Page last updated: 2024-11-06

moricizine

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Description

Moricizine is a class I antiarrhythmic drug used to treat ventricular tachycardia. It is a synthetic compound with a complex structure and a chiral center. Moricizine works by blocking sodium channels in the heart, which helps to regulate the electrical activity of the heart and reduce the frequency of abnormal heartbeats. It has been shown to be effective in treating both chronic and acute ventricular tachycardia, and it is often used in patients with heart failure. Moricizine is generally well-tolerated, but it can cause side effects such as nausea, dizziness, and headache. It is important to note that Moricizine is not approved for use in all countries. It is a significant drug in the treatment of arrhythmias because it offers an alternative to other treatments that may have more severe side effects or be less effective. Moricizine is frequently studied to explore its potential in treating other cardiac conditions and to understand its complex mechanism of action.'

Moricizine: An antiarrhythmia agent used primarily for ventricular rhythm disturbances. [Medical Subject Headings (MeSH), National Library of Medicine, extracted Dec-2023]

moricizine : A phenothiazine substituted on the nitrogen by a 3-(morpholin-4-yl)propanoyl group, and at position 2 by an (ethoxycarbonyl)amino group. [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]

Cross-References

ID SourceID
PubMed CID16133238
MeSH IDM0024900
PubMed CID34633
CHEMBL ID1075
CHEBI ID6997
SCHEMBL ID16794
MeSH IDM0024900

Synonyms (83)

Synonym
gtpl2257
pacap-27
BIDD:GT0499
en-313 free base
CHEMBL1075
chebi:6997 ,
PRESTWICK2_001051
BRD-K21548250-003-03-5
moracizinum
moracizina
ethyl [10-(3-morpholin-4-ylpropanoyl)-10h-phenothiazin-2-yl]carbamate
phenothiazine-2-carbamic acid, 10-(3-morpholinopropionyl)-, ethyl ester
moracizina [inn-spanish]
moracizine
en-313
ethyl (10-(3-(4-morpholinyl)-1-oxopropyl)-10h-phenothiazin-2-yl)carbamate
moracizinum [inn-latin]
carbamic acid, (10-(3-(4-morpholinyl)-1-oxopropyl)-10h-phenothiazin-2-yl)-, ethyl ester
c22h25n3o4s
einecs 250-854-5
moricizine [usan]
g 214
TIMTEC1_000772
cas-31883-05-3
CBDIVE_008814
BSPBIO_001002
D05077
moracizine (inn)
moricizine (usan)
OPREA1_701257
AB00514710
ethyl {10-[3-(morpholin-4-yl)propanoyl]-10h-phenothiazin-2-yl}carbamate
STK370502
C07743
moricizine
31883-05-3
ethyl 10-(3-morpholinopropionyl)phenothiazine-2-carbamate
ethyl 10-(beta-n-morpholinylpropionyl)phenothiazine-2-carbamate
DB00680
[10-(3-morpholin-4-yl-propionyl)-10h-phenothiazin-2-yl]-carbamic acid ethyl ester
PRESTWICK0_001051
PRESTWICK1_001051
SPBIO_002931
OPREA1_682904
BPBIO1_001104
PRESTWICK3_001051
MLS001201823
smr000059585
NCGC00074074-03
HMS1536D02
AKOS001487682
ethyl n-[10-(3-morpholin-4-ylpropanoyl)phenothiazin-2-yl]carbamate
ethyl n-{10-[3-(morpholin-4-yl)propanoyl]-10h-phenothiazin-2-yl}carbamate
NCGC00016809-03
NCGC00016809-04
NCGC00016809-02
moracizine [inn]
2gt1d0tmx1 ,
unii-2gt1d0tmx1
HMS2852B19
FT-0630560
n-{10-[3-(morpholin-4-yl)propanoyl]-10h-phenothiazin-2-yl}ethoxycarboximidic acid
gtpl7244
moracizine [who-dd]
moricizine [vandf]
moricizine [mi]
moracizine [mart.]
HY-B0615
AB00514710-13
SCHEMBL16794
FUBVWMNBEHXPSU-UHFFFAOYSA-N
ethyl (10-(3-morpholinopropanoyl)-10h-phenothiazin-2-yl)carbamate
DTXSID4023335
carbamic acid, [10-[3-(4-morpholinyl)-1-oxopropyl]-10h-phenothiazin-2-yl]-, ethyl ester
ethyl 10-(3-morpholinopropanoyl)-10h-phenothiazin-2-ylcarbamate
[10-[3-(4-morpholinyl)-1-oxopropyl]-10h-phenothiazin-2-yl]-, ethyl ester
BCP14374
Q904071
carbamicacid,[10-[3-(4-morpholinyl)-1-oxopropyl]-10h-phenothiazin-2-yl]-,ethylester
A853599
EN300-18530976
carbamic acid,[10-[3-(4-morpholinyl)-1-oxopropyl]-10h-phenothiazin-2-yl]-,ethyl ester
ethyl 10-(beta-morpholinopropionyl)phenothiazine-2-carbamate

Research Excerpts

Overview

Moricizine is a phenothiazine derivative with Vaughan Williams class 1 antiarrhythmic properties. Moricizine appears to be a well-tolerated drug with low occurrence of noncardiac adverse effects without significant serious organ toxicity.

ExcerptReferenceRelevance
"Moricizine is a novel phenothiazine antiarrhythmic agent that depresses the activity of ectopic foci, has a low incidence of adverse effects relative to other agents, and is useful in treating pediatric atrial ectopic tachycardia. "( Pharmacokinetics of moricizine in young patients.
LeClair, IO; Mehta, AV; Rice, PJ; Stone, WL, 1995
)
2.06
"Moricizine is a Class I antiarrhythmic drug currently approved for the treatment of life-threatening ventricular arrhythmias. "( Moricizine-induced proarrhythmia.
Cowan, MD; Seaborg, SM, 1992
)
3.17
"Moricizine (Ethmozine) is a phenothiazine derivative recently approved in the United States for the treatment of malignant ventricular arrhythmias. "( Moricizine: pharmacodynamic, pharmacokinetic, and therapeutic profile of a new antiarrhythmic.
Maloney, JD; Vanerio, G,
)
3.02
"Moricizine (moracizine) is a new class I antiarrythmic drug which is undergoing a large scale clinical trial at present. "( The effect of pretreatment with moricizine on early arrhythmia resulting from myocardial ischemia in rats.
Hashimoto, K; He, ZS; Komori, S; Tamura, K, 1992
)
2.01
"Moricizine is a phenothiazine derivative with Vaughan Williams class 1 antiarrhythmic properties. "( Moricizine: a novel antiarrhythmic agent.
Carnes, CA; Coyle, JD,
)
3.02
"Moricizine is a class I antiarrhythmic drug. "( Cardiac electrophysiologic effects of moricizine hydrochloride.
Bigger, JT, 1990
)
1.99
"Moricizine appears to be a well-tolerated antiarrhythmic drug with low occurrence of noncardiac adverse effects without significant serious organ toxicity."( Noncardiac adverse effects and organ toxicity of moricizine during short- and long-term studies.
Kennedy, HL, 1990
)
1.25
"Moricizine hydrochloride is an orally effective antiarrhythmic agent currently marketed in the Soviet Union and undergoing clinical testing in the United States. "( Determination of unlabeled and 13C6-labeled moricizine in human plasma using thermospray liquid chromatography-mass spectrometry.
Garner, DM; Isensee, RK; Page, GO; Pieniaszek, HJ; Shalaby, LM; Shen, HS; Whitney, CC, 1989
)
1.98
"Moricizine HCl is a phenothiazine derivative with antiarrhythmic properties. "( Pharmacokinetics of moricizine HCl.
Fogoros, RN; Humphries, JO; Mason, DT; McMahon, FG; Morganroth, J; Williams, RL; Woosley, RL, 1987
)
2.04
"Moricizine HCl is a promising primary drug for atrial ectopic tachycardia."( Ethmozine (moricizine HCl): a promising drug for "automatic" atrial ectopic tachycardia.
Evans, VL; Garson, A; McNamara, DG; McVey, P; Moak, JP; Smith, RT, 1987
)
1.38

