Page last updated: 2024-11-13

charybdotoxin

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

Cross-References

ID SourceID
PubMed CID56842037
MeSH IDM0028373

Synonyms (9)

Synonym
quinquestriatus toxin
115422-61-2
charybdotoxin ,
ctx toxin
95751-30-7
charybdotoxin (reduced)
charybdotoxin (native)
lqh alpha it recombinant
DTXSID30897182

Research Excerpts

Overview

Charybdotoxin is a 37-residue polypeptide toxin from scorpion venom, which acts by blocking voltage-gated and Ca(2+)-activated K+ channels. It is rigidly held in active conformation by three disulfide bonds. CharyBDotoxin (ChTX) is a potent blocker of the high-conductance Ca(++)-activated channel in smooth muscle.

ExcerptReferenceRelevance
"Charybdotoxin is a non-specific inhibitor of BK and other K"( Development of charybdotoxin Q18F variant as a selective peptide blocker of neuronal BK(α + β4) channel for the treatment of epileptic seizures.
Cao, C; Ji, Y; Lan, W; Li, G; Liu, X; Tao, J; Wang, C; Xue, H; Yao, Y; Zhang, S, 2022
)
1.8
"Charybdotoxin (CTX) is a peptide of known structure that inhibits Shaker K+ channels by a pore-blocking mechanism. "( The charybdotoxin receptor of a Shaker K+ channel: peptide and channel residues mediating molecular recognition.
Goldstein, SA; Miller, C; Pheasant, DJ, 1994
)
2.29
"Charybdotoxin is a 37-residue polypeptide toxin from scorpion venom, which acts by blocking voltage-gated and Ca(2+)-activated K+ channels. "( Synthesis and structural characterisation of analogues of the potassium channel blocker charybdotoxin.
Byrnes, ME; Duggan, BM; Dyke, TR; Kem, WR; Norton, RS; Pennington, MW, 1996
)
1.96
"Charybdotoxin is a small peptide blocker of K+ channels, rigidly held in active conformation by three disulfide bonds. "( Interaction of Ca2(+)-activated K+ channels with refolded charybdotoxins mutated at a central interaction residue.
Dang, W; Kozlowski, E; Miller, C; Naini, AA; Shaikh, T; Shimony, E, 1996
)
1.98
"Charybdotoxin (ChTX) is a specific blocker of Ca(2+)-activated K+ channels. "( Charybdotoxin block of Ca(2+)-activated K+ channels in colonic muscle depends on membrane potential dynamics.
Carl, A; Frey, BW; Publicover, NG, 1998
)
3.19
"Charybdotoxin (ChTX) is a potent blocker of the high-conductance Ca(++)-activated K+ channel in smooth muscle and produces a concentration-dependent contraction of guinea pig trachea."( Selective inhibition of relaxation of guinea-pig trachea by charybdotoxin, a potent Ca(++)-activated K+ channel inhibitor.
Charette, L; Garcia, ML; Jones, TR; Kaczorowski, GJ, 1990
)
1.24
"Charybdotoxin is a high-affinity specific inhibitor of the high-conductance Ca2+-activated K+ channel found in the plasma membranes of many vertebrate cell types. "( Purification of charybdotoxin, a specific inhibitor of the high-conductance Ca2+-activated K+ channel.
Miller, C; Phillips, M; Smith, C, 1986
)
2.06

Actions

Charybdotoxin can increase quantal content, but this is more likely to result from block of voltage-dependent K+ channels than Ca(2+)-activated channels. The increase in transmitter release occurred in conditions in which little IKCa would be present. CharyBDotoxin did not inhibit the sickling of sickle cells under deoxygenation.

ExcerptReferenceRelevance
"Charybdotoxin can increase quantal content, but this is more likely to result from block of voltage-dependent K+ channels than Ca(2+)-activated channels: the increase in transmitter release occurred in conditions in which little IKCa would be present; higher concentration of charybdotoxin and longer exposure times were required to increase transmitter release than those needed to block IKCa, and the facilitatory effects of charybdotoxin and toxin 18-2 correlated more with their effects on dendrotoxin binding than on block of IKCa."( Neuromuscular effects of some potassium channel blocking toxins from the venom of the scorpion Leiurus quinquestriatus hebreus.
Bouet, F; Boyot, P; Doljansky, Y; Harvey, AL; Marshall, DL; Ménez, A; Pinkasfeld, S; Vatanpour, H, 1994
)
1.01
"Charybdotoxin did not inhibit the sickling of sickle cells under deoxygenation."( Inhibition of the in vitro formation of dense cells and of irreversibly sickled cells by charybdotoxin, a specific inhibitor of calcium-activated potassium efflux.
Katagi, C; Katagi, H; Ohnishi, ST, 1989
)
1.22

