Page last updated: 2024-12-06

eedq

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Description

EEDQ: peptide coupling reagent [Medical Subject Headings (MeSH), National Library of Medicine, extracted Dec-2023]

Cross-References

ID SourceID
PubMed CID27833
CHEMBL ID1527785
SCHEMBL ID338
MeSH IDM0040601

Synonyms (82)

Synonym
HMS1776O14
AC-2881
brn 0533048
1(2h)-quinolinecarboxylic acid, 2-ethoxy-, ethyl ester
ethyl n-(2-ethoxy-1,2-dihydroquinoline)carboxylate
einecs 240-418-2
n-carbethoxy-2-ethoxy-1,2-dihydroquinoline
nsc 147831
n-ethoxycarbonyl-2-ethoxy-1,2-dihydroquinoline
smr000059033
MLS000069601 ,
2-ethoxy-1-ethoxycarbonyl-1,2-dihydroquinoline
eedq
16357-59-8
2-ethoxy-1(2h)-quinolinecarboxylic acid, ethyl ester
nsc147831
bc 681
wln: t66 bn chj bvo2 co2
nsc-147831
2-ethoxy-1-ethoxycarbonyl-1,2-dihydroquinoline, >=99%
(3z)-3-(ethoxy-hydroxymethylidene)-1-methylquinoline-2,4-dione
gkqlysroiskdll-uhfffaoysa-
inchi=1/c14h17no3/c1-3-17-13-10-9-11-7-5-6-8-12(11)15(13)14(16)18-4-2/h5-10,13h,3-4h2,1-2h3
AKOS001075463
1-ethoxycarbonyl-2-ethoxy-1,2-dihydroquinoline
E0363
ethyl 2-ethoxy-2h-quinoline-1-carboxylate
STK802369
ethyl 2-ethoxyquinoline-1(2h)-carboxylate
A810487
NCGC00246989-01
5-21-03-00028 (beilstein handbook reference)
unii-60o971an19
60o971an19 ,
ethyl 1,2-dihydro-2-ethoxyquinoline-1-carboxylate
BBL011113
FT-0606405
AM20050163
ethyl 1,2-dihydro-2-ethoxy-1-quinolinecarboxylate
SCHEMBL338
2-ethoxy-1-ethoxycarbonyl-1,2-dihydroquinoline (eedq)
mfcd00006703
SY003226
2-ethoxy-1-ethoxycarbonyl-1,2dihydroquinoline
1-carbethoxy-2-ethoxy-1,2-dihydroquinoline
2-ethoxy-n-ethoxycarbonyl-1,2-dihydroquinoline
2-ethyoxy-1-ethoxycarbonyl-1,2-dihydroquinoline
2-ethoxy-1-ethoxycarbonyl-1.2-dihydroquinoline
1-carbethoxy-2-ethoxy-l,2-dihydroquinoline
2-ethoxy-1(2h)-quinolinecarboxylic acid ethyl ester
ethyl 2-ethoxy-1,2-dihydroquinoline-1-carboxylate
2-ethoxy-l-ethoxycarbonyl-1,2-dihydroquinoline
2-ethoxy-1-ethoxycarbonyl-1,2-dihydrochinolin
2-ethoxy- 1(2h)-quinolinecarboxylic acid ethyl ester
1-ethoxycabonyl-2-ethoxy-1,2-dihydroquinoline
AKOS016842289
bdbm40545
cid_27833
2-ethoxy-2h-quinoline-1-carboxylic acid ethyl ester
ethyl 2-ethoxy-1,2-dihydro-1-quinolinecarboxylate
2-ethoxy-n-(ethoxycarbonyl)-1,2-dihydroquinoline
eedq [mi]
ethyl 2-ethoxy-1(2h)-quinolinecarboxylate
bc-681
CHEMBL1527785
OPERA_ID_1846
n-ethoxycarbonyl-2-ethoxy-1,2-dhydroqunolne
J-523556
F0001-0593
P16694
J-010063
Z85921046
BP-24399
DTXSID50871969
2-ethoxy-1-(ethoxycarbonyl)-1,2-dihydroquinoline
AS-15469
Q10859667
CS-0017180
1-ethoxycarbonyl-2-ethoxy-1
ethyl2-ethoxyquinoline-1(2h)-carboxylate
SB40704
EN300-18587

Research Excerpts

Overview

EEDQ irreversibly inactivates serotonergic receptors which are coupled to G proteins. EEDQ is an effective alkylating agent for DA(T) in vitro, but not to evaluate metabolic turnover or function of DA( T) in vivo.

