Page last updated: 2024-12-05

chlorisondamine

Description Research Excerpts Clinical Trials Roles Classes Pathways Study Profile Bioassays Related Drugs Related Conditions Protein Interactions Research Growth Market Indicators

Description

Chlorisondamine: A nicotinic antagonist used primarily as a ganglionic blocker in animal research. It has been used as an antihypertensive agent but has been supplanted by more specific drugs in most clinical applications. [Medical Subject Headings (MeSH), National Library of Medicine, extracted Dec-2023]

Cross-References

ID SourceID
PubMed CID6244
CHEMBL ID1398654
CHEBI ID135514
SCHEMBL ID14340042
MeSH IDM0004145

Synonyms (26)

Synonym
chlorisondamine
PDSP1_000172
PDSP2_000171
NCGC00024930-01
tocris-1001
NCGC00163230-01
CHEBI:135514
NCGC00024930-02
7701-62-4
4,5,6,7-tetrachloro-2-methyl-2-(2-(trimethylammonio)ethyl)isoindolinium
unii-jd3m24f66i
isoindolinium, 4,5,6,7-tetrachloro-2-methyl-2-(2-(trimethylammonio)ethyl)-
jd3m24f66i ,
cas_6243
bdbm84948
nsc_6243
CHEMBL1398654
chlorisondamine ion
chlorisondamine cation
isoindolinium, 4,5,6,7-tetrachloro-2-methyl-2-(2- (trimethylammonio)ethyl)-
chlorisondamine [who-dd]
1h-isoindolium, 4,5,6,7-tetrachloro-2,3-dihydro-2-methyl-2-(2- (trimethylammonio)ethyl)-
SCHEMBL14340042
DTXSID0048395
Q5102966
chlorisondamine-diiodide

Research Excerpts

Overview

Chlorisondamine is a charged molecule that acts as long-acting nicotinic antagonist in many species.

ExcerptReferenceRelevance
"Chlorisondamine is a charged molecule that acts as long-acting nicotinic antagonist in many species, including pigeon. "( Chlorisondamine inhibits the nicotine-induced stimulation of c-fos in the pigeon brain for up to 2 weeks.
Chadman, KK; Stitzel, J; Woods, JH, 2007
)
3.23

Effects

ExcerptReferenceRelevance
"Chlorisondamine (CSD) has been used to assess the neurogenic contribution to blood pressure (BP) and vasomotor sympathetic tone in animal models. "( Use of chlorisondamine to assess the neurogenic contribution to blood pressure in mice: An evaluation of method.
Cooper, SG; Feng Earley, Y; Souza, LA; Thakore, P; Worker, CJ, 2021
)
2.52

Actions

Chlorisondamine failed to lower heart rate significantly in 4 or 7 day old rats, but lowered the rate by 50 to 80 beats per min in the older animals. Atropine had little or no effect on heart rate. Chlorisonamine inhibited the increase in ganglionic DOPAC following preganglionic stimulation (5 Hz, 30 min) by 30-50%.

ExcerptReferenceRelevance
"3. Chlorisondamine failed to lower heart rate significantly in 4 or 7 day old rats, but lowered the rate by 50 to 80 beats per min in the older animals and eliminated the difference in rate between 16 day old and the other ages; atropine had little or no effect on heart rate."( Presynaptic and postsynaptic contributions to ontogeny of sympathetic control of heart rate in the pre-weanling rat.
Seidler, FJ; Slotkin, TA, 1979
)
0.77
"Chlorisondamine inhibited the increase in ganglionic DOPAC following preganglionic stimulation (5 Hz, 30 min) by 30-50% and it even better reduced the biochemical changes in the salivary gland."( Stimulation of the synthesis of catecholamines in a sympathetic ganglion via cholinergic and non-cholinergic mechanisms.
Andén, NE; Grabowska-Andén, M; Klaesson, L, 1986
)
0.99

Treatment

Chlorisondamine treatment depressed heart rate, blood pressure and plasma levels of NPY-LI. Pretreatment with chlorisondam inhibited the Il-6 responses, while it had little influence on the TNF responses.