Effects

Moricizine hydrochloride has been shown to be effective in the treatment of a variety of ventricular arrhythmias. The drug depresses abnormal automaticity and delayed after-depolarizations but has little effect on normal automaticity. Moricizine carries a considerable risk for life-threatening proarrhythmia.

ExcerptReferenceRelevance
"Moricizine has a low rate of efficacy and carries a considerable risk for life-threatening proarrhythmia in patients with serious ventricular arrhythmias and inducible ventricular tachycardia who have failed therapy with other class I antiarrhythmic agents."( Efficacy and risks of moricizine in inducible sustained ventricular tachycardia.
Brooks, R; Damle, R; Frumkin, W; Goldberger, J; Greenberg, S; Kadish, AH; Levine, J; Matos, J, 1992
)
2.04
"Moricizine has been touted as having a low incidence of proarrhythmic effects. "( Exercise induced fatal sinusoidal ventricular tachycardia secondary to moricizine.
Bauman, J; Ivanovich, L; Kehoe, RF; Nazari, J; Pham, T, 1992
)
1.96
"Moricizine hydrochloride has been shown to be effective in the treatment of a variety of ventricular arrhythmias. "( Efficacy of moricizine in malignant ventricular arrhythmias.
Horowitz, LN, 1990
)
2.1
"Moricizine has a low rate of efficacy and carries a considerable risk for life-threatening proarrhythmia in patients with serious ventricular arrhythmias and inducible ventricular tachycardia who have failed therapy with other class I antiarrhythmic agents."( Efficacy and risks of moricizine in inducible sustained ventricular tachycardia.
Brooks, R; Damle, R; Frumkin, W; Goldberger, J; Greenberg, S; Kadish, AH; Levine, J; Matos, J, 1992
)
2.04
"Moricizine has proved to be more effective than disopyramide and propranolol in suppressing ventricular ectopic activity, of comparable efficacy to quinidine, but less effective than encainide and flecainide."( Moricizine. A review of its pharmacological properties, and therapeutic efficacy in cardiac arrhythmias.
Buckley, MT; Fitton, A, 1990
)
2.44
"Moricizine HCl has demonstrated a low incidence of generally mild and transient side effects."( Drug interactions with Ethmozine (moricizine HCl).
Kennedy, HL; MacFarland, RT; Wood, AJ, 1987
)
1.27
"Moricizine HCl has been used primarily for ventricular rhythm disturbances; the drug depresses abnormal automaticity and delayed after-depolarizations but has little effect on normal automaticity."( Ethmozine (moricizine HCl): a promising drug for "automatic" atrial ectopic tachycardia.
Evans, VL; Garson, A; McNamara, DG; McVey, P; Moak, JP; Smith, RT, 1987
)
1.38

Toxicity

Moricizine is well tolerated in a wide variety of patients, and therefore, may be a safe and effective agent for treating AF.

ExcerptReferenceRelevance
"Older age increases the susceptibility to adverse cardiac events from a class of relatively toxic antiarrhythmic agents."( Effects of advancing age on the efficacy and side effects of antiarrhythmic drugs in post-myocardial infarction patients with ventricular arrhythmias. The CAST Investigators.
Akiyama, T; Barker, AH; Campbell, WB; Friedman, L; Josephson, RA; Keller, M; Papa, L; Pawitan, Y; Rubbert, P, 1992
)
0.28
"To determine the tolerance and safety of moricizine, the incidence and nature of its noncardiac adverse effects and organ toxicity reported during short- and long-term clinical studies were examined."( Noncardiac adverse effects and organ toxicity of moricizine during short- and long-term studies.
Kennedy, HL, 1990
)
0.8
" Besides its significant antiarrhythmic activity, ethacizin displayed a number of adverse cardiac effects, such as excessive negative inotropic and dromotropic ones."( [Possibilities of correcting adverse effects of anti-arrhythmia agents].
Bartashevich, VV; Galenko-Iaroshevskiĭ, PA; Kanorskiĭ, SG; Khankoeva, AI; Skibitskiĭ, VV; Uvarov, AV, 1996
)
0.29
" Moricizine is well tolerated in a wide variety of patients, and therefore, may be a safe and effective agent for treating AF."( Efficacy and safety of moricizine in the maintenance of sinus rhythm in patients with recurrent atrial fibrillation.
Carlson, MD; Geller, JC; Geller, M; Waldo, AL, 2001
)
1.53
"5 million adverse drug reaction (ADR) reports for 8620 drugs/biologics that are listed for 1191 Coding Symbols for Thesaurus of Adverse Reaction (COSTAR) terms of adverse effects."( Assessment of the health effects of chemicals in humans: II. Construction of an adverse effects database for QSAR modeling.
Benz, RD; Contrera, JF; Kruhlak, NL; Matthews, EJ; Weaver, JL, 2004
)
0.32

Pharmacokinetics

The potential for a pharmacokinetic interaction between the investigational antiarrhythmic drug ethmozine (moricizine HCl, the generic name that is infrequently used in existing literature) and digoxin was evaluated in nine healthy male adults. Under steady-state conditions, there was a two-way (opposing) pharmacokinetics drug interaction.