Bioavailability

ExcerptReferenceRelevance
"Endothelial dysfunction has been linked to a decrease in nitric oxide (NO) bioavailability and attenuated endothelium-derived hyperpolarizing factor (EDHF)-mediated relaxation."( Upregulation of intermediate calcium-activated potassium channels counterbalance the impaired endothelium-dependent vasodilation in stroke-prone spontaneously hypertensive rats.
Carneiro, FS; Carneiro, ZN; Dorrance, A; Giachini, FR; Lima, VV; Tostes, RC; Webb, RC, 2009
)
0.35
" These results demonstrate that quercetin-mediated stimulation of eNOS phosphorylation increases NO bioavailability in endothelial cells and can thus play a role in the vascular protective effects associated with improved endothelial cell function."( Dietary flavonoid quercetin stimulates vasorelaxation in aortic vessels.
Constance, C; Inoue, T; Khoo, NK; Parks, DA; Patel, RP; Pozzo-Miller, L; White, CR; Zhou, F, 2010
)
0.36

Dosage Studied

ExcerptRelevanceReference
"05) without affecting exogenously applied acetylcholine dose-response curves."( Role of K+ channels in the modulation of cholinergic neural responses in guinea-pig and human airways.
Barnes, PJ; Belvisi, MG; Miura, M; Stretton, CD; Yacoub, MH, 1992
)
0.28
"5 microM) had no significant effect on relaxation dose-response curves (DRCs) to ACh, NTG or NO."( Role of calcium-activated K+ channels in vasodilation induced by nitroglycerine, acetylcholine and nitric oxide.
Khan, SA; Mathews, WR; Meisheri, KD, 1993
)
0.29
" Hydrochlorothiazide (10 microM) and cicletanine (10 microM) were weak calcium antagonists shifting the calcium dose-response curve half a log unit to the right."( Ion channel involvement in the acute vascular effects of thiazide diuretics and related compounds.
Calder, JA; Schachter, M; Sever, PS, 1993
)
0.29
" However, the inhibition of the combined CPA and CCh response was reduced and the dose-response curve of SIN-1 shifted to the right."( Involvement of intracellular Ca2+ stores in inhibitory effects of NO donor SIN-1 and cGMP.
Allescher, HD; Franck, H; Puschmann, A; Schusdziarra, V; Storr, M, 1998
)
0.3
" The model in which the occupancy of one of four binding sites by melatonin is sufficient to block the channels gives the best fit to the dose-response relationship, although all four binding sites can be occupied by the drug."( Multiple binding sites for melatonin on Kv1.3.
Csécsei, G; Damjanovich, S; Gáspár, R; Panyi, G; Péter, M; Pieri, C; Varga, Z, 2001
)
0.31
" These results suggest that MET is endowed with peculiar hypophagic effects at dosage levels that are not able to affect gross behaviour in mice."( Methylamine and benzylamine induced hypophagia in mice: modulation by semicarbazide-sensitive benzylamine oxidase inhibitors and aODN towards Kv1.1 channels.
Banchelli, G; Galeotti, N; Ghelardini, C; Pirisino, R; Raimondi, L, 2001
)
0.31
[information is derived through text-mining from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Research

Studies (1,132)

TimeframeStudies, This Drug (%)All Drugs %
pre-199044 (3.89)18.7374
1990's604 (53.36)18.2507
2000's375 (33.13)29.6817
2010's103 (9.10)24.3611
2020's6 (0.53)2.80
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Market Indicators

Research Demand Index: 30.08

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 Index30.08 (24.57)
Research Supply Index7.05 (2.92)
Research Growth Index5.66 (4.65)
Search Engine Demand Index39.83 (26.88)
Search Engine Supply Index2.00 (0.95)

This Compound (30.08)

All Compounds (24.57)

Study Types

Publication TypeThis drug (%)All Drugs (%)
Trials0 (0.00%)5.53%
Reviews14 (1.22%)6.00%
Case Studies0 (0.00%)4.05%
Observational0 (0.00%)0.25%
Other1,136 (98.78%)84.16%
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]