ExcerptReferenceRelevance
"Chlorisondamine treatment exacerbated the decrease in mean arterial pressure in male mice infused with sPRR."( Soluble Prorenin Receptor Increases Blood Pressure in High Fat-Fed Male Mice.
Gatineau, E; Gong, MC; Yiannikouris, F, 2019
)
1.24
"Chlorisondamine pretreatment (2.5 mg/kg, 20 min beforehand) prevented restraint-elicited defaecation and body weight decreases."( Effects of chlorisondamine and restraint on cortical [3H]ketanserin binding, 5-HT2A receptor-mediated head shakes, and behaviours in models of anxiety.
Baudrie, V; Chaouloff, F; Coupry, I,
)
1.24
"Chlorisondamine pretreatment depressed heart rate, blood pressure and plasma levels of NPY-LI."( Reserpine-induced depletion of neuropeptide Y from cardiovascular nerves and adrenal gland due to enhanced release.
Al-Saffar, A; Lundberg, JM; Saria, A; Theodorsson-Norheim, E, 1986
)
0.99
"Pretreatment with chlorisondamine (0.2-5 micromol/kg, i.p.) only partially blocked the effects of ABT-594 at the higher doses tested."( ABT-594 (a nicotinic acetylcholine agonist): anti-allodynia in a rat chemotherapy-induced pain model.
Decker, MW; Honore, P; Lynch, JJ; Mikusa, JP; Wade, CL, 2005
)
0.65
"Treatment with chlorisondamine, which blocks nicotinic ganglionic transmission, also increased SP, reproducing the effects of decentralization."( Regulation of substance P in adult rat sympathetic ganglia.
Black, IB; Kessler, JA, 1982
)
0.6
"Pretreatment with chlorisondamine (EC) and phentolamine (PT) did not alter the HC-induced hyperglycemia but did result in higher plasma insulin levels in response to the higher glucose levels."( Insulin release after acute hydrocortisone treatment in mice.
Fletcher, HP; Longano, CA, 1983
)
0.59
"Pretreatment with chlorisondamine, a ganglionic blocking agent, inhibited the Il-6 responses, while it had little influence on the TNF responses."( Central IL-1 differentially regulates peripheral IL-6 and TNF synthesis.
Kitamura, H; Morimatsu, M; Okamoto, S; Saito, M; Shimamoto, Y; Terao, A, 1998
)
0.62
"Pretreatment with chlorisondamine or verapamil prevented the cocaine-induced enhancement of the maximal response to noradrenaline and the response to isoproterenol, but it did not inhibit potentiation of submaximal doses."( Post-junctional mechanisms involved in the potentiation of cardiac adrenergic responses by cocaine.
Bechara, G; El-Bizri, NM; Khoury, HA; Sabra, R; Sharaf, LH, 2000
)
0.63
"Pretreatment with chlorisondamine (1 mg/kg i.v."( Mechanisms involved in the hyperglycemic effect of the 5-HT1C/5-HT2 receptor agonist, DOI.
Baudrie, V; Chaouloff, F, 1992
)
0.61
"Treatment with chlorisondamine, which blocks synaptic transmission in sympathetic ganglia, produces a significant increase in SV levels in the SCG after 7 d of treatment."( Plasticity of expression of a synaptic vesicle antigen in adult rat superior cervical ganglion.
Greif, KF, 1986
)
0.61

Dosage Studied

ExcerptRelevanceReference
"From a study on the interrelationship between electroshock-induced convulsions, autonomic function, catecholamines, and cardiovascular homeostasis in dogs, the authors found that: (1) the asystole of electroshock (ES) was significnatly prolonged by high spinal anesthesia but not by relative alpha- or beta-adrenergic blockade; (2) increased levels of circulating catecholamines were solely responsible for the marked hypertensive response to ES, since the pressor effect could be blocked by preventing the release of catecholamines with high spinal anesthesia or by inhibiting alpha-adrenergic receptors with phenoxybenzamine; (3) the adrenal medulla appeared to be the source of most of the ES-induced increase in circulating catecholamines; (4) the asystole and arrhythmias of ES were a cholinergic effect, since they were blocked by atropine; (5) there was a dose-response relationship between the coulombs of electricity administered and the catecholamine and cardiovascular responses; and (6) that the adverse cardiovascular effects of ES therapy could be ameliorated pharmacologically."( Autonomic blockade and the cardiovascular and catecholamine response to electroshock.
Anton, AH; Redderson, CL; Uy, DS,
)
0.13
"3-3 mg/kg); the former effect was not dose dependent (bell-shaped dose-response curve), whereas the latter effect was dose-dependent."( Cardiovascular effects of cocaine in conscious rats: relative significance of central sympathetic stimulation and peripheral neuronal monoamine uptake and release mechanisms.
Goldberg, SR; Schindler, CW; Tella, SR, 1992
)
0.28
" The phenylephrine dose-response curves for mean arterial blood pressure and total peripheral vascular resistance were shifted to the right but the maximal responses were not decreased."( Alpha 1-adrenoceptor subtypes and the regulation of peripheral hemodynamics in the conscious rat.
Barron, KW; Kusiak, JW; Piascik, MT, 1990
)
0.28
") evoked dose-dependent shifts to the right of the dose-response curves to B-HT 933 whilst having minimal effects on the methoxamine dose-response curve."( An investigation into the selectivity of a novel series of benzoquinolizines for alpha 2-adrenoceptors in vivo.
Paciorek, PM; Pierce, V; Shepperson, NB; Waterfall, JF, 1984
)
0.27
" The whole-cell dose-response curve suggests that activation of current by ACh increases up to at least 100 microM and that multiple ligand binding steps are involved."( Activation of nicotinic acetylcholine receptors on cultured Drosophila and other insect neurones.
Albert, JL; Lingle, CJ, 1993
)
0.29
" In the presence of chlorisondamine, McN-A-343 increased both RNA and BP in dose-related fashion, and the dose-response curves of McN-A-343 shifted to the right in the presence of pirenzepine."( Role of muscarinic receptors in ganglionic transmission in rabbits.
Kim, JH; Ro, YB, 1996
)
0.62
" Mean arterial pressure (MAP), heart rate (HR), and renal blood flow (RBF) were recorded from conscious unrestrained rats while five-point cumulative dose-response curves were constructed during infusion or bolus injection of BK (5-80 microg kg(-1))."( Bradykinin B2-receptors mediate the pressor and renal hemodynamic effects of intravenous bradykinin in conscious rats.
Hoagland, KM; Maddox, DA; Martin, DS, 1999
)
0.3
" Cocaine shifted the dose-response curve of noradrenaline to the left and enhanced its maximal effects."( Post-junctional mechanisms involved in the potentiation of cardiac adrenergic responses by cocaine.
Bechara, G; El-Bizri, NM; Khoury, HA; Sabra, R; Sharaf, LH, 2000
)
0.31
" Halothane shifted the ACh dose-response curve for the alpha 4 beta 2-type currents in the direction of lower ACh concentrations and slowed its apparent rate of desensitization."( Modulation of neuronal nicotinic acetylcholine receptors by halothane in rat cortical neurons.
Aistrup, GL; Marszalec, W; Mori, T; Narahashi, T; Nishikawa, K; Yeh, JZ; Zhao, X; Zuo, Y, 2001
)
0.31
[information is derived through text-mining from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Drug Classes (1)