ExcerptReferenceRelevance
" For the pharmacokinetic study, rats (4 males and 4 females) were treated with 40 mg/kg oral MRZ once daily for 7 days."( Effects of multiple doses of moricizine hydrochloride on its pharmacokinetics and hepatic microsomal enzymes in rats.
Davidson, AF; King, SY; Pieniaszek, HJ; Powel, RJ; Quon, CY; Vincent, DR; Wong, YN, 1992
)
0.57
" More importantly, there was no evidence of a pharmacodynamic interaction based on the prothrombin time profile."( Effect of moricizine on the pharmacokinetics and pharmacodynamics of warfarin in healthy volunteers.
Agra, AM; Benedek, IH; King, SY; Pieniaszek, HJ; Powell, RJ; Schary, WL, 1992
)
0.69
" This necessitates a pharmacokinetic monitoring of such patients prescribed ethmozine and a correction of the drug dose, if necessary."( [Ethmozine pharmacokinetics in liver insufficiency].
Gneushev, ET; Kukes, VG; Kurapov, AP; Nekrasova, OV; Ryzhenkova, AP, 1990
)
0.28
" The elimination half-life of moricizine is 2 to 6 hours, but its duration of antiarrhythmic action is much longer suggesting active metabolites."( Clinical pharmacokinetics of moricizine.
Barbey, JT; Schwartz, SL; Siddoway, LA; Woosley, RL, 1990
)
0.86
"Problems in studying pharmacokinetic interactions with digoxin were evaluated using as a test model the examination of a possible interaction between digoxin and ethmozine in a group of 11 patients with cardiac disease."( Drug interactions with cardiac glycosides: evaluation of a possible digoxin-ethmozine pharmacokinetic interaction.
Antman, EM; Arnold, M; Bosak, M; Friedman, PL; Smith, TW; White, H, 1987
)
0.27
" There is a 4-fold variability in range for its elimination half-life and in volumes of distribution and clearance."( Pharmacokinetics of moricizine HCl.
Fogoros, RN; Humphries, JO; Mason, DT; McMahon, FG; Morganroth, J; Williams, RL; Woosley, RL, 1987
)
0.6
" The pharmacokinetic parameters obtained indicate that ethacizine is characterized by a less value of clearance and greater period of half-elimination as compared to ethmozine."( [Clinical pharmacokinetics and hemodynamics of ethacizin in the acute period of myocardial infarct].
Beloborodov, VL; Kaverina, NV; Klimov, AV; Pokazeeva, ET; Tiukavkina, NA,
)
0.13
"The potential for a pharmacokinetic interaction between the investigational antiarrhythmic drug ethmozine (moricizine HCl, the generic name that is infrequently used in existing literature) and digoxin was evaluated in nine healthy male adults."( Assessment of the potential pharmacokinetic interaction between digoxin and ethmozine.
MacFarland, RT; Marcus, FI; Moeller, VR; Pieniaszek, HJ; Whitney, CC, 1985
)
0.48
" It was demonstrated that the drug half-life was on the average 164 +/- 24."( [Pharmacokinetics of the new Soviet anti-arrhythmia preparation etacizin].
Gneushev, ET; Kukes, VG; Kurapov, AP; Ponomarenko, EL,
)
0.13
" The peak concentration in plasma (2."( [Pharmacokinetics of moracizine and moracizine sulfoxide in healthy volunteers].
Guo, WY; Jiang, WD; Li, ZS; Yang, JM; Zhu, JR, 1993
)
0.29
" Theophylline pharmacokinetic profiles were obtained over 36 h after all theophylline administrations."( Effect of moricizine on the pharmacokinetics of single-dose theophylline in healthy subjects.
Benedek, IH; Davidson, AF; Pieniaszek, HJ, 1993
)
0.69
" Under steady-state conditions, there was a two-way (opposing) pharmacokinetic drug interaction when moricizine and diltiazem were coadministered in healthy volunteers."( Pharmacokinetic interactions of moricizine and diltiazem in healthy volunteers.
Benedek, IH; Davidson, AF; Flamenbaum, W; Pieniaszek, HJ; Robinson, CA; Shum, L; Widner, PJ, 1996
)
0.79

Compound-Compound Interactions

ExcerptReferenceRelevance
" Thus the objective of this investigation was to evaluate the antifibrillatory properties of moricizine (a new antiarrhythmic agent) alone and in combination with lidocaine (an established antifibrillatory agent)."( Antifibrillatory and electrophysiologic actions of moricizine alone and in combination with lidocaine: a prospective, randomized trial.
Chow, MS; Fan, C; Kluger, J; O'Rangers, EA; Ujhelyi, MR, 1993
)
0.76
"5 mg/kg/hr infusion, or saline bolus and infusion), and drug combined with lidocaine (5 mg/kg loading dose, 4 mg/kg/hr infusion)."( Antifibrillatory and electrophysiologic actions of moricizine alone and in combination with lidocaine: a prospective, randomized trial.
Chow, MS; Fan, C; Kluger, J; O'Rangers, EA; Ujhelyi, MR, 1993
)
0.54
"4 mA at baseline during saline infusion, and when saline was combined with lidocaine, respectively."( Antifibrillatory and electrophysiologic actions of moricizine alone and in combination with lidocaine: a prospective, randomized trial.
Chow, MS; Fan, C; Kluger, J; O'Rangers, EA; Ujhelyi, MR, 1993
)
0.54
" They were divided into a control group (CG, metoprolol, n = 156) and an observation group (OG, moracizine combined with metoprolol, n = 160) based on the treatment they received."( Effects of Moracizine Combined with Metoprolol on Hemodynamic Indices of the Left Atrium and Quality of Life in Patients with Atrial Fibrillation.
Fu, T; Han, G; Zhang, Y, 2023
)
0.91
"Moracizine combined with metoprolol is an effective treatment for AF patients."( Effects of Moracizine Combined with Metoprolol on Hemodynamic Indices of the Left Atrium and Quality of Life in Patients with Atrial Fibrillation.
Fu, T; Han, G; Zhang, Y, 2023
)
0.91

Bioavailability

Moricizine is well absorbed after oral administration and undergoes extensive first-pass metabolism.

ExcerptReferenceRelevance
" It undergoes extensive first-pass metabolism, has a bioavailability of 34-38 percent, and is 95 percent bound to plasma proteins."( Moricizine: a novel antiarrhythmic agent.
Carnes, CA; Coyle, JD,
)
1.57
"Moricizine is well absorbed after oral administration and undergoes extensive first-pass metabolism."( Clinical pharmacokinetics of moricizine.
Barbey, JT; Schwartz, SL; Siddoway, LA; Woosley, RL, 1990
)
2.01
" This method was successfully used to assay human plasma samples from a pilot moricizine bioavailability study in which tablets and solution containing moricizine hydrochloride and [13C6]moricizine, respectively, were simultaneously administered."( Determination of unlabeled and 13C6-labeled moricizine in human plasma using thermospray liquid chromatography-mass spectrometry.
Garner, DM; Isensee, RK; Page, GO; Pieniaszek, HJ; Shalaby, LM; Shen, HS; Whitney, CC, 1989
)
0.77
" The bioavailability of moricizine HCl connotes extensive first-pass effect, or presystemic metabolism."( Pharmacokinetics of moricizine HCl.
Fogoros, RN; Humphries, JO; Mason, DT; McMahon, FG; Morganroth, J; Williams, RL; Woosley, RL, 1987
)
0.9
"05) instead of decreased as one would expect because of enzyme induction, presumably due to a decrease in systemic bioavailability and its influence on the oral volume of distribution."( Enzyme induction by moricizine: time course and extent in healthy subjects.
Benedek, IH; Davidson, AF; Pieniaszek, HJ, 1994
)
0.61
" Study of metacisin pharmacokinetics showed that it possesses bioavailability twice that of ethmosin tablets taken separately and four times that of ethasicin."( [The pharmacology of the new combined anti-arrhythmia preparation metatsizin].
Beloborodov, VL; Bugriĭ, EM; Chichkanov, GG; Kaverina, NV; Kryzhanovskiĭ, SA; Lyskovtsev, VV; Rodionov, AP; Tolmacheva, EA; Turilova, AI; Vititnova, MB,
)
0.13
"The relative bioavailability of a 200 mg film-coated tablet of [12C]moricizine."( Moricizine bioavailability via simultaneous, dual, stable isotope administration: bioequivalence implications.
Adams, MP; Barrett, JS; Mayersohn, M; Pieniaszek, HJ; Reinhart, RJ, 1999
)
1.98
"The quantitative structure-bioavailability relationship of 232 structurally diverse drugs was studied to evaluate the feasibility of constructing a predictive model for the human oral bioavailability of prospective new medicinal agents."( QSAR model for drug human oral bioavailability.
Topliss, JG; Yoshida, F, 2000
)
0.31

Dosage Studied

Moricizine HCl was titrated up to a maximum of 400 mg 3 times daily or 15 mg/kg daily, based on arrhythmia suppression and occurrence of side effects. Patients had plasma moricizine concentration determined over a dosing interval, and had standard 12-lead ECG and 24-hour ambulatory ECG recorded.