ExcerptReferenceRelevance
"EEDQ is an alkylating agent which irreversibly inactivates serotonergic receptors which are coupled to G proteins."( N-ethoxycarbonyl-2-ethoxy-1,2-dihydroquinoline (EEDQ) administration for studies of 5-HT1A receptor binding site inactivation and turnover.
Keck, BJ; Lakoski, JM, 1997
)
1.27
"EEDQ is an effective alkylating agent for DA(T) in vitro, but not to evaluate metabolic turnover or function of DA(T) in vivo."( Alkylation of rat dopamine transporters and blockade of dopamine uptake by EEDQ.
Baldessarini, RJ; Kula, NS; Tarazi, FI; Zhang, K, 2000
)
1.26

Treatment

EDQ treatment reduced the sodium current considerably and irreversibly, regardless of the presence of a primary amine in the Ringer's solution. In EEDQ-pretreated rats (6 mg/kg, i.p., 6 h), clonidine caused a rapid and dose-dependent (320-5120 micrograms/kg) increase in the firing rate of NA-LC neurones.

ExcerptReferenceRelevance
"EEDQ pretreatment on the SCC response to aldosterone and amphotericin B revealed nearly identical characteristics; 5) in contrast, amphotericin B stimulation of SCC was limited when Na+ transport was limited by antimycin A (an inhibitor of energy production) or by ouabain."( Modification of carboxyl of Na+ channel inhibits aldosterone action on Na+ transport.
Fanestil, DD; Kipnowski, J; Park, CS, 1983
)
0.99
"EEDQ treatment reduced the sodium current considerably and irreversibly, regardless of the presence of a primary amine in the Ringer's solution."( Effects of chemical modification of carboxyl groups on the voltage-clamped nerve fiber of the frog.
Rack, M; Woll, KH, 1984
)
0.99
"In EEDQ-pretreated rats (6 mg/kg, i.p., 6 h), clonidine caused a rapid and dose-dependent (320-5120 micrograms/kg, i.v.) increase in the firing rate of NA-LC neurones (ED50 = 809 micrograms/kg, Emax = 90%)."( The stimulatory effect of clonidine through imidazoline receptors on locus coeruleus noradrenergic neurones is mediated by excitatory amino acids and modulated by serotonin.
García-Sevilla, JA; Pineda, J; Ruiz-Ortega, JA; Ugedo, L, 1995
)
0.81
"EEDQ treatment shifted the dose-response curve for 5-HT to the right by 6-7-fold, accompanied by a reduction (30-50%) in maximal response."( Receptor reserve masks partial agonist activity of drugs in a cloned rat 5-hydroxytryptamine1B receptor expression system.
Adham, N; Branchek, T; Ellerbrock, B; Hartig, P; Weinshank, RL, 1993
)
1.01
"In EEDQ-pretreated membranes (10(-5) M, 30 min at 25 degrees C), the density of I2-imidazoline sites (Bmax = 80 +/- 4 fmol/mg of protein) was not different from that determined in untreated membranes in the presence of (10(-6) M (-)-adrenaline (Bmax = 83 +/- 4 fmol/mg of protein), and both densities were lower (24%, p < 0.05) than the total native density of [3H]idazoxan binding sites (Bmax = 107 +/- 6 fmol/mg of protein) (I2-imidazoline sites plus alpha 2-adrenoceptors)."( Differential effects of the alkylating agent N-ethoxycarbonyl-2-ethoxy-1,2-dihydroquinoline on brain alpha 2-adrenoceptors and I2-imidazoline sites in vitro and in vivo.
García-Sevilla, JA; Miralles, A; Olmos, G; Ribas, C, 1993
)
0.8
"For EEDQ-treated animals, a drastic decrease of 5-HT(1A) receptor binding activity was noted; this loss was greater in hippocampus than in cerebral cortex."( Alkylation of [3H]8-OH-DPAT binding sites in rat cerebral cortex and hippocampus.
Afkhami-Dastjerdian, S; Carli, M; Nénonéné, EK; Radja, F; Reader, TA; van Gelder, NM, 1996
)
0.77