ClassDescription
isoindoles
[compound class information is derived from Chemical Entities of Biological Interest (ChEBI), Hastings J, Owen G, Dekker A, Ennis M, Kale N, Muthukrishnan V, Turner S, Swainston N, Mendes P, Steinbeck C. (2016). ChEBI in 2016: Improved services and an expanding collection of metabolites. Nucleic Acids Res]

Protein Targets (4)

Potency Measurements

ProteinTaxonomyMeasurementAverage (µ)Min (ref.)Avg (ref.)Max (ref.)Bioassay(s)
15-lipoxygenase, partialHomo sapiens (human)Potency15.84890.012610.691788.5700AID887
cytochrome P450 2D6 isoform 1Homo sapiens (human)Potency15.84890.00207.533739.8107AID891
cytochrome P450 2C19 precursorHomo sapiens (human)Potency5.01190.00255.840031.6228AID899
histone acetyltransferase KAT2A isoform 1Homo sapiens (human)Potency17.03900.251215.843239.8107AID504327
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Bioassays (4)

Assay IDTitleYearJournalArticle
AID504749qHTS profiling for inhibitors of Plasmodium falciparum proliferation2011Science (New York, N.Y.), Aug-05, Volume: 333, Issue:6043
Chemical genomic profiling for antimalarial therapies, response signatures, and molecular targets.
AID766732Noncompetitive inhibition of nicotinic cholinergic receptor in rat PC12 cells assessed as inhibition of 100 to 1000 uM nicotine-induced [3H]-norepinephrine release at 5 uM after 30 mins by liquid scintillation counting analysis2013Bioorganic & medicinal chemistry, Sep-15, Volume: 21, Issue:18
Development of a pharmacophore model for the catecholamine release-inhibitory peptide catestatin: virtual screening and functional testing identify novel small molecule therapeutics of hypertension.
AID1347154Primary screen GU AMC qHTS for Zika virus inhibitors2020Proceedings of the National Academy of Sciences of the United States of America, 12-08, Volume: 117, Issue:49
Therapeutic candidates for the Zika virus identified by a high-throughput screen for Zika protease inhibitors.
AID1508630Primary qHTS for small molecule stabilizers of the endoplasmic reticulum resident proteome: Secreted ER Calcium Modulated Protein (SERCaMP) assay2021Cell reports, 04-27, Volume: 35, Issue:4
A target-agnostic screen identifies approved drugs to stabilize the endoplasmic reticulum-resident proteome.
[information is prepared from bioassay data collected from National Library of Medicine (NLM), extracted Dec-2023]

Research

Studies (584)

TimeframeStudies, This Drug (%)All Drugs %
pre-1990389 (66.61)18.7374
1990's123 (21.06)18.2507
2000's53 (9.08)29.6817
2010's16 (2.74)24.3611
2020's3 (0.51)2.80
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Market Indicators

Research Demand Index: 19.31

According to the monthly volume, diversity, and competition of internet searches for this compound, as well the volume and growth of publications, there is estimated to be moderate demand-to-supply ratio for research on this compound.

MetricThis Compound (vs All)
Research Demand Index19.31 (24.57)
Research Supply Index6.41 (2.92)
Research Growth Index4.08 (4.65)
Search Engine Demand Index23.28 (26.88)
Search Engine Supply Index2.00 (0.95)

This Compound (19.31)

All Compounds (24.57)

Study Types

Publication TypeThis drug (%)All Drugs (%)
Trials1 (0.17%)5.53%
Reviews6 (0.99%)6.00%
Case Studies0 (0.00%)4.05%
Observational0 (0.00%)0.25%
Other597 (98.84%)84.16%
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]