ExcerptRelevanceReference
"5 mg/kg/h infusion) and lidocaine (5 mg/kg loading dose, 4 mg/kg/h infusion) were dosed to achieve therapeutic concentrations."( Defibrillation energy requirements during moricizine and moricizine-lidocaine therapy.
Chow, M; Fan, C; Kluger, J; O'Rangers, EA; Ujhelyi, MR, 1992
)
0.55
" The suggested dosage is 600 to 900 mg per day in three divided doses."( Moricizine: pharmacodynamic, pharmacokinetic, and therapeutic profile of a new antiarrhythmic.
Maloney, JD; Vanerio, G,
)
1.57
" Thus, dynamic changes were observed for intraventricular conduction (fQRS, QRS) and ventricular repolarization (JTc) over the dosing interval."( Time course of moricizine's effect on signal-averaged and 12 lead electrocardiograms: insights into mechanism of action.
Giardina, EG; Steinberg, JS; Wechsler, ME, 1991
)
0.63
" It was concluded that moricizine follows first-order or linear pharmacokinetics after multiple dosing and exhibits dose proportional pharmacokinetics in the dosage-range studies."( Dose proportionality of moricizine after escalating multiple doses in healthy volunteers.
Benedek, IH; Garner, DM; Pieniaszek, HJ, 1991
)
0.9
"The chemistry, pharmacology, pharmacokinetics, clinical efficacy, adverse effects, and dosage of the Class I antiarrhythmic agent moricizine hydrochloride are reviewed."( Moricizine: a new class I antiarrhythmic.
Mann, HJ, 1990
)
1.93
" Ventricular function as assessed by echocardiography during drug dosing showed no significant changes from placebo."( Comparison of ethmozine to propranolol and the combination for ventricular arrhythmias.
Butman, SM; Gardin, JM; Knoll, ML, 1987
)
0.27
") 10(-5)/ms) were used to predict the time course of INa block in response to repeated depolarizations and the dose-response relationship of steady-state used-dependent block measured in independent experiments."( Use-dependent block of sodium current by ethmozin in voltage-clamped internally perfused canine cardiac Purkinje cells.
Alpert, LA; Fozzard, HA; Hanck, DA; Makielski, JC; Nesterenko, VV; Rosenshtraukh, LV; Sheets, MF; Undrovinas, AI, 1988
)
0.27
" Serious adverse reactions necessitate a change in antiarrhythmic therapy, as opposed to lowering drug dosage to an ineffective level."( Antiarrhythmic drug therapy. Recent advances and current status.
Somberg, J, 1985
)
0.27
" During a double-blind drug and dose selection phase, investigators were permitted to change drug or dosage to achieve greater than or equal to 70% suppression in VPC frequency and greater than 90% suppression of runs of VPC with the exception of patients assigned to placebo, who continued receiving it."( Effects of encainide, flecainide, imipramine and moricizine on ventricular arrhythmias during the year after acute myocardial infarction: the CAPS.
, 1988
)
0.53
" A dose-response relation between moricizine HCl and the percentage of reduction in frequency of benign or potentially lethal ventricular arrhythmias was documented."( Efficacy and tolerance of Ethmozine (moricizine HCl) in placebo-controlled trials.
Baker, BJ; Kennedy, HL; Mason, DT; Morganroth, J; Platt, ML; Pratt, CM; Singh, SN, 1987
)
0.82
" The dosage of moricizine HCl was 200 mg 3 times daily, and during 5 to 6 days was titrated up to a maximum of 400 mg 3 times daily or 15 mg/kg daily, based on arrhythmia suppression and occurrence of side effects."( Ethmozine (moricizine HCl) therapy for complex ventricular arrhythmias.
Hession, MJ; Lampert, S; Lown, B; Podrid, PJ, 1987
)
1.02
" Ethmozine dosing was repeated 15 days later after cimetidine, 300 mg four times a day for 7 days."( Cimetidine inhibition of ethmozine metabolism.
Biollaz, J; Shaheen, O; Wood, AJ, 1985
)
0.27
" There were five 7-day phases in which the first, third, and fifth were placebo dosing and the second and fourth were randomized as to moricizine dosage regimen (every 8 hours vs every 12 hours)."( Safety and efficacy of a twice-daily dosing regimen for moricizine (ethmozine).
Morganroth, J, 1985
)
0.72
" If side effects intervene that may cause continued therapy to be intolerable, changing the antiarrhythmic agent, as opposed to decreasing the dosage to an ineffective range, may be appropriate."( New directions in antiarrhythmic drug therapy.
Somberg, JC, 1984
)
0.27
" Although both drugs significantly reduced VPDs relative to placebo, ethmozine was a superior antiarrhythmic drug in ach9eving near-total abolition of VPDs (30% of patients), which was never observed during disopyramide dosing (p less than ."( Comparative effect of disopyramide and ethmozine in suppressing complex ventricular arrhythmias by use of a double-blind, placebo-controlled, longitudinal crossover design.
English, L; Francis, MJ; Kopelen, H; Mann, DE; Norton, HJ; Pratt, CM; Quinones, MA; Roberts, R; Taylor, AA; Young, JB, 1984
)
0.27
" During steady-state moricizine therapy, patients had plasma moricizine concentration determined over a dosing interval, and had standard 12-lead ECG and a 24-hour ambulatory ECG recorded."( Moricizine concentration to guide arrhythmia treatment: with attention to elderly patients.
Dolgopiatova, M; Giardina, EG; Sciacca, R; Wechsler, ME, 1994
)
2.05
" We conclude that the moricizine dose required for arrhythmia patients with hepatic disease should be lower, and perhaps, the dosing frequency should be less than in patients with normal liver function."( The effect of hepatic disease on the disposition of moricizine in humans.
Davidson, AF; Mayersohn, M; McEntegart, CM; Pieniaszek, HJ; Quon, CY; Sampliner, RE, 1994
)
0.85
"HCl was studied in 12 male volunteers dosed with 250 mg (300 microCi) 14C-radiolabelled drug."( Human moricizine metabolism. II. Quantification and pharmacokinetics of plasma and urinary metabolites.
Chaney, JE; Davidson, AF; Mayersohn, M; Pieniaszek, HJ; Robinson, CA; Shum, L, 1999
)
0.78
[information is derived through text-mining from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Roles (1)

