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C5366

Sigma-Aldrich

Chlorisondamine diiodide

≥98% (HPLC), white, solid

Sinónimos:

4,5,6,7-Tetrachloro-2,3-dihydro-2-methyl-2-[2-(trimethylammonio)ethyl]-2H-isoindolium diiodide

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About This Item

Fórmula empírica (notación de Hill):
C14H20Cl4I2N2
Número de CAS:
96750-66-2
Peso molecular:
611.94
Número MDL:
MFCD01074794
Código UNSPSC:
12352116
ID de la sustancia en PubChem:
24724443
NACRES:
NA.77

Ensayo

≥98% (HPLC)

Formulario

solid

condiciones de almacenamiento

protect from light

color

white

solubilidad

H2O: ≥2 mg/mL
DMSO: >20 mg/mL

temp. de almacenamiento

2-8°C

cadena SMILES

[I-].[I-].C[N+](C)(C)CC[N+]1(C)Cc2c(Cl)c(Cl)c(Cl)c(Cl)c2C1

InChI

1S/C14H20Cl4N2.2HI/c1-19(2,3)5-6-20(4)7-9-10(8-20)12(16)14(18)13(17)11(9)15;;/h5-8H2,1-4H3;2*1H/q+2;;/p-2

Clave InChI

FPNVAOZHQUJJJQ-UHFFFAOYSA-L

Aplicación

Chlorisondamine diiodide has been used:
  • as a nicotinic receptor antagonist to test its effect on trinitrobenzene sulfonic acid (TNBS)-induced colitis
  • as an irreversible nicotinic acetylcholine(nAChR) blocker to pre-treat brain samples to test its effect on cytochrome P450 2B (CYP2B) induction
  • as a ganglionic blocker to test its effect on regulating corticosterone levels in rat with chronic stress

Acciones bioquímicas o fisiológicas

Chlorisondamine diiodide mediates ganglionic and central blockade.
Irreversible, long-lasting nicotinic acetylcholine receptor antagonist.

Características y beneficios

This compound is a featured product for Neuroscience research. Click here to discover more featured Neuroscience products. Learn more about bioactive small molecules for other areas of research at sigma.com/discover-bsm.
This compound is featured on the Acetylcholine Receptors (Nicotinic) page of the Handbook of Receptor Classification and Signal Transduction. To browse other handbook pages, click here.

Pictogramas

Exclamation markEnvironment
GHS07,GHS09

Palabra de señalización

Warning

Frases de peligro

H302,H400

Consejos de prudencia

P273 - P301 + P312 + P330

Clasificaciones de peligro

Acute Tox. 4 Oral - Aquatic Acute 1

Código de clase de almacenamiento

11 - Combustible Solids

Clase de riesgo para el agua (WGK)

WGK 2

Punto de inflamabilidad (°F)

Not applicable

Punto de inflamabilidad (°C)

Not applicable

Equipo de protección personal

dust mask type N95 (US), Eyeshields, Gloves

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Certificados de análisis (COA)

Lot/Batch Number
0000258200
0000258199
0000190009
BGBC4599
BGBC2796

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Jibran Y Khokhar et al.
Brain research, 1348, 1-9 (2010-07-06)
CYP2B is a drug-metabolizing enzyme expressed in the liver and brain that metabolizes a variety of centrally acting drugs (e.g. propofol, bupropion and nicotine), endogenous neurochemicals (e.g. serotonin and testosterone) and toxins (e.g. chlorpyrifos). Human CYP2B6 is found at higher
T Mori et al.
Molecular pharmacology, 59(4), 732-743 (2001-03-22)
Inhalational general anesthetics have recently been shown to inhibit neuronal nicotinic acetylcholine (ACh) receptors (nnAChRs) expressed in Xenopus laevis oocytes and in molluscan neurons. However, drug actions on these systems are not necessarily the same as those seen on native
G Costa et al.
Brain research, 888(2), 336-342 (2001-01-11)
While the work of several groups has shown the neuroprotective effects of nicotine in vitro, evidences for the same effects in vivo are controversial, mainly regarding neuroprotection in experimental models of Parkinson's disease. In this context, we investigated the capability
T Marenco et al.
British journal of pharmacology, 129(1), 147-155 (2000-02-29)
Chlorisondamine blocks central nicotinic receptors for many weeks via an unknown mechanism. Intracerebroventricular administration of [(3)H]-chlorisondamine in rats results in an anatomically restricted and persistent intracellular accumulation of radioactivity. The initial aim of the present study was to test whether
A Bai et al.
Scandinavian journal of immunology, 66(5), 538-545 (2007-10-24)
Inflammatory bowel diseases (IBD) are characterized by proinflammatory cytokines, tissue damage and loss of neuron in inflamed mucosa, which implies the cholinergic anti-inflammatory pathway may be destroyed during the process of inflammatory response. In the study, we identified the effect
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