"EEDQ-pretreated animals lost their stereotypic response to apomorphine but showed increased vacuous jaw movements in response to apomorphine or SKF38393."( Dopaminergic behaviors and signal transduction mediated through adenylate cyclase and phospholipase C pathways.
Beardsley, K; Berki, AC; Undie, AS, 2000
)
1.03
"EEDQ treatment dose-dependently reduced the maximal inhibitory effect of 5-HT [percentage of inhibition: control, 23.6; EEDQ (1 mg/kg), 13.4; EEDQ (6 mg/kg), 8.9], without altering either the slope factor (1.01) or the EC50 (96.4 nM)."( Lack of apparent receptor reserve at postsynaptic 5-hydroxytryptamine1A receptors negatively coupled to adenylyl cyclase activity in rat hippocampal membranes.
Iben, L; Meller, E; Yocca, FD, 1992
)
1
"EEDQ pretreatment reduced inhibition of the ISO response by both NE and the alpha 2-agonist UK 14,304, and inhibition of the forskolin response by UK 14,304."( Occupancy-response relationships for beta- and alpha 2-adrenergic receptors exerting opposing effects on cAMP production.
Atkinson, BN; Minneman, KP, 1992
)
1
"EEDQ treatment did not affect the overflow of radioactivity evoked by POP, but greatly facilitated overflow at 36 or 72 pulses/3 Hz indicating that the autoinhibition seen under the latter conditions is totally lacking with POP stimulation."( Estimation of agonist dissociation constants at central presynaptic alpha-2 autoreceptors in the absence of autoinhibition.
Agneter, E; Drobny, H; Singer, EA, 1991
)
1
"EEDQ treatment decreased receptor density in the cortex in both LRZ- and vehicle-treated groups by approximately 50%, with no change in apparent affinity as previously reported."( Accelerated benzodiazepine receptor recovery after lorazepam discontinuation.
Greenblatt, DJ; Lumpkin, M; Miller, LG; Shader, RI, 1991
)
1
"EEDQ treatment of cytochrome-c oxidase vesicles influenced ferrocytochrome c-induced proton pumping by reducing maximally the H+/e- stoichiometry from 0.84 (control) to 0.24, but had only small effects on respiration, respiratory control ratio, and proton conductivity of the proteoliposomes."( Influence of N-ethoxycarbonyl-2-ethoxy-1,2-dihydroquinoline modification on proton translocation and membrane potential of reconstituted cytochrome-c oxidase support "proton slippage".
Kadenbach, B; Steverding, D, 1991
)
1
"EEDQ treatment significantly (P less than 0.01) suppressed serum testosterone levels only when administered at the higher dose of 5 mg/kg."( The effect of neuroleptic drugs on serum testosterone level in the male rat.
Bradshaw, WG; Couceyro, P; Okonmah, AD; Soliman, KF, 1986
)
0.99
"EEDQ treatment had no effect on [3H]NE uptake or base-line release."( Receptor reserve at the alpha-2 adrenergic receptor in the rat cerebral cortex.
Adler, CH; Goldstein, M; Meller, E, 1987
)
0.99
"Pretreatment with EEDQ (24 h, subcutaneous [s.c.]) inhibited foot-shock-induced ultrasonic vocalisation (effective dose50=0.95 micromol/kg) and decreased [3H]-8-OH-DPAT and [3H]-ketanserin binding in the brain."( N-ethoxycarbonyl-2-ethoxy-1,2-dihydroquinoline studies on the role of 5-HT1A and 5-HT2 receptors in mediating foot-shock-induced ultrasonic vocalisation in adult rats.
Mørk, A; Sánchez, C, 1999
)
0.63

Dosage Studied

EEDQ treatment shifted the dose-response curve for 5-HT to the right by 6-7-fold, accompanied by a reduction (30-50%) in maximal response. The measured reduction in dopamine D2 receptor density after EEDQ was of the same magnitude as the reduction in receptor number predicted from the EedQ induced shift in the full dopamine D1 receptor agonist NPA.