RoleDescription
anti-arrhythmia drugA drug used for the treatment or prevention of cardiac arrhythmias. Anti-arrhythmia drugs may affect the polarisation-repolarisation phase of the action potential, its excitability or refractoriness, or impulse conduction or membrane responsiveness within cardiac fibres.
[role 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]

Drug Classes (3)

ClassDescription
phenothiazines
morpholinesAny compound containing morpholine as part of its structure.
carbamate esterAny ester of carbamic acid or its N-substituted derivatives.
[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 (33)

Potency Measurements

ProteinTaxonomyMeasurementAverage (µ)Min (ref.)Avg (ref.)Max (ref.)Bioassay(s)
Chain A, Beta-lactamaseEscherichia coli K-12Potency25.11890.044717.8581100.0000AID485341
glp-1 receptor, partialHomo sapiens (human)Potency7.94330.01846.806014.1254AID624417
hypoxia-inducible factor 1, alpha subunit (basic helix-loop-helix transcription factor)Homo sapiens (human)Potency1.58490.00137.762544.6684AID914; AID915
cytochrome P450 family 3 subfamily A polypeptide 4Homo sapiens (human)Potency2.45450.01237.983543.2770AID1645841
GVesicular stomatitis virusPotency30.90080.01238.964839.8107AID1645842
cytochrome P450 2D6Homo sapiens (human)Potency21.87610.00108.379861.1304AID1645840
euchromatic histone-lysine N-methyltransferase 2Homo sapiens (human)Potency0.89130.035520.977089.1251AID504332
gemininHomo sapiens (human)Potency32.64270.004611.374133.4983AID624296
peripheral myelin protein 22Rattus norvegicus (Norway rat)Potency0.08700.005612.367736.1254AID624032
cytochrome P450 3A4 isoform 1Homo sapiens (human)Potency5.01190.031610.279239.8107AID884; AID885
histone acetyltransferase KAT2A isoform 1Homo sapiens (human)Potency0.19950.251215.843239.8107AID504327
lamin isoform A-delta10Homo sapiens (human)Potency0.00040.891312.067628.1838AID1487
Gamma-aminobutyric acid receptor subunit piRattus norvegicus (Norway rat)Potency5.01191.000012.224831.6228AID885
Interferon betaHomo sapiens (human)Potency30.90080.00339.158239.8107AID1645842
HLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)Potency30.90080.01238.964839.8107AID1645842
Gamma-aminobutyric acid receptor subunit beta-1Rattus norvegicus (Norway rat)Potency5.01191.000012.224831.6228AID885
Gamma-aminobutyric acid receptor subunit deltaRattus norvegicus (Norway rat)Potency5.01191.000012.224831.6228AID885
Gamma-aminobutyric acid receptor subunit gamma-2Rattus norvegicus (Norway rat)Potency5.01191.000012.224831.6228AID885
Gamma-aminobutyric acid receptor subunit alpha-5Rattus norvegicus (Norway rat)Potency5.01191.000012.224831.6228AID885
Gamma-aminobutyric acid receptor subunit alpha-3Rattus norvegicus (Norway rat)Potency5.01191.000012.224831.6228AID885
Gamma-aminobutyric acid receptor subunit gamma-1Rattus norvegicus (Norway rat)Potency5.01191.000012.224831.6228AID885
Gamma-aminobutyric acid receptor subunit alpha-2Rattus norvegicus (Norway rat)Potency5.01191.000012.224831.6228AID885
Gamma-aminobutyric acid receptor subunit alpha-4Rattus norvegicus (Norway rat)Potency5.01191.000012.224831.6228AID885
Gamma-aminobutyric acid receptor subunit gamma-3Rattus norvegicus (Norway rat)Potency5.01191.000012.224831.6228AID885
Gamma-aminobutyric acid receptor subunit alpha-6Rattus norvegicus (Norway rat)Potency5.01191.000012.224831.6228AID885
Gamma-aminobutyric acid receptor subunit alpha-1Rattus norvegicus (Norway rat)Potency5.01191.000012.224831.6228AID885
Gamma-aminobutyric acid receptor subunit beta-3Rattus norvegicus (Norway rat)Potency5.01191.000012.224831.6228AID885
Guanine nucleotide-binding protein GHomo sapiens (human)Potency11.22021.995325.532750.1187AID624287
Gamma-aminobutyric acid receptor subunit beta-2Rattus norvegicus (Norway rat)Potency5.01191.000012.224831.6228AID885
GABA theta subunitRattus norvegicus (Norway rat)Potency5.01191.000012.224831.6228AID885
Inositol hexakisphosphate kinase 1Homo sapiens (human)Potency30.90080.01238.964839.8107AID1645842
Gamma-aminobutyric acid receptor subunit epsilonRattus norvegicus (Norway rat)Potency5.01191.000012.224831.6228AID885
cytochrome P450 2C9, partialHomo sapiens (human)Potency30.90080.01238.964839.8107AID1645842
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Biological Processes (50)

Processvia Protein(s)Taxonomy
cell surface receptor signaling pathway via JAK-STATInterferon betaHomo sapiens (human)
response to exogenous dsRNAInterferon betaHomo sapiens (human)
B cell activation involved in immune responseInterferon betaHomo sapiens (human)
cell surface receptor signaling pathwayInterferon betaHomo sapiens (human)
cell surface receptor signaling pathway via JAK-STATInterferon betaHomo sapiens (human)
response to virusInterferon betaHomo sapiens (human)
positive regulation of autophagyInterferon betaHomo sapiens (human)
cytokine-mediated signaling pathwayInterferon betaHomo sapiens (human)
natural killer cell activationInterferon betaHomo sapiens (human)
positive regulation of peptidyl-serine phosphorylation of STAT proteinInterferon betaHomo sapiens (human)
cellular response to interferon-betaInterferon betaHomo sapiens (human)
B cell proliferationInterferon betaHomo sapiens (human)
negative regulation of viral genome replicationInterferon betaHomo sapiens (human)
innate immune responseInterferon betaHomo sapiens (human)
positive regulation of innate immune responseInterferon betaHomo sapiens (human)
regulation of MHC class I biosynthetic processInterferon betaHomo sapiens (human)
negative regulation of T cell differentiationInterferon betaHomo sapiens (human)
positive regulation of transcription by RNA polymerase IIInterferon betaHomo sapiens (human)
defense response to virusInterferon betaHomo sapiens (human)
type I interferon-mediated signaling pathwayInterferon betaHomo sapiens (human)
neuron cellular homeostasisInterferon betaHomo sapiens (human)
cellular response to exogenous dsRNAInterferon betaHomo sapiens (human)
cellular response to virusInterferon betaHomo sapiens (human)
negative regulation of Lewy body formationInterferon betaHomo sapiens (human)
negative regulation of T-helper 2 cell cytokine productionInterferon betaHomo sapiens (human)
positive regulation of apoptotic signaling pathwayInterferon betaHomo sapiens (human)
response to exogenous dsRNAInterferon betaHomo sapiens (human)
B cell differentiationInterferon betaHomo sapiens (human)
natural killer cell activation involved in immune responseInterferon betaHomo sapiens (human)
adaptive immune responseInterferon betaHomo sapiens (human)
T cell activation involved in immune responseInterferon betaHomo sapiens (human)
humoral immune responseInterferon betaHomo sapiens (human)
positive regulation of T cell mediated cytotoxicityHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
adaptive immune responseHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
antigen processing and presentation of endogenous peptide antigen via MHC class I via ER pathway, TAP-independentHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
regulation of T cell anergyHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
defense responseHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
immune responseHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
detection of bacteriumHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
regulation of interleukin-12 productionHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
regulation of interleukin-6 productionHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
protection from natural killer cell mediated cytotoxicityHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
innate immune responseHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
regulation of dendritic cell differentiationHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
antigen processing and presentation of endogenous peptide antigen via MHC class IbHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
negative regulation of inflammatory response to antigenic stimulusGuanine nucleotide-binding protein GHomo sapiens (human)
renal water homeostasisGuanine nucleotide-binding protein GHomo sapiens (human)
G protein-coupled receptor signaling pathwayGuanine nucleotide-binding protein GHomo sapiens (human)
regulation of insulin secretionGuanine nucleotide-binding protein GHomo sapiens (human)
cellular response to glucagon stimulusGuanine nucleotide-binding protein GHomo sapiens (human)
inositol phosphate metabolic processInositol hexakisphosphate kinase 1Homo sapiens (human)
phosphatidylinositol phosphate biosynthetic processInositol hexakisphosphate kinase 1Homo sapiens (human)
negative regulation of cold-induced thermogenesisInositol hexakisphosphate kinase 1Homo sapiens (human)
inositol phosphate biosynthetic processInositol hexakisphosphate kinase 1Homo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Molecular Functions (20)

