bioscience
4 Citations for Chlorisondamine diiodide
Citations are publications that use Tocris products. Selected citations for Chlorisondamine diiodide include:
Sabharwal et al (2015) Angiotensin-dependent autonomic dysregulation precedes dilated cardiomyopathy in a mouse model of muscular dystrophy. J Exp Med 100 776 PMID: 25921929
Bucci et al (2013) Cross-talk between toll-like receptor 4 (TLR4) and proteinase-activated receptor 2 (PAR(2) ) is involved in vascular function. Br J Pharmacol 168 411 PMID: 22957757
Luyer et al (2005) Nutritional stimulation of cholecystokinin receptors inhibits inflammation via the vagus nerve. Clin Sci (Lond) 202 1023 PMID: 16216887
Sabharwal et al (2014) Chronic oral administration of Ang-(1-7) improves skeletal muscle, autonomic and locomotor phenotypes in muscular dystrophy. J Cereb Blood Flow Metab 127 101 PMID: 24502705
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Literature in this Area
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Peripheral sensitization is the reduction in the threshold of excitability of sensory neurons that results in an augmented response to a given external stimulus. This poster outlines the excitatory and inhibitory signaling pathways involved in modulation of peripheral sensitization. The role of ion channels, GPCRs, neurotrophins, and cytokines in sensory neurons are also described.