ExcerptRelevanceReference
" After acquisition of the discrimination, the dose-response function for SKF (2."( Effects of chronic SCH 23390 or acute EEDQ on the discriminative stimulus effects of SKF 38393.
Cao, GH; Perry, BD; Woolverton, WL, 1992
)
0.55
"Irreversible inactivation of striatal D2 dopamine (DA) autoreceptors with N-ethoxycarbonyl-2-ethoxy-1,2-dihydroquinoline (EEDQ) or inactivation of striatal guanine nucleotide binding proteins (G proteins) with pertussis toxin (PT) shifted the dose-response curve for N-n-propylnorapomorphine (NPA)-mediated inhibition of gamma-butyrolactone (GBL)-induced elevation of L-3,4-dihydroxyphenylalanine (L-DOPA) to the right, with a decrease in the maximum response."( The effects of pertussis toxin on dopamine D2 and serotonin 5-HT1A autoreceptor-mediated inhibition of neurotransmitter synthesis: relationship to receptor reserve.
Bohmaker, K; Bordi, F; Meller, E, 1992
)
0.49
"Synaptoneurosomes, incubated with amphetamine, showed a biphasic dose-response change in activity of PKC and release of DA."( Protein kinase C and dopamine transport--2. Effects of amphetamine in vitro.
Giambalvo, CT, 1992
)
0.28
" Pretreatment with the receptor-inactivating agent N-ethoxycarbonyl-2-ethoxy-1,2-dihydroquinoline (1 and 2 x 6 mg/kg) progressively shifted the dose-response curve for NPA to the right, but PRL secretion was still maximally inhibited."( Receptor reserve for D2 dopaminergic inhibition of prolactin release in vivo and in vitro.
Friedhoff, AJ; Meller, E; Miller, JC; Puza, T; Schweitzer, JW, 1991
)
0.28
"1-810 nmol) caused a rightward shift of dose-response curve and reduction of maximal effect of alpha-2 agonists used."( Relative efficacy of spinal alpha-2 agonists, dexmedetomidine, clonidine and ST-91, determined in vivo by using N-ethoxycarbonyl-2-ethoxy-1,2-dihydroquinoline, an irreversible antagonist.
Takano, Y; Yaksh, TL, 1991
)
0.28
" Rats were treated with vehicle or EEDQ (2 or 6 mg/kg) and 24 hr later dose-response curves were constructed for inhibition of 5-hydroxytrytophan (5-HTP) accumulation (after decarboxylase inhibition with NSD-1015) by the selective 5-HT1A agonists 8-hydroxy-2(di-n-propylamino)tetralin (8-OH-DPAT) (0."( Receptor reserve for 5-hydroxytryptamine1A-mediated inhibition of serotonin synthesis: possible relationship to anxiolytic properties of 5-hydroxytryptamine1A agonists.
Bohmaker, K; Goldstein, M; Meller, E, 1990
)
0.56
" In the first series of experiments, dose-response curves were constructed for the inhibition of A9 and A10 dopamine cell firing by intravenous administration of the potent dopamine agonist, R-(-)-N-n-propylnorapomorphine (NPA)."( Irreversible receptor inactivation reveals differences in dopamine receptor reserve between A9 and A10 dopamine systems: an electrophysiological analysis.
Cox, RF; Waszczak, BL, 1990
)
0.28
" However, antagonist properties were also evident inasmuch as immediate pretreatment with a low dose of (S)-(+)-NPA caused a significant rightward shift of the (R)-(-)-NPA dose-response curve."( Differences in dopamine receptor reserve for N-n-propylnorapomorphine enantiomers: single unit recording studies after partial inactivation of receptors by N-ethoxycarbonyl-2-ethoxy-1,2-dihydroquinoline.
Cox, RF; Waszczak, BL, 1989
)
0.28