Processvia Protein(s)Taxonomy
cytokine activityInterferon betaHomo sapiens (human)
cytokine receptor bindingInterferon betaHomo sapiens (human)
type I interferon receptor bindingInterferon betaHomo sapiens (human)
protein bindingInterferon betaHomo sapiens (human)
chloramphenicol O-acetyltransferase activityInterferon betaHomo sapiens (human)
TAP bindingHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
signaling receptor bindingHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
protein bindingHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
peptide antigen bindingHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
TAP bindingHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
protein-folding chaperone bindingHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
G protein activityGuanine nucleotide-binding protein GHomo sapiens (human)
adenylate cyclase activator activityGuanine nucleotide-binding protein GHomo sapiens (human)
inositol-1,3,4,5,6-pentakisphosphate kinase activityInositol hexakisphosphate kinase 1Homo sapiens (human)
inositol hexakisphosphate kinase activityInositol hexakisphosphate kinase 1Homo sapiens (human)
inositol heptakisphosphate kinase activityInositol hexakisphosphate kinase 1Homo sapiens (human)
inositol hexakisphosphate 5-kinase activityInositol hexakisphosphate kinase 1Homo sapiens (human)
protein bindingInositol hexakisphosphate kinase 1Homo sapiens (human)
ATP bindingInositol hexakisphosphate kinase 1Homo sapiens (human)
inositol hexakisphosphate 1-kinase activityInositol hexakisphosphate kinase 1Homo sapiens (human)
inositol hexakisphosphate 3-kinase activityInositol hexakisphosphate kinase 1Homo sapiens (human)
inositol 5-diphosphate pentakisphosphate 5-kinase activityInositol hexakisphosphate kinase 1Homo sapiens (human)
inositol diphosphate tetrakisphosphate kinase activityInositol hexakisphosphate kinase 1Homo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Ceullar Components (22)

Processvia Protein(s)Taxonomy
extracellular spaceInterferon betaHomo sapiens (human)
extracellular regionInterferon betaHomo sapiens (human)
Golgi membraneHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
endoplasmic reticulumHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
Golgi apparatusHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
plasma membraneHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
cell surfaceHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
ER to Golgi transport vesicle membraneHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
membraneHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
secretory granule membraneHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
phagocytic vesicle membraneHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
early endosome membraneHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
recycling endosome membraneHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
extracellular exosomeHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
lumenal side of endoplasmic reticulum membraneHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
MHC class I protein complexHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
extracellular spaceHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
external side of plasma membraneHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
plasma membraneGamma-aminobutyric acid receptor subunit gamma-2Rattus norvegicus (Norway rat)
plasma membraneGamma-aminobutyric acid receptor subunit alpha-1Rattus norvegicus (Norway rat)
plasma membraneGuanine nucleotide-binding protein GHomo sapiens (human)
plasma membraneGamma-aminobutyric acid receptor subunit beta-2Rattus norvegicus (Norway rat)
fibrillar centerInositol hexakisphosphate kinase 1Homo sapiens (human)
nucleoplasmInositol hexakisphosphate kinase 1Homo sapiens (human)
cytosolInositol hexakisphosphate kinase 1Homo sapiens (human)
nucleusInositol hexakisphosphate kinase 1Homo sapiens (human)
cytoplasmInositol hexakisphosphate kinase 1Homo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Bioassays (110)

Assay IDTitleYearJournalArticle
AID1346459Human PAC1 receptor (VIP and PACAP receptors)2006Neuropharmacology, Nov, Volume: 51, Issue:6
A systematic comparison of intracellular cyclic AMP and calcium signalling highlights complexities in human VPAC/PAC receptor pharmacology.
AID1346454Human VPAC1 receptor (VIP and PACAP receptors)2006Neuropharmacology, Nov, Volume: 51, Issue:6
A systematic comparison of intracellular cyclic AMP and calcium signalling highlights complexities in human VPAC/PAC receptor pharmacology.
AID1346433Human VPAC2 receptor (VIP and PACAP receptors)2006Neuropharmacology, Nov, Volume: 51, Issue:6
A systematic comparison of intracellular cyclic AMP and calcium signalling highlights complexities in human VPAC/PAC receptor pharmacology.
AID1346433Human VPAC2 receptor (VIP and PACAP receptors)2002Diabetes, May, Volume: 51, Issue:5
A potent and highly selective VPAC2 agonist enhances glucose-induced insulin release and glucose disposal: a potential therapy for type 2 diabetes.
AID1346459Human PAC1 receptor (VIP and PACAP receptors)1999Journal of neuroendocrinology, Dec, Volume: 11, Issue:12
N-terminal splice variants of the type I PACAP receptor: isolation, characterization and ligand binding/selectivity determinants.
AID1346454Human VPAC1 receptor (VIP and PACAP receptors)
AID1346459Human PAC1 receptor (VIP and PACAP receptors)
AID1346435Rat PAC1 receptor (VIP and PACAP receptors)1995European journal of pharmacology, Feb-15, Volume: 288, Issue:3
Pharmacological properties of two recombinant splice variants of the PACAP type I receptor, transfected and stably expressed in CHO cells.
AID1346454Human VPAC1 receptor (VIP and PACAP receptors)1998Annals of the New York Academy of Sciences, Dec-11, Volume: 865Analogues of VIP, helodermin, and PACAP discriminate between rat and human VIP1 and VIP2 receptors.
AID1346434Rat VPAC1 receptor (VIP and PACAP receptors)1998Annals of the New York Academy of Sciences, Dec-11, Volume: 865Analogues of VIP, helodermin, and PACAP discriminate between rat and human VIP1 and VIP2 receptors.
AID1346433Human VPAC2 receptor (VIP and PACAP receptors)1998Annals of the New York Academy of Sciences, Dec-11, Volume: 865Analogues of VIP, helodermin, and PACAP discriminate between rat and human VIP1 and VIP2 receptors.
AID1346470Rat VPAC2 receptor (VIP and PACAP receptors)1998Annals of the New York Academy of Sciences, Dec-11, Volume: 865Analogues of VIP, helodermin, and PACAP discriminate between rat and human VIP1 and VIP2 receptors.
AID1346454Human VPAC1 receptor (VIP and PACAP receptors)1996European journal of pharmacology, Apr-29, Volume: 302, Issue:1-3
Stable expression of the recombinant human VIP1 receptor in clonal Chinese hamster ovary cells: pharmacological, functional and molecular properties.
AID1346433Human VPAC2 receptor (VIP and PACAP receptors)
AID1079934Highest frequency of acute liver toxicity observed during clinical trials, expressed as a percentage. [column '% AIGUE' in source]
AID588215FDA HLAED, alkaline phosphatase increase2004Current drug discovery technologies, Dec, Volume: 1, Issue:4
Assessment of the health effects of chemicals in humans: II. Construction of an adverse effects database for QSAR modeling.
AID1079935Cytolytic liver toxicity, either proven histopathologically or where the ratio of maximal ALT or AST activity above normal to that of Alkaline Phosphatase is > 5 (see ACUTE). Value is number of references indexed. [column 'CYTOL' in source]
AID625292Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) combined score2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID588219FDA HLAED, gamma-glutamyl transferase (GGT) increase2004Current drug discovery technologies, Dec, Volume: 1, Issue:4
Assessment of the health effects of chemicals in humans: II. Construction of an adverse effects database for QSAR modeling.
AID625291Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for liver function tests abnormal2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID588217FDA HLAED, serum glutamic pyruvic transaminase (SGPT) increase2004Current drug discovery technologies, Dec, Volume: 1, Issue:4
Assessment of the health effects of chemicals in humans: II. Construction of an adverse effects database for QSAR modeling.
AID28681Partition coefficient (logD6.5)2000Journal of medicinal chemistry, Jun-29, Volume: 43, Issue:13
QSAR model for drug human oral bioavailability.
AID29359Ionization constant (pKa)2000Journal of medicinal chemistry, Jun-29, Volume: 43, Issue:13
QSAR model for drug human oral bioavailability.
AID1079931Moderate liver toxicity, defined via clinical-chemistry results: ALT or AST serum activity 6 times the normal upper limit (N) or alkaline phosphatase serum activity of 1.7 N. Value is number of references indexed. [column 'BIOL' in source]
AID588218FDA HLAED, lactate dehydrogenase (LDH) increase2004Current drug discovery technologies, Dec, Volume: 1, Issue:4
Assessment of the health effects of chemicals in humans: II. Construction of an adverse effects database for QSAR modeling.
AID1079940Granulomatous liver disease, proven histopathologically. Value is number of references indexed. [column 'GRAN' in source]
AID625281Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for cholelithiasis2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID1474166Liver toxicity in human assessed as induction of drug-induced liver injury by measuring severity class index2016Drug discovery today, Apr, Volume: 21, Issue:4
DILIrank: the largest reference drug list ranked by the risk for developing drug-induced liver injury in humans.
AID1079933Acute liver toxicity defined via clinical observations and clear clinical-chemistry results: serum ALT or AST activity > 6 N or serum alkaline phosphatases activity > 1.7 N. This category includes cytolytic, choleostatic and mixed liver toxicity. Value is
AID625287Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for hepatomegaly2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID1079941Liver damage due to vascular disease: peliosis hepatitis, hepatic veno-occlusive disease, Budd-Chiari syndrome. Value is number of references indexed. [column 'VASC' in source]
AID1079942Steatosis, proven histopathologically. Value is number of references indexed. [column 'STEAT' in source]
AID588214FDA HLAED, liver enzyme composite activity2004Current drug discovery technologies, Dec, Volume: 1, Issue:4
Assessment of the health effects of chemicals in humans: II. Construction of an adverse effects database for QSAR modeling.
AID1079944Benign tumor, proven histopathologically. Value is number of references indexed. [column 'T.BEN' in source]
AID1079948Times to onset, minimal and maximal, observed in the indexed observations. [column 'DELAI' in source]
AID567091Drug absorption in human assessed as human intestinal absorption rate2011European journal of medicinal chemistry, Jan, Volume: 46, Issue:1
Prediction of drug intestinal absorption by new linear and non-linear QSPR.
AID1079936Choleostatic liver toxicity, either proven histopathologically or where the ratio of maximal ALT or AST activity above normal to that of Alkaline Phosphatase is < 2 (see ACUTE). Value is number of references indexed. [column 'CHOLE' in source]
AID625288Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for jaundice2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID1079949Proposed mechanism(s) of liver damage. [column 'MEC' in source]
AID1079946Presence of at least one case with successful reintroduction. [column 'REINT' in source]
AID1079943Malignant tumor, proven histopathologically. Value is number of references indexed. [column 'T.MAL' in source]
AID27167Delta logD (logD6.5 - logD7.4)2000Journal of medicinal chemistry, Jun-29, Volume: 43, Issue:13
QSAR model for drug human oral bioavailability.
AID1079947Comments (NB not yet translated). [column 'COMMENTAIRES' in source]
AID625290Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for liver fatty2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID1474167Liver toxicity in human assessed as induction of drug-induced liver injury by measuring verified drug-induced liver injury concern status2016Drug discovery today, Apr, Volume: 21, Issue:4
DILIrank: the largest reference drug list ranked by the risk for developing drug-induced liver injury in humans.
AID1079939Cirrhosis, proven histopathologically. Value is number of references indexed. [column 'CIRRH' in source]
AID625289Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for liver disease2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID625279Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for bilirubinemia2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID625285Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for hepatic necrosis2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID625282Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for cirrhosis2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID29812Oral bioavailability in human2000Journal of medicinal chemistry, Jun-29, Volume: 43, Issue:13
QSAR model for drug human oral bioavailability.
AID588216FDA HLAED, serum glutamic oxaloacetic transaminase (SGOT) increase2004Current drug discovery technologies, Dec, Volume: 1, Issue:4
Assessment of the health effects of chemicals in humans: II. Construction of an adverse effects database for QSAR modeling.
AID1079945Animal toxicity known. [column 'TOXIC' in source]
AID1079932Highest frequency of moderate liver toxicity observed during clinical trials, expressed as a percentage. [column '% BIOL' in source]
AID588220Literature-mined public compounds from Kruhlak et al phospholipidosis modelling dataset2008Toxicology mechanisms and methods, , Volume: 18, Issue:2-3
Development of a phospholipidosis database and predictive quantitative structure-activity relationship (QSAR) models.
AID625283Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for elevated liver function tests2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID625284Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for hepatic failure2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID1079938Chronic liver disease either proven histopathologically, or through a chonic elevation of serum amino-transferase activity after 6 months. Value is number of references indexed. [column 'CHRON' in source]
AID1079937Severe hepatitis, defined as possibly life-threatening liver failure or through clinical observations. Value is number of references indexed. [column 'MASS' in source]
AID625280Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for cholecystitis2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID625286Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for hepatitis2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID1460598Inhibition of NorA in Staphylococcus aureus SA1199B harboring GrlA A116E mutant assessed as inhibition of ethidium bromide efflux at 50 uM measured after 5 mins by fluorometric method relative to control2017Journal of medicinal chemistry, 02-23, Volume: 60, Issue:4
Pharmacophore-Based Repositioning of Approved Drugs as Novel Staphylococcus aureus NorA Efflux Pump Inhibitors.
AID588501High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Lethal Factor Protease, MLPCN compound set2010Current protocols in cytometry, Oct, Volume: Chapter 13Microsphere-based flow cytometry protease assays for use in protease activity detection and high-throughput screening.
AID588501High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Lethal Factor Protease, MLPCN 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.
AID588501High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Lethal Factor Protease, MLPCN 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.
AID588499High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain A protease, MLPCN compound set2010Current protocols in cytometry, Oct, Volume: Chapter 13Microsphere-based flow cytometry protease assays for use in protease activity detection and high-throughput screening.
AID588499High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain A protease, MLPCN 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.
AID588499High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain A protease, MLPCN 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.
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.
AID588497High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain F protease, MLPCN compound set2010Current protocols in cytometry, Oct, Volume: Chapter 13Microsphere-based flow cytometry protease assays for use in protease activity detection and high-throughput screening.
AID588497High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain F protease, MLPCN 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.
AID588497High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain F protease, MLPCN 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.
AID651635Viability Counterscreen for Primary qHTS for Inhibitors of ATXN expression
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.
AID1745845Primary qHTS for Inhibitors of ATXN expression
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.
AID1347091qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for SJ-GBM2 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
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.
AID1347407qHTS to identify inhibitors of the type 1 interferon - major histocompatibility complex class I in skeletal muscle: primary screen against the NCATS Pharmaceutical Collection2020ACS chemical biology, 07-17, Volume: 15, Issue:7
High-Throughput Screening to Identify Inhibitors of the Type I Interferon-Major Histocompatibility Complex Class I Pathway in Skeletal Muscle.
AID1296008Cytotoxic Profiling of Annotated Libraries Using Quantitative High-Throughput Screening2020SLAS discovery : advancing life sciences R & D, 01, Volume: 25, Issue:1
Cytotoxic Profiling of Annotated and Diverse Chemical Libraries Using Quantitative High-Throughput Screening.
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.
AID1347425Rhodamine-PBP qHTS Assay for Modulators of WT P53-Induced Phosphatase 1 (WIP1)2019The Journal of biological chemistry, 11-15, Volume: 294, Issue:46
Physiologically relevant orthogonal assays for the discovery of small-molecule modulators of WIP1 phosphatase in high-throughput screens.
AID1347102qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for Rh18 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347090qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for DAOY cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347092qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for A673 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347101qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for BT-12 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347424RapidFire Mass Spectrometry qHTS Assay for Modulators of WT P53-Induced Phosphatase 1 (WIP1)2019The Journal of biological chemistry, 11-15, Volume: 294, Issue:46
Physiologically relevant orthogonal assays for the discovery of small-molecule modulators of WIP1 phosphatase in high-throughput screens.
AID1347095qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for NB-EBc1 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347094qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for BT-37 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347104qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for RD cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347099qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for NB1643 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347107qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for Rh30 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347098qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for SK-N-SH cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347082qHTS for Inhibitors of the Functional Ribonucleoprotein Complex (vRNP) of Lassa (LASV) Arenavirus: LASV Primary Screen - GLuc reporter signal2020Antiviral research, 01, Volume: 173A cell-based, infectious-free, platform to identify inhibitors of lassa virus ribonucleoprotein (vRNP) activity.
AID1347100qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for LAN-5 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347086qHTS for Inhibitors of the Functional Ribonucleoprotein Complex (vRNP) of Lymphocytic Choriomeningitis Arenaviruses (LCMV): LCMV Primary Screen - GLuc reporter signal2020Antiviral research, 01, Volume: 173A cell-based, infectious-free, platform to identify inhibitors of lassa virus ribonucleoprotein (vRNP) activity.
AID1347096qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for U-2 OS cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347093qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for SK-N-MC cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347105qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for MG 63 (6-TG R) cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347108qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for Rh41 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347106qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for control Hh wild type fibroblast cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347089qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for TC32 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347103qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for OHS-50 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347083qHTS for Inhibitors of the Functional Ribonucleoprotein Complex (vRNP) of Lassa (LASV) Arenavirus: Viability assay - alamar blue signal for LASV Primary Screen2020Antiviral research, 01, Volume: 173A cell-based, infectious-free, platform to identify inhibitors of lassa virus ribonucleoprotein (vRNP) activity.
AID1347097qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for Saos-2 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1159607Screen for inhibitors of RMI FANCM (MM2) intereaction2016Journal of biomolecular screening, Jul, Volume: 21, Issue:6
A High-Throughput Screening Strategy to Identify Protein-Protein Interaction Inhibitors That Block the Fanconi Anemia DNA Repair Pathway.
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.
AID1794808Fluorescence-based screening to identify small molecule inhibitors of Plasmodium falciparum apicoplast DNA polymerase (Pf-apPOL).2014Journal of biomolecular screening, Jul, Volume: 19, Issue:6
A High-Throughput Assay to Identify Inhibitors of the Apicoplast DNA Polymerase from Plasmodium falciparum.
AID1794808Fluorescence-based screening to identify small molecule inhibitors of Plasmodium falciparum apicoplast DNA polymerase (Pf-apPOL).
[information is prepared from bioassay data collected from National Library of Medicine (NLM), extracted Dec-2023]