" Pretreatment with sulpiride (200 mg/kg) produced a parallel, 40-fold shift to the right of the dose-response curve for NPA."( Hypothermia in mice: D2 dopamine receptor mediation and absence of spare receptors.
Hizami, R; Kreuter, L; Meller, E, 1989
)
0.28
" After irreversible dopamine (DA) receptor inactivation with N-ethoxycarbonyl-2-ethoxy-1,2-dihydroquinoline (EEDQ), neither the ED50 nor the slope of the dose-response curve for NPA was altered, whereas the maximal response was reduced to 56% of control."( Absence of receptor reserve at striatal dopamine receptors regulating cholinergic neuronal activity.
Enz, A; Goldstein, M; Meller, E, 1988
)
0.49
" In contrast, the major effect of a similar degree of irreversible blockade (86%) on the dose-response curve for the autoreceptor-selective agent EMD 23,448 was a reduction in maximal response (60% of control), indicating that EMD 23,448 is a partial agonist."( Receptor reserve at striatal dopamine autoreceptors: implications for selectivity of dopamine agonists.
Adler, CH; Bohmaker, K; Friedhoff, AJ; Goldstein, M; Helmer-Matyjek, E; Meller, E, 1986
)
0.27
" Type I, parallel shift of the dose-response curve towards higher concentration by modification of COO- groups by N-ethoxycarbonyl-2-ethoxy-1,2-dihydroquinoline (EEDQ)."( Three types of chemical modification-effects induced by various chemical reagents on the glutamate receptors in molluscan neurons.
Kato, M; Kusano, K; Maruhashi, J; Oomura, Y, 1984
)
0.46
" The measured reduction in dopamine D2 receptor density after EEDQ was of the same magnitude as the reduction in receptor number predicted from the EEDQ induced shift in the dose-response curve of the full dopamine D2 receptor agonist NPA."( A high dose of EEDQ reduces pituitary dopamine D2 receptor density and the prolactin suppressive potency of agonists.
Ekman, A; Eriksson, E, 1993
)
0.88
" Dose-response curves were obtained for 8-OH-DPAT (0."( Differential receptor reserve for 5-HT1A receptor-mediated regulation of plasma neuroendocrine hormones.
Bohmaker, K; Meller, E, 1994
)
0.29
" EEDQ treatment shifted the dose-response curve for 5-HT to the right by 6-7-fold, accompanied by a reduction (30-50%) in maximal response."( Receptor reserve masks partial agonist activity of drugs in a cloned rat 5-hydroxytryptamine1B receptor expression system.
Adham, N; Branchek, T; Ellerbrock, B; Hartig, P; Weinshank, RL, 1993
)
1.2
" Moreover, dose-response curves to R(-)-NPA were shifted 10-fold to the right and the maximum inhibitory response was depressed."( Inhibition of substantia nigra dopamine cell firing by R(-)-N-n-propylnorapomorphine: electrophysiological and autoradiographic studies after regional inactivation of dopamine receptors by microinjection of N-ethoxycarbonyl-2-ethoxy-1,2-dihydroquinoline.
Cox, RF; Waszczak, BL, 1993
)
0.29
" EEDQ decreased the number of 5-HT1A binding sites and shifted the dose-response curves (DRCs) of each agonist either to the right or, at higher EEDQ doses, to the right and downward."( In vivo estimates of efficacy at 5-HT1A receptors: effects of EEDQ on the ability of agonists to produce lower-lip retraction in rats.
Assié, MB; France, CP; Koek, W; Zernig, G, 2000
)
1.46
[information is derived through text-mining from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Protein Targets (4)