Research

Studies (344)

TimeframeStudies, This Drug (%)All Drugs %
pre-1990170 (49.42)18.7374
1990's139 (40.41)18.2507
2000's11 (3.20)29.6817
2010's16 (4.65)24.3611
2020's8 (2.33)2.80
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Market Indicators

Research Demand Index: 32.93

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 Index32.93 (24.57)
Research Supply Index6.11 (2.92)
Research Growth Index4.44 (4.65)
Search Engine Demand Index45.89 (26.88)
Search Engine Supply Index2.00 (0.95)

This Compound (32.93)

All Compounds (24.57)

Study Types

Publication TypeThis drug (%)All Drugs (%)
Trials0 (0.00%)5.53%
Trials85 (23.29%)5.53%
Reviews0 (0.00%)6.00%
Reviews34 (9.32%)6.00%
Case Studies0 (0.00%)4.05%
Case Studies14 (3.84%)4.05%
Observational0 (0.00%)0.25%
Observational0 (0.00%)0.25%
Other7 (100.00%)84.16%
Other232 (63.56%)84.16%
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Clinical Trials (3)

Trial Overview

TrialPhaseEnrollmentStudy TypeStart DateStatus
[NCT00000556]Phase 30 participants Interventional1995-03-31Completed
[NCT00000504]Phase 20 participants Interventional1982-09-30Completed
[NCT00000526]Phase 30 participants Interventional1986-08-31Completed
[information is prepared from clinicaltrials.gov, extracted Sep-2024]