Potency Measurements

ProteinTaxonomyMeasurementAverage (µ)Min (ref.)Avg (ref.)Max (ref.)Bioassay(s)
Chain A, Beta-lactamaseEscherichia coli K-12Potency100.00000.044717.8581100.0000AID485294
survival motor neuron protein isoform dHomo sapiens (human)Potency1.41250.125912.234435.4813AID1458
lamin isoform A-delta10Homo sapiens (human)Potency1.41250.891312.067628.1838AID1487
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Activation Measurements

ProteinTaxonomyMeasurementAverageMin (ref.)Avg (ref.)Max (ref.)Bioassay(s)
Estrogen receptor 1Homo sapiens (human)EC50 (µMol)9,999.00009.219915.159423.4895AID737
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Bioassays (14)

Assay IDTitleYearJournalArticle
AID588460High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain A protease, Validation Compound Set2010Current protocols in cytometry, Oct, Volume: Chapter 13Microsphere-based flow cytometry protease assays for use in protease activity detection and high-throughput screening.
AID588460High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain A protease, Validation Compound Set2006Cytometry. Part A : the journal of the International Society for Analytical Cytology, May, Volume: 69, Issue:5
Microsphere-based protease assays and screening application for lethal factor and factor Xa.
AID588460High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain A protease, Validation Compound Set2010Assay and drug development technologies, Feb, Volume: 8, Issue:1
High-throughput multiplex flow cytometry screening for botulinum neurotoxin type a light chain protease inhibitors.
AID588459High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain F protease, Validation compound set2010Current protocols in cytometry, Oct, Volume: Chapter 13Microsphere-based flow cytometry protease assays for use in protease activity detection and high-throughput screening.
AID588459High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain F protease, Validation compound set2006Cytometry. Part A : the journal of the International Society for Analytical Cytology, May, Volume: 69, Issue:5
Microsphere-based protease assays and screening application for lethal factor and factor Xa.
AID588459High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain F protease, Validation compound set2010Assay and drug development technologies, Feb, Volume: 8, Issue:1
High-throughput multiplex flow cytometry screening for botulinum neurotoxin type a light chain protease inhibitors.
AID588461High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Lethal Factor Protease, Validation compound set2010Current protocols in cytometry, Oct, Volume: Chapter 13Microsphere-based flow cytometry protease assays for use in protease activity detection and high-throughput screening.
AID588461High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Lethal Factor Protease, Validation compound set2006Cytometry. Part A : the journal of the International Society for Analytical Cytology, May, Volume: 69, Issue:5
Microsphere-based protease assays and screening application for lethal factor and factor Xa.
AID588461High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Lethal Factor Protease, Validation compound set2010Assay and drug development technologies, Feb, Volume: 8, Issue:1
High-throughput multiplex flow cytometry screening for botulinum neurotoxin type a light chain protease inhibitors.
AID504810Antagonists of the Thyroid Stimulating Hormone Receptor: HTS campaign2010Endocrinology, Jul, Volume: 151, Issue:7
A small molecule inverse agonist for the human thyroid-stimulating hormone receptor.
AID504812Inverse Agonists of the Thyroid Stimulating Hormone Receptor: HTS campaign2010Endocrinology, Jul, Volume: 151, Issue:7
A small molecule inverse agonist for the human thyroid-stimulating hormone receptor.
AID588519A screen for compounds that inhibit viral RNA polymerase binding and polymerization activities2011Antiviral research, Sep, Volume: 91, Issue:3
High-throughput screening identification of poliovirus RNA-dependent RNA polymerase inhibitors.
AID540299A screen for compounds that inhibit the MenB enzyme of Mycobacterium tuberculosis2010Bioorganic & medicinal chemistry letters, Nov-01, Volume: 20, Issue:21
Synthesis and SAR studies of 1,4-benzoxazine MenB inhibitors: novel antibacterial agents against Mycobacterium tuberculosis.
AID1224864HCS microscopy assay (F508del-CFTR)2016PloS one, , Volume: 11, Issue:10
Increasing the Endoplasmic Reticulum Pool of the F508del Allele of the Cystic Fibrosis Transmembrane Conductance Regulator Leads to Greater Folding Correction by Small Molecule Therapeutics.
[information is prepared from bioassay data collected from National Library of Medicine (NLM), extracted Dec-2023]

Research

Studies (314)

TimeframeStudies, This Drug (%)All Drugs %
pre-1990101 (32.17)18.7374
1990's166 (52.87)18.2507
2000's31 (9.87)29.6817
2010's16 (5.10)24.3611
2020's0 (0.00)2.80
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Market Indicators

Research Demand Index: 33.75

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 Index33.75 (24.57)
Research Supply Index5.80 (2.92)
Research Growth Index4.31 (4.65)
Search Engine Demand Index50.49 (26.88)
Search Engine Supply Index2.00 (0.95)

This Compound (33.75)

All Compounds (24.57)

Study Types

Publication TypeThis drug (%)All Drugs (%)
Trials0 (0.00%)5.53%
Reviews4 (1.22%)6.00%
Case Studies0 (0.00%)4.05%
Observational0 (0.00%)0.25%
Other325 (98.78%)84.